Cardiovascular effects of vasopressors in halothane-anesthetized dogs before and after hemorrhage

Exogenously administered vasopressors (sympathomimetics) were evaluated in halothane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure (SAP), heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Dobutamine administered at the low dose before hemorrhage increased SAP and dP/dT. At the high and medium dose, dobutamine significantly increased CI, dP/dT, and SAP, with no significant change in HR or SVR. The medium dose of epinephrine was the most effective dose of epinephrine at increasing key variables (CI, SI, dP/dT). The response of CI and SI to this dose was not significantly different from the changes seen with high-dose administration of dobutamine. The dP/dT was significantly lower with epinephrine than with dobutamine, and SVR and HR were unchanged with epinephrine, except at the low dose, which decreased SVR.     

Comparative cardiovascular, analgesic, and sedative effects of medetomidine, medetomidine-hydromorphone, and medetomidine-butorphanol in dogs

OBJECTIVE: To compare sedative, analgesic, and cardiopulmonary effects after IV administration of medetomidine (20 microg/kg), medetomidine-hydromorphone (20 microg of medetomidine/kg and 0.1 mg of hydromorphone/kg), and medetomidine-butorphanol (20 microg of medetomidine/kg and 0.2 mg of butorphanol tartrate/kg) in dogs. ANIMALS: 6 dogs healthy mixed-breed dogs. PROCEDURE: Instruments were surgically inserted, and heart rate (HR), respiratory rate (RR), systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), mean pulmonary arterial pressure (MPAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), core body temperature, and cardiac output (CO) were measured 0, 5, 10, 15, 30, 45, and 60 minutes after injection. Cardiac index (CI), stroke volume (SV), stroke index (SI), systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR) were calculated. Arterial samples for blood gas analysis were collected 0, 15, and 45 minutes after injection. Intensity of analgesia, degree of sedation, and degree of muscle relaxation were evaluated at aforementioned time points and 75, 90, 120, 150, 180, and 210 minutes after injection. RESULTS: Administration of medetomidine, medetomidine-hydromorphone, and medetomidine-butorphanol was associated with increases in SAP, MAP, DAP, MPAP, PCWP, CVP, SVR, PVR, core body temperature, and PaCO2 and decreases in HR, CO, CI, SV, SI, RR, pH, and PaO2. Clinically important differences were not detected among treatments. Medetomidine-hydromorphone and medetomidine-butorphanol provided a longer duration of sedation and better quality of analgesia, compared with medetomidine alone. CONCLUSIONS AND CLINICAL RELEVANCE: Medetomidine-hydromorphone or medetomidine-butorphanol is associated with improved analgesia and sedation but has cardiopulmonary effects comparable to those for medetomidine alone.     

Noninvasive estimation of cardiac systolic function using continuous-wave Doppler echocardiography in dogs with experimental mitral regurgitation

OBJECTIVE: To evaluate the feasibility of noninvasive estimation of cardiac systolic function using transthoracic continuous-wave Doppler echocardiography in dogs with mitral regurgitation. PROCEDURE: Seven mongrel dogs with experimental mitral regurgitation were used. Left ventriculography and measurement of pulmonary capillary wedge pressure were performed under inhalational anaesthesia. A micromanometer-tipped catheter was placed into the left ventricle and transthoracic echocardiography was carried out. The peak rate of left ventricular pressure rise (peak dP/dt) was derived simultaneously by continuous-wave Doppler and manometer measurements. The Doppler-derived dP/dt was compared with the catheter-measured peak dP/dt in the dogs. RESULTS: Classification of the severity of mitral regurgitation in the dogs was as follows: 1+, 2 dogs; 2+, 1 dog; 3+, 2 dogs; 4+, 1 dog; and not examined, 1 dog. We were able to derive dP/dt from the transthoracic continuous-wave Doppler echocardiography in all dogs. Doppler-derived dP/dt had a significant correlation with the catheter-measured peak dP/dt (r = 0.90, P < 0.0001). CONCLUSION: It was demonstrated that transthoracic continuous-wave Doppler echocardiography is a feasible method of noninvasive estimation of cardiac systolic function in dogs with experimental mitral regurgitation and may have clinical usefulness in canine patients with spontaneous mitral regurgitation.     

Use of right ventricular pressure increase rate to evaluate cardiac contractility in horses

OBJECTIVE: To establish reference values for right ventricular maximal rate of increase in pressure (dP/dt(max)) in horses and determine the usefulness of this variable to evaluate cardiac contractility. ANIMALS: 15 crossbred horses, 3 to 20 years old. PROCEDURE: Cardiac catheterization was performed, using a high-fidelity catheter tip micromanometer, to determine right ventricular dP/dt(max). The following mathematic corrections were made: for preload, (dP/dt(max))/instantaneous total pressure, (dP/dt(max))/instantaneous developed pressure, and (dP/dt(max))/end diastolic pressure; for afterload, (dP/dtCPIP)/common peak isovolumic pressure. Wedge pressure was measured simultaneously, using a Swan-Ganz catheter. A negative inotropic drug, detomidine hydrochloride, was administered to 6 horses to examine the effect of the negative inotropic drug on right ventricular dP/dt(max) and derived variables. RESULTS: The mean right ventricular dP/dt(max) was 477 (+/- 84.1) mm Hg/s in 15 horses. A 40% decrease in dP/dt(max) was found for 30 minutes after detomidine administration. Variables that correct for preload and afterload were influenced similarly. Detomidine administration also caused a 24% increase in mean wedge pressure, probably indicating reduced left-sided cardiac contractility. CONCLUSIONS AND CLINICAL RELEVANCE: Right ventricular dP/dt(max) may be a useful clinical variable for determining acute changes in cardiac contractility in horses.     

Noninvasive estimation of cardiac systolic function using continuous-wave Doppler echocardiography in dogs with experimental mitral regurgitation

Objective To evaluate the feasibility of noninvasive estimation of cardiac systolic function using transthoracic continuous-wave Doppler echocardiography in dogs with mitral regurgitation.
Procedure Seven mongrel dogs with experimental mitral regurgitation were used. Left ventriculography and measurement of pulmonary capillary wedge pressure were performed under inhalational anaesthesia. A micromanometer-tipped catheter was placed into the left ventricle and transthoracic echocardiography was carried out. The peak rate of left ventricular pressure rise (peak dP/dt) was derived simultaneously by continuous-wave Doppler and manometer measurements. The Doppler-derived dP/dt was compared with the catheter-measured peak dP/dt in the dogs.
Results Classification of the severity of mitral regurgitation in the dogs was as follows: 1+, 2 dogs; 2+, 1 dog; 3+, 2 dogs; 4+, 1 dog; and not examined, 1 dog. We were able to derive dP/dt from the transthoracic continuous-wave Doppler echocar-diography in all dogs. Doppler-derived dP/dt had a significant correlation with the catheter-measured peak dP/dt (r = 0.90, P < 0.0001).
Conclusion It was demonstrated that transthoracic continuous-wave Doppler echocardiography is a feasible method of noninvasive estimation of cardiac systolic function in dogs with experimental mitral regurgitation and may have clinical usefulness in canine patients with spontaneous mitral regurgitation.     

Cardiovascular effects of desflurane following acute hemorrhage in dogs

Objective: To determine the cardiovascular effects of desflurane in dogs following acute hemorrhage. Design: Experimental study. Animals: Eight mix breed dogs. Interventions: Hemorrhage was induced by withdrawal of blood until mean arterial pressure (MAP) dropped to 60 mmHg in conscious dogs. Blood pressure was maintained at 60 mmHg for 1 hour by further removal or replacement of blood. Desflurane was delivered by facemask until endotracheal intubation could be performed and a desflurane expiratory end‐tidal concentration of 10.5 V% was maintained. Measurements and main results: Systolic, diastolic, and mean arterial blood pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), stroke volume (SV), cardiac index (CI), systemic vascular resistance (SVR), heart rate (HR), respiratory rate (RR), partial pressure of carbon dioxide in arterial blood (PaCO₂), and arterial pH were recorded before and 60 minutes after hemorrhage, and 5, 15, 30, 45 and 60 minutes after intubation. Sixty minutes after hemorrhage, SAP, DAP, MAP, CVP, CO, CI, SV, PaCO₂, and arterial pH decreased, and HR and RR increased when compared with baselines values. Immediately after intubation, MAP and arterial pH decreased, and PaCO₂ increased. Fifteen minutes after intubation SAP, DAP, MAP, arterial pH, and SVR decreased. At 30 and 45 minutes, MAP and DAP remained decreased and PaCO₂ increased, compared with values measured after hemorrhage. Arterial pH increased after 30 minutes of desflurane administration compared with values measured 5 minutes after intubation. Conclusions: Desflurane induced significant changes in blood pressure and arterial pH when administered to dogs following acute hemorrhage.     

Assessment of longitudinal tissue Doppler imaging of the left ventricular septum and free wall as an indicator of left ventricular systolic function in dogs

OBJECTIVE: To evaluate tissue Doppler imaging (TDI) of the left ventricular (LV) free wall (FW) and ventricular septum (VS) as an indicator of LV systolic function in dogs. ANIMALS: 7 healthy Beagles. PROCEDURES: Doses of dobutamine (5 and 10 microg/kg/min) and esmolol (50 and 100 microg/kg/min) were infused into the LV of each dog. With each dose, heart rate; myocardial performance index (MPI); transmitral inflow and ejection time (determined via pulsed-wave Doppler [PWD] echocardiography); and FW and VS velocities of the mitral valve annulus (determined via TDI during systole [S'], early diastole [E'], and late diastole [A']) were assessed. RESULTS: With each dose, dobutamine significantly increased heart rate and the first derivatives of LV pressure (+dP/dt and -dP/dt), whereas esmolol significantly decreased the +dP/dt and -dP/dt values, compared with baseline. Esmolol (100 microg/kg/min) significantly decreased the VS-TDI-derived S' velocity and FW-TDI-derived E' velocity; dobutamine significantly increased transmitral inflow and TDI velocities. Regression coefficient between VS-TDI-derived S' velocity and +dP/dt was higher than that between FW-TDI-derived S' velocity and +dP/dt. Compared with baseline, the PWD- and VS-TDI-derived MPI were significantly decreased by dobutamine and significantly increased by esmolol at each dose. Values of FW-TDI-derived MPI were higher than values derived via the other techniques. Correlation between +dP/dt and VS-TDI-derived MPI was greater than that between +dP/dt and FW-TDI- or PWD-derived MPI. CONCLUSIONS AND CLINICAL RELEVANCE: In healthy dogs, the VS-TDI-derived S' velocity and MPI appear to be reliable assessments for evaluating LV systolic function.     

Hemodynamic Effects of Intravenous Midazolam-Xylazine-Butorphanol in Dogs

The hemodynamic effects of a mixture of midazolam (1.0 mg/kg), xylazine (0.44 mg/kg), and butorphanol (0.1 mg/kg) were evaluated in six adult dogs. The dogs were anesthetized with isoflurane for instrumentation. As the dogs returned to consciousness, baseline values were recorded and the midazolam-xylazine-butorphanol mixture and glycopyrrolate (0.01 mg/kg) were administered intravenously (IV). Hemodynamic data were recorded 3, 10, 20, 30, 40, 50, and 60 minutes after injection. Mean arterial pressure (AP), mean pulmonary arterial pressure (PAP), heart rate (HR), rate-pressure product (RPP), mean pulmonary capillary wedge pressure (PCWP), systemic vascular resistance (SVR), and right ventricular stroke work index (RVSWI) were increased significantly above baseline values. Cardiac output (CO), stroke volume (SV), cardiac index (CI), stroke index (SI), mean central venous pressure (CVP), and left ventricular stroke work index (LVSWI) were decreased significantly below baseline values. When administered IV at the dosages used in this study, midazolam-xylazine-butorphanol-glycopyrrolate induced profound acute alterations in several critical hemodynamic variables.     

The effects of a hemoglobin-based oxygen carrier (HBOC-301) on left ventricular systolic function in anesthetized dogs

OBJECTIVE: To evaluate the effects of a hemoglobin-based oxygen carrier (HBOC-301) on left ventricular preload, afterload, contractility, and ventriculo-arterial coupling in anesthetized dogs. STUDY DESIGN: A prospective experimental study. ANIMALS: Seven adult male dogs weighing 2.3 to 2.7 kg. METHODS: The study was performed on intact, closed-chest, chloralose-anesthetized dogs. Heart rate, left ventricular end-systolic and end-diastolic volume and pressure, cardiac output, stroke volume, blood resistivity, mean arterial pressure (MAP), dP/dtmax, end-systolic elastance (Ees), systemic vascular resistance (SVR), effective arterial elastance (Ea), left ventricular-arterial coupling (Ees/Ea), and myocardial oxygen consumption (MVO2) were determined during a 90-minute infusion of 30 mL/kg (20 mL/kg/h) of HBOC-301 and for 90 minutes thereafter. RESULTS: The administration of HBOC-301 significantly decreased packed cell volume, blood resistivity, heart rate, cardiac output, and dP/dtmax and significantly increased left ventricular end-diastolic and end-systolic pressure, MAP, and SVR. The Ea, Ees, Ees/Ea and MVO2 did not change. CONCLUSIONS: HBOC-301 produced insignificant changes in load independent indexes of cardiac performance (Ees, E, Ees/Ea) in anesthetized dogs. The collective directional changes in these variables, however, in conjunction with significant increases in SVR were most likely responsible for a decrease in cardiac output. Increases in SVR and the volume load (30 mL/kg) contributed to increases in left ventricular end-diastolic pressure. CLINICAL RELEVANCE: HBOC-301 infusion should be monitored and administered cautiously to dogs with poor ventricular function.     

Influence of sotalol on the time constant of isovolumic left ventricular relaxation in anesthetized dogs.

OBJECTIVE: To determine the effects of various doses of sotalol on myocardial relaxation in healthy dogs. ANIMALS: 12 healthy adult mixed-breed dogs anesthetized with thiopental and alpha-chloralose. PROCEDURES: Left ventricular pressure (LVP), aortic pressure, and aortic flow velocity were measured. The time constant of isovolumic relaxation (tau) was determined by means of linear regression of the natural logarithm of LVP and by means of direct measurement from the LVP-versus-time curve. Sotalol was administered IV at cumulative doses of 1, 2, 4, and 8 mg/kg to 6 dogs; the other 6 were used as controls. Mean systolic aortic pressure was used to assess afterload, and maximal rate of increase in LVP versus time (dP/dt) was used as an index of contractility. RESULTS: After administration of the first dose of sotalol, tau was increased significantly, and maximum dP/dt was decreased significantly, compared with baseline values. Administration of additional doses of sotalol did not result in any additional change in tau, but maximum dP/dt increased, and maximum dP/dt after administration of the final dose of sotalol was significantly higher than maximum dP/dt after administration of the first dose. There were no significant changes in mean systolic aortic pressure. CONCLUSIONS AND CLINICAL RELEVANCE: In healthy dogs, sotalol did not have any negative effect on myocardial relaxation beyond those attributable to its beta-blocking properties, despite an increase in intracellular ionized calcium concentration, as suggested by an increase in maximum dP/dt after an initial decrease.     

Cardiovascular effects of vasopressors in isoflurane-anesthetized dogs before and after hemorrhage

Exogenously administered vasopressors (sympathomimetics) were evaluated in isoflurane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and isoflurane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure, heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Before hemorrhage, administration of high doses of dobutamine and medium and high doses of epinephrine were equally effective at increasing CI and SI. The dP/dT was increased to the greatest degree by administration of high doses of dobutamine. Administration of the low dose of dobutamine increased dP/dT, whereas administration of the low dose of epinephrine increased CI, HR, and SI, and decreased SVR. The HR and SVR were not increased by administration of any dose of dobutamine or of the medium and high doses of epinephrine. However, methoxamine increased SVR and decreased HR. Methoxamine decreased CI, SI, and dP/dT, but increased systemic arterial pressure to the same degree as that attributed to administration of high doses of dobutamine and epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of 2.0% end-tidal isoflurane with and without atropine prior to dexmedetomidine administration on cardiovascular variables in dogs

The purpose of this study was to determine the cardiovascular effects of 2.0% end‐tidal isoflurane in dogs administered dexmedetomidine (DEX). Using a randomized crossover design and allowing at least 2 weeks between treatments 12 adult hound dogs of either sex weighing 22 ± 1.7 SD kg were anesthetized by face mask administration of either sevoflurane or isoflurane to facilitate instrumentation prior to administration of treatment drugs. Dogs were intubated and instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP) and diastolic (DAP) arterial pressures, mean pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), and cardiac output (CO) via thermodilution using 5 mL of 5% dextrose, and recording the average of three replicate measurements. Cardiac index (CI) and systemic (SVR) and pulmonary vascular resistances were calculated. Following completion of instrumentation, dogs were allowed to recover for 40 minutes. After collection of baseline data, dogs were administered one of four treatments at T‐10 minutes prior to injection of DEX (500? g M^–2 IM): 1) saline (SAL); 2) atropine [ATR, 0.02 (n = 6) or 0.04 (n = 6) mg kg^–1 IM]; 3) ISO (2.0% end tidal concentration); or 4) ISO + ATR. Cardiovascular data were collected at T‐20 and T‐5 minutes prior to administration of DEX, and at 5, 10 , 20, 30, 40, and 60 min following DEX. Data were analyzed using anova for repeated measures with post‐hoc differences between means identified using Bonferroni's method (p < 0.05). Differences in ATR dose were not found to be significant and thus results for ATR dose groups were pooled. Administration of SAL (dexmedetomidine alone) was associated with decreases in HR and CO and increases in SAP, MAP, DAP, CVP, and SVR. Administration of ATR was associated with an increase in HR and CO compared with SAL. Administration of ISO was associated with an increase in HR and a decrease in SVR, MAP and CVP compared with SAL. Administration of ISO + ATR was associated with effects similar to that of ISO or ATR alone. We conclude that administration of ISO reduces the increase in SVR associated with administration of DEX and does not adversely affect CO.     

Effects of sodium nitroprusside after load reduction and/or atropine pre-treatment prior to dexmedetomidine administration on cardiovascular variables in dogs

The purpose of this study was to determine the cardiovascular effects of sodium nitroprusside (SNP)‐induced after load reduction in dogs administered dexmedetomidine (DEX). Using a randomized crossover design and allowing at least 2 weeks between treatments 12 adult hound dogs of either sex weighing 22 ± 1.7 SD kg were anesthetized by face mask administration of 2.9% ET sevoflurane to facilitate instrumentation prior to administration of treatment drugs. Dogs were intubated and instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP) and diastolic (DAP) arterial pressures, mean pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), and cardiac output (CO). Systemic (SVR) and pulmonary vascular resistances were calculated. Following completion of instrumentation dogs were allowed to recover for 40 minutes. After collection of baseline data, dogs were administered one of four treatments at T–10 minutes prior to injection of DEX (500? g M^–2 IM): 1) saline (SAL); 2) atropine (ATR, 0.02 [n = 6] or 0.04 [n = 6] mg kg^–1 IM); 3) SAL + SNP (infused at 1–10 ?g kg^–1 minute^–1, IV as needed to maintain MAP between 90–110 mm Hg; or 4) ATR + SNP. Cardiovascular data were collected at T‐20 minutes prior to administration of DEX, T‐5 and at 5, 10, 20, 30, 40, and 60 minutes following DEX. Data were analyzed using anova for repeated measures with post hoc differences between means identified using Bonferroni's method (p < 0.05). Differences in ATR dose were not found to be significant and thus results for ATR dose groups were pooled. Administration of SAL (dexmedetomidine alone) was associated with decreases in HR and CO and increases in SAP, MAP, DAP, CVP, and SVR. Administration of ATR was associated with an increase in HR and CO compared with SAL. Administration of SNP was associated with an increase in HR and CO and a decrease in SVR, MAP and CVP compared with SAL. Administration of SNP + ATR was associated with effects similar to that of SNP or ATR alone and resulted in an additive increase in CO. We conclude that SNP‐induced afterload reduction with or without atropine is effective in mitigating DEX‐induced impairment of cardiovascular function.     

Effects of naloxone in treating hemorrhagic shock in dogs with maintained baroreceptor responsiveness

The efficacy of treating hemorrhagic shock with naloxone in conjunction with fluids, compared with fluid therapy alone, was studied. Previously instrumented dogs were anesthetized with 0.04 mg of fentanyl/kg + 2.2 mg of droperidol/kg and pentobarbital sodium (to effect). Blood was withdrawn from each animal to achieve and maintain a mean arterial blood pressure of 40 to 50 mm of Hg for the first 2 hours of the experiment (t = 0 to 120 minutes). At t = 120 minutes, IV fluid administration was begun (all dogs) and continued for 1 hour (lactated Ringer's solution at a dosage of 70 ml/kg/hr). Hypothermia was corrected. Control dogs were given no other treatment. Dogs in the naloxone plus fluids group were given an IV bolus of naloxone (1 mg/kg) at t = 120 minutes and 1 mg of naloxone/kg/hr in the fluids from t = 120 to t = 180 minutes. Treatment (either naloxone plus fluids or fluids alone) was stopped at t = 180 minutes, and measuring of response was continued for an additional hour (posttherapeutic period). Significant differences were not seen in mean arterial pressures, left ventricular peak systolic pressures, dP/dt max, time constant T (a measure of left ventricular elasticity), and mean pulmonary arterial pressures between the dogs given naloxone and fluid therapy and those given fluid therapy alone. All dogs in both groups survived the procedure.     

The Effects of Medetomidine on Cardiac Contractility in Autonomically Blocked Dogs

The effects of medetomidine on load-dependent and relatively load-independent indices of left ventricular contractility and hemodynamics were studied in 8 chloralose-anesthetized, autonomic-blocked dogs. Left ventricular contractility was assessed by the maximum rate of increase in pressure (dP/dt_max), the slope of the end-systolic pressure volume relationship (Ees), preload recruitable stroke work (PRSW), and dP/dt_max-end-diastolic volume relation (SdPV). Dogs received 5 or 10 μg/kg of medetomidine IV. The dP/dt_max decreased significantly 30 minutes after both doses of medetomidine. The Ees did not change. Both SdPV and PRSW increased 5 minutes after both doses of medetomidine. Mean arterial pressure, left-ventricular end-diastolic and end-systolic pressures, peripheral vascular resistance and effective arterial elastance increased 5 minutes after both doses of medetomidine. Stroke volume, cardiac output, and stroke work decreased 5 minutes after medetomidine administration. End-diastolic volume did not change. End-systolic volume increased but the difference was not significant. Our study suggests that medetomidine increases inotropy and vascular resistance in autonomic-blocked dogs and that both ventricular and vascular responses to pharmacological manipulation must be considered for a complete assessment of the inotropic effects of a drug.     

Effect of cardiac arrhythmia on left ventricular and aortic blood pressure parameters in the horse

Transaortic blood pressures were recorded in seven horses using catheter mounted transducers during various types of supraventricular arrhythmia. Changes in left ventricular (LV) and aortic (Ao) pulse contours were associated with variation in pulse interval (PI). When PI lengthened there was a rise in LV end diastolic pressure (LVEDP) associated with a prolonged filling time. In contrast, a long PI resulted in a reduced end diastolic Ao pressure (AoEDP) due to a prolonged arterial 'run off'. LVdP/dt max representing the peak rate of rise of pressure during the isovolumic contraction period was not consistently affected by changes in PI. Stepwise linear regression was used to examine the simultaneous relationships of a number of variables derived from the LV and Ao contours. Peak LV pressure (LVPp) was directly related to AoEDP (seven of seven horses) and LVEDP (four of seven). Ao systolic pulse pressure (SPP) was directly related to LVEDP (four of seven) and inversely related to AoEDP (three of seven). Neither LVPp nor SPP were consistently related to LVdP/dt max. The peak positive gradient between LV and Ao pressures was inversely related to AoEDP (six of seven) and directly related to LVEDP and LVdP/dt max (three of seven). The peak rate of rise of the Ao pressure contour during ejection (AodP/dt max) was inversely related to AoEDP (seven of seven) and directly related to LVEDP (four of seven). It was also directly related to LVdP/dt max in four horses but was inversely related in one. The peak rate of fall of the LV pressure contour during relaxation (-LVdP/dt max) was directly related to LVPp (five of seven).     

Modification of cardiopulmonary and intestinal motility effects of xylazine with glycopyrrolate in horses.

Xylazine (XYL) administration in horses is accompanied by significant cardiovascular depression characterized by a 25-35% decrease in cardiac output (CO) which is likely to compromise tissue oxygen delivery (DO2), and usually vagally mediated bradycardia is an important cause of this reduced cardiovascular performance. To examine the possible benefit of preventing the bradycardiac response, 6 healthy horses were treated with intravenous (IV) saline (SAL) or 2.5 micrograms/kg glycopyrrolate (GLY) in a blinded, randomized, crossover trial. Fifteen minutes later, 1 mg/kg XYL was administered IV and systolic, diastolic and mean blood pressures (SBP, DBP, and MBP, respectively), central venous pressure (CVP), mean pulmonary artery pressure, heart rate (HR), CO, and arterial and mixed venous blood gases were measured at the following times: baseline, 2, 5, and 10 min post-SAL or GLY; and 2, 5, 10, 15, 30, 45 and 60 min post-XYL. Determination of cardiac index (CI), stroke index (SI), left ventricular work, systemic vascular resistance (SVR), DO2, oxygen uptake, and oxygen extraction ratio were made at the same time. Gastrointestinal (GI) motility was evaluated by four-quadrant auscultation for 24 h post-XYL. Statistical analysis of continuous variables was carried out using ANOVA for repeated measures and Wilcoxon's rank-sum test for non-parametric data. In GLY treated horses, HR, SBP, MBP, DBP, CI, DO2 and mixed venous oxygen tension were significantly higher up to 30 min after XYL (P < or = 0.02) while CVP and SI were significantly lower 2 and 5 min post-XYL, respectively. In both groups, GI motility as assessed by auscultation was virtually abolished for an hour, with a non-significant tendency for the decrease in motility to last longer in the GLY/XYL group. None of the treated horses developed abdominal discomfort. No significant difference was observed in the other variables. The study shows that 2.5 micrograms/kg GLY premedication reduces the cardiovascular depression caused by 1 mg/kg XYL, without adversely affecting GI motility.     

Some physiological and biochemical effects of intravenous fluid administration during halothane anaesthesia in the dog

Six dogs with previously implanted arterial, central venous, pulmonary arterial and left atrial catheters received halothane anaesthesia, and halothane anaesthesia plus administration of a balanced electrolyte solution given over one hour, in a cross-over experiment. Parameters measured included temperature, heart rate (HR), respiratory rate (f), arterial and mixed venous blood-gases and acid-base parameters, mean arterial pressure ( AP ), mean pulmonary artery pressure ( PAP ), mean left atrial pressure ( LAP ), mean central venous pressure ( CVP ), packed cell volume (PCV), total plasma protein (TPP), plasma sodium, potassium and chloride concentrations, and urinary sodium and potassium concentrations.
During halothane anaesthesia there were significant decreases in AP , PCV, TPP, f, and significant increases in arterial and mixed venous oxygen, and glucose concentrations, when compared with conscious control values. When intravenous fluid was administered during anaesthesia, there were significant decreases in temperature, AP , PCV and TPP, with significant increases in PAP , CVP and f, when compared with values during anaesthesia alone. After one hour recovery period from anaesthesia, dogs receiving intravenous fluids had significantly decreased PaO₂ values and significantly increased pH when compared with anaesthesia alone. There was an average urinary excretion of 7 mmol of sodium and 5 mmol of potassium during anaesthesia, and 36 mmol of sodium and 8 mmol potassium during fluid administration.     

Cardiopulmonary effects of medetomidine, oxymorphone, or butorphanol in selegiline-treated dogs

OBJECTIVES: To determine if chronic selegiline HCl administration affects the cardiopulmonary response to medetomidine, oxymorphone, or butorphanol in dogs. STUDY DESIGN: Prospective randomized experimental study. ANIMALS: Twenty-eight adult, random source, hound dogs weighing 21-33 kg. METHODS: Dogs were assigned to the following treatment groups: selegiline + medetomidine (MED; n = 6); placebo + MED (n = 6), selegiline + oxymorphone (OXY; n = 6); placebo + OXY (n = 6); selegiline + butorphanol (BUT; n = 7) or placebo + BUT (n = 6). Nine dogs were treated with two of the three pre-medicants. Dogs were treated with selegiline (1 mg kg(-1) PO, q 24 hours) or placebo for at least 44 days prior to pre-medicant administration. On the day of the experiment, arterial blood for blood gas analysis, blood pressure measurements, ECG, cardiac ultrasound (mM-mode, 2-D, and continuous wave Doppler), and behavioral observations were obtained by blinded observers. An IV injection of MED (750 micro g m(-2)), OXY (0.1 mg kg(-1)) or BUT (0.4 mg kg(-1)) was given. Cardiopulmonary and behavioral data were collected at 1, 2, 5, 15, 30, and 60 minutes after injection. RESULTS: Selegiline did not modify responses to any of the pre-medicant drugs. Medetomidine caused a significant decrease in heart rate (HR), cardiac output (CO), and fractional shortening (FS). Mean arterial pressure (MAP), systemic vascular resistance (SVR), and central venous pressure (CVP) were increased. Level of consciousness and resistance to restraint were both decreased. Oxymorphone did not affect MAP, CO, CVP, or SVR, but RR and PaCO(2) were increased. Level of consciousness and resistance to restraint were decreased. BUT decreased heart rate at 1 and 5 minutes. All other cardiovascular parameters were unchanged. BUT administration was associated with decreased arterial pH and increased PaCO(2). BUT decreased level of consciousness and resistance to restraint. CONCLUSIONS AND CLINICAL RELEVANCE: Although pre-medicants themselves altered cardiopulmonary and behavioral function, selegiline did not affect the response to medetomidine, oxymorphone, or butorphanol in this group of normal dogs.     

Inotropic mechanisms of dopexamine hydrochloride in horses.

Mechanisms responsible for the positive inotropic effects of dopexamine were investigated in 8 halothane-anesthetized horses. The hemodynamic effects of increasing infusions of dopexamine (5, 10, 15 micrograms/kg of body weight/min) were determined before and after sequential administration of specific antagonists. Using glycopyrrolate and chlorisondamine, and atenolol and ICI 118,551, muscarinic and nicotinic ganglionic, and beta 1, and beta 2-adrenergic receptor blockade, respectively, was induced. Dopexamine infusions induced increase in heart rate, cardiac output, systolic and mean arterial blood pressure, and maximal rate of left ventricular pressure development (+dP/dtmax). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and +dP/dtmax responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. beta 1-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and +dP/dtmax from baseline values and markedly reduced the response to dopexamine infusion. beta 2-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on +dP/dtmax. These data indicate that baroreflex activity, beta 1- and beta 2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.