Cardiovascular and respiratory effects of propofol administration in hypovolemic dogs.

Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 6 mg of propofol/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.     

Cardiovascular and respiratory effects of three rapidly acting barbiturates in dogs

The cardiovascular and respiratory effects of 3 rapidly acting barbiturates, thiopental sodium, thiamylal sodium, and methohexital sodium, were studied in dogs from completion of injection until 12.5 minutes after injection. The doses administered were 19.4 mg of thiopental/kg of body weight, 18.4 mg of thiamylal/kg, and 9.7 mg of methohexital/kg, which were chosen as equipotent doses necessary to inhibit the laryngoscopic reflex in 50% of the population. To determine the cardiovascular and respiratory effects for each drug, the values at each measurement time following injection were compared with baseline values (T0). At the 15- and 30-second measurement times following thiopental administration, stroke volume (SV) decreased; heart rate (HR), left atrial pressure, and mean pulmonary arterial pressure increased; and cardiac index (CI), myocardial contractility, and systemic and pulmonary vascular resistances were not different from baseline values. Mean arterial pressure (MAP) was not different from the baseline value at 15 seconds, but was increased from 30 seconds to 2 minutes. All values except HR had returned to baseline values by 7.5 minutes. At all measurement times, arterial oxygen tension and arterial pH were decreased, and arterial carbon dioxide tension increased from baseline values. Although the cardiovascular and respiratory changes following administration of thiamylal and methohexital were similar to those described for thiopental, some differences were found. Following thiamylal administration, systemic vascular resistance increased at 1 minute, pulmonary vascular resistance increased at 1 and 2 minutes, and myocardial contractility increased at 1 and 2 minutes. Following methohexital administration, MAP decreased at 15 seconds, and SV decreased at all measurement times.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular and respiratory effects of medetomidine in dogs and influence of anticholinergics

A total of 10 laboratory beagles was used to determine the cardiovascular and respiratory effects of medetomidine. The effects of atropine sulphate and glycopyrrolate on heart rate were also observed. Xylazine was included as a positive control. Medetomidine induced initial hypertension followed by a longer lasting hypotensive period. Evident bradycardia with second degree atrioventricular blocks and decrease in respiratory frequency was observed. Atropine sulphate and glycopyrrolate transiently abolished the bradycardic effect of medetomidine. Xylazine exhibited a similar cardiovascular and respiratory pattern to medetomidine.     

Cardiopulmonary effects of etomidate in hypovolemic dogs.

Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered IV to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.     

Cardiovascular effects of butorphanol administration in isoflurane-O2 anesthetized healthy dogs

Cardiovascular consequences of butorphanol tartrate (0.2 mg/kg of body weight, IV) administration during isoflurane (1.7% end-tidal concentration) anesthesia were determined in mechanically ventilated healthy dogs. Butorphanol administration caused significant (P less than or equal to 0.05) reductions in mean, systolic, and diastolic arterial blood pressures; cardiac output; and rate-pressure product.     

Cardiovascular and respiratory effects of ketamine infusions in isoflurane-anesthetized dogs before and during noxious stimulation

OBJECTIVE: To characterize the effects of ketamine administration on the cardiovascular and respiratory systems and on acid-base balance and to record adverse effects of ketamine in isoflurane-anesthetized dogs. ANIMALS: 6 healthy adult mongrel dogs. PROCEDURE: Dogs were anesthetized with isoflurane (1.25 times the individual minimum alveolar concentration) in oxygen, and ketamine was administered IV to target pseudo-steady-state plasma concentrations of 0, 0.5, 1, 2, 5, 8, and 11 microg/mL. Isoflurane concentration was reduced to an equipotent concentration. Cardiovascular, respiratory, and acid-base variables; body temperature; urine production; and adverse effects were recorded before and during noxious stimulation. Cardiac index, stroke index, rate-pressure product, systemic vascular resistance index, pulmonary vascular resistance index, left ventricular stroke work index, right ventricular stroke work index, arterial oxygen concentration, mixed-venous oxygen concentration, oxygen delivery, oxygen consumption, oxygen extraction ratio, alveolar-arterial oxygen partial pressure gradient, and venous admixture were calculated. Plasma ketamine and norketamine concentrations were measured. RESULTS: Overall, ketamine administration improved ventilation, oxygenation, hemodynamics, and oxygen delivery in isoflurane-anesthetized dogs in a dosedependent manner. With the addition of ketamine, core body temperature was maintained or increased and urine production was maintained at an acceptable amount. However, at the higher plasma ketamine concentrations, adverse effects such as spontaneous movement and profuse salivation were observed. Myoclonus and dysphoria were observed during recovery in most dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Infusion of ketamine appears to be a suitable technique for balanced anesthesia with isoflurane in dogs. Plasma ketamine concentrations between 2 to 3 microg/mL elicited the most benefits with minimal adverse effects.     

Cardiovascular effects of romifidine in dogs

OBJECTIVE: To characterize the cardiovascular effects of romifidine at doses ranging from 5 to 100 microg/kg of body weight, IV. ANIMALS: 25 clinically normal male Beagles. PROCEDURE: Romifidine was administered IV at a dose of 5, 10, 25, 50, or 100 microg/kg (n = 5/group). Heart rate, arterial pressure, central venous pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, body temperature, cardiac output, and PCV were measured immediately prior to and at selected times after romifidine administration. Cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, and left and right ventricular stroke work indices were calculated. Degree of sedation was assessed by an observer who was blinded to the dose administered. RESULTS: Romifidine induced a decrease in heart rate, pulmonary arterial pressure, rate-pressure product, cardiac index, and right ventricular stroke work index and an increase in central venous pressure, pulmonary capillary wedge pressure, and systemic vascular resistance index. In dogs given romifidine at a dose of 25, 50, or 100 microg/kg, an initial increase followed by a prolonged decrease in arterial pressure was observed. Arterial pressure immediately decreased in dogs given romifidine at a dose of 5 or 10 microg/kg. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that IV administration of romifidine induces dose-dependent cardiovascular changes in dogs. However, the 2 lowest doses (5 and 10 microg/kg) induced less cardiovascular depression, and doses > or = 25 microg/kg induced similar cardiovascular changes, suggesting that there may be a ceiling on the cardiovascular effects of romifidine.     

Cardiovascular effects of intravenous gadolinium administration to anaesthetized dogs undergoing magnetic resonance imaging

Objective To assess changes in heart rate and arterial blood pressure following intravenous (IV) gadolinium‐based contrast media administration to sevoflurane‐anaesthetized dogs undergoing magnetic resonance imaging (MRI). Study design Prospective clinical study. Animals Fifty client‐owned dogs (31 male, 19 female; aged 6–156 months; weighing 4.2–45.4 kg; ASA 2–3). Methods Heart rate and oscillometric blood pressures (systolic, mean and diastolic) were recorded at 10 minutes, 5 minutes and immediately pre‐administration of IV gadolinium contrast medium (time 0), then at 1, 2, 3, 5 and 10 minutes post‐gadolinium administration. Repeated measures anova was used to compare cardiovascular variables pre and post‐gadolinium administration. Significance was set at p < 0.05. Results There were no significant changes in cardiovascular variables following the IV administration of gadolinium. Conclusions and clinical relevance Administration IV of gadolinium‐based contrast media was not associated with adverse cardiovascular effects in these sevoflurane‐anaesthetized dogs undergoing MRI.     

Cardiovascular effects of butorphanol in halothane-anesthetized dogs

Cardiovascular effects of butorphanol (0.2 mg/kg of body weight, IV) and responses associated with subsequent administration of naloxone (0.04 mg/kg, IV) were studied in halothane (1.2% end-tidal concentration)-anesthetized dogs. Transient, but statistically significant (P less than 0.05), decreases in heart rate, mean and diastolic arterial blood pressures, and rate-pressure product were observed after butorphanol administration. Cardiac index, stroke volume, and systemic vascular resistance did not change significantly. Except for the decrease in heart rate, changes in the values of the cardiovascular variables measured after butorphanol administration did not appear to be clinically relevant. Sixty minutes after butorphanol administration, naloxone was given. Statistically significant (P less than 0.05) increases in heart rate, arterial blood pressures, cardiac index, and rate-pressure product, along with dysrhythmias were observed. Stroke volume and systemic vascular resistance remained unchanged after administration of naloxone. Naloxone administration was associated with changes indicative of increased myocardial oxygen consumption.     

Cardiovascular effects of epidural blocks in dogs

Cardiovascular and respiratory function was studied after epidural injection of lignocaine hydrochloride (3 mg kg¹) at the lumbosacral space in dogs premedicated with methadone (0–8 mg kg¹), acepromazine (0.3 mg kg¹) and atropine (0.6 to 1.2 mg). Analgesia was produced caudal to the third to fifth thoracic dermatomes; there was no significant change in cardiovascular function, respiratory rate, arterial blood pH or blood gas tensions. Relaxation of the hind leg and abdominal muscles was profound and haemorrhage caused a rapid fall in arterial blood pressure accompanied by tachycardia.     

Cardiovascular and subjective evaluations of oxymorphone/diazepam and hydromorphone/diazepam induction in experimentally induced hypovolemic dogs

Carprofen is an oral nonsteroidal anti-inflammatory drug commonly used for treatment of chronic osteoarthritic pain. The injectable formulation has some efficacy for treatment of acute surgical orthopedic pain. The purpose of this project was to assess the efficacy of oral preoperative carprofen for control of postoperative pain in dogs undergoing knee surgery for repair of ruptured cranial cruciate ligaments.
This was a randomized, placebo controlled, parallel study that investigated the effectiveness of carprofen compared to placebo. Nineteen dogs, presented to the CSU VTH, were entered into the study and randomly assigned to the carprofen (C) ( n  = 10) or placebo (P) ( n  = 9) group. Dogs received either a loading dose of carprofen (2.2 mg kg⁻¹ PO BID) or placebo starting 24 hours prior to surgery including the morning of surgery. The placebo contained lactose and liver flavoring. Pain was assessed using a pain scoring system, visual analog scale, and a loaded pressure threshold device preoperatively, and at 1, 2, 4, 6, 24, and 48 hours and 10 and 21 days postoperatively. The treatment continued for 21 days. Blood for cortisol analysis was drawn at all assessment times. Data were analyzed using a likelihood-based mixed effect model repeated measures. Data were considered significant if p  < 0.05.
Eight of 10 C dogs and 5/9 P dogs were given at least 1 dose of morphine. The mean relative dose of morphine was greater in the C group at 1 hour ( p  = 0.01) and 24 hours ( p  = 0.02). The heart rate and respiratory rate decreased postoperatively in a similar manner for both groups. There were no significant postoperative differences in cortisol levels or any measured variable. It appears that the scoring system used was not sensitive enough to detect differences in pain between a known analgesic and a placebo.     

Cardiovascular effects of doxacurium chloride in isoflurane-anaesthetised dogs

The cardiovascular effects of doxacurium were studied in 6 isoflurane-anaesthetised dogs. Each dog was anaesthetised twice, receiving doxacurium (0.008 mg/kg bwt) or placebo iv. Dogs were ventilated to normocapnia. Heart rate, cardiac index, systolic, diastolic, and mean arterial blood pressures, stroke volume, pulmonary vascular resistance, pulmonary artery wedge pressure, systemic vascular resistance, and pulmonary arterial pressure were determined. Neuromuscular blockade was assessed using the train-of-four technique. After recording baseline values, dogs randomly received either doxacurium or placebo iv, and data were recorded at 5, 10, 15, 30, 45, 60, 75, 90, 105 and 120 min. At 120 min, dogs treated with doxacurium received edrophonìum (0.5 mg/kg bwt iv) to antagonise neuromuscular blockade; dogs treated with placebos received saline iv. No statistically significant differences were detected after doxacurium compared to placebo. In both the doxacurium and placebo groups, significant increases in systolic arterial blood pressure, cardiac index, and stroke volume and a significant decrease in systemic vascular resistance occurred with time. Doxacurium depressed twitch tension 100% in all dogs (time to maximal twitch depression, 11 ± 7 min). First twitch tension was less than 10% of baseline values in all dogs at the time (120 min) of edrophonium administration. Additional edrophonium (1.0 ± 0.4 mg/kg iv) was required to obtain a fourth twitch to first twitch ratio of greater than 0.70. In conclusion, doxacurium is a long-acting neuromuscular blocking agent with no significant cardiovascular effects in isoflurane-anesthetised dogs. In dogs, doxacurium is indicated primarily for long surgical procedures requiring neuromuscular blockade and cardiovascular stability.     

Propofol versus thiopental: effects on peri-induction intraocular pressures in normal dogs

ObjectiveTo determine the effects of propofol or thiopental induction on intraocular pressures (IOP) in normal dogs.Study designProspective randomized experimental study.AnimalsTwenty-two random-source dogs weighing 19.5 ± 5.3 kg.MethodsDogs were randomly assigned to receive propofol 8 mg kg⁻¹ IV (group P) or thiopental 18 mg kg⁻¹ IV (group T) until loss of jaw tone. Direct arterial blood pressure, arterial blood gasses, and IOP were measured at baseline, after pre-oxygenation but before induction, before endotracheal intubation, and after intubation.ResultsThere were no significant differences between groups with regard to weight, body condition score, breed group, or baseline or before-induction IOP, arterial blood pressure, or blood gases. The baseline IOP was 12.9 mmHg. Before endotracheal intubation, IOP was significantly higher compared to baseline and before induction in dogs receiving propofol. After intubation with propofol, IOP was significantly higher compared to thiopental and was significantly higher compared to before induction. After intubation, IOP was significantly lower compared to before intubation in dogs receiving thiopental. Propofol increased IOP before intubation by 26% over the before-induction score and thiopental increased IOP by 6% at the same interval. The IOP in group P remained 24% over the before induction score whereas thiopental ultimately decreased IOP 9% below baseline after intubation. There was no significant relationship between any cardiovascular or blood gas parameter and IOP at any time. There was no significant relationship between the changes in any cardiovascular or blood gas parameter and the changes in IOP between time points.Conclusions and clinical relevancePropofol caused a significant increase in IOP compared to baseline and thiopental. Thiopental caused an insignificant increase in IOP which decreased after intubation. Propofol should be avoided when possible in induction of anesthesia in animals where a moderate increase in IOP could be harmful.     

Cardiovascular effects of epidural administration of methadone, ropivacaine 0.75% and their combination in isoflurane anaesthetized dogs

ObjectiveTo compare the cardiovascular effects of four epidural treatments in isoflurane anaesthetised dogs.Study designProspective, randomized. experimental study.AnimalsSix female, neutered Beagle dogs (13.3 ± 1.0 kg), aged 3.6 ± 0.1 years.MethodsAnaesthesia was induced with propofol (8.3 ± 1.1 mg kg^?1) and maintained with isoflurane in a mixture of oxygen and air [inspiratory fraction of oxygen (FiO₂) = 40%], using intermittent positive pressure ventilation. Using a cross-over model, NaCl 0.9% (P); methadone 1% 0.1 mg kg^?1 (M); ropivacaine 0.75% 1.65 mg kg^?1 (R) or methadone 1% 0.1 mg kg^?1 + ropivacaine 0.75% 1.65 mg kg^?1 (RM) in equal volumes (0.23 mL kg^?1) using NaCl 0.9%, was administered epidurally at the level of the lumbosacral space. Treatment P was administered to five dogs only. Cardiovascular and respiratory variables, blood gases, and oesophageal temperature were recorded at T-15 and for 60 minutes after epidural injection (T0).ResultsMean overall heart rate (HR in beats minute^?1) was significantly lower after treatment M (119 ± 16) (p = 0.0019), R (110 ± 18) (p < 0.0001) and RM (109 ± 13) (p < 0.0001), compared to treatment P (135 ± 21). Additionally, a significant difference in HR between treatments RM and M was found (p = 0.04). After both ropivacaine treatments, systemic arterial pressures (sAP) were significantly lower compared to other treatments. No significant overall differences between treatments were present for central venous pressure, cardiac output, stroke volume, systemic vascular resistance, oxygen delivery and arterial oxygen content (CaO₂). Heart rate and sAP significantly increased after treatment P and M compared to baseline (T-15). With all treatments significant reductions from baseline were observed in oesophageal temperature, packed cell volume and CaO₂. A transient unilateral Horner’s syndrome occurred in one dog after treatment R.Conclusions and clinical relevanceClinically important low sAPs were observed after the ropivacaine epidural treatments in isoflurane anaesthetised dogs. Systemic arterial pressures were clinically acceptable when using epidural methadone.     

Cardiovascular and respiratory effects of two doses of fentanyl in the presence or absence of bradycardia in isoflurane-anesthetized dogs

Objective

To compare the cardiopulmonary effects of low and high doses of fentanyl before and after the correction of bradycardia in isoflurane-anesthetized dogs.

Cardiovascular and respiratory effects of the acaricide amitraz

Amitraz is a formamidine compound used as a topical acaricide mainly in dogs and cattle. In an initial attempt to explain some of its side-effects, the actions of amitraz were studied on the cardiovascular and respiratory systems in thiopentone/methoxyflurane-anaesthetized dogs. In separate experiments, amitraz, at doses of 1, 2 and 5 mg/kg i.v., dissolved in DMSO, increased blood pressure for 1 hour. Heart rate decreased initially then showed a dose-related return towards control values. Tidal volume, respiratory rate and respiratory minute volume all showed initial transient depression. Hyperventilation was a feature after high doses of amitraz. Cumulative doses of amitraz of 0.5, 1, 2, 5 and 10 mg/kg i.v., at intervals of 5 min, increased blood pressure. Heart rate decreased at lower doses but increased slightly after higher doses. Five minutes after injection, cardiac index had returned to control values while total peripheral resistance showed a dose-related increase. The mechanism of action of amitraz in dogs cannot be determined from these results; however, other reports have described an alpha 2-adrenoceptor agonist action of this formamidine compound.     

Cardiovascular effects of hydralazine HCl administration in horses

Six standing awake adult horses were instrumented for measurement of mean arterial, central venous, and pulmonary arterial blood pressures (mm of Hg), thermodilution cardiac output (ml/kg/min), and pulmonary arterial blood temperature (C). Total peripheral resistance was calculated from these values. Base-line data were accumulated, and a single dose of hydralazine HCl (0.5 mg/kg) was administered IV. Horses were monitored for 420 minutes after hydralazine administration. Mean arterial and central venous blood pressures did not change from the base-line values. Cardiac output and heart rate were increased above base-line values for 260 minutes. Total peripheral resistance was decreased for 240 minutes. Pulmonary arterial blood temperature was decreased for 60 minutes after drug administration. Mean pulmonary arterial pressure relative to the base-line mean was intermittently decreased during the study. Intravenously administered hydralazine HCl appears to be an effective vasodilator, with moderate duration of action in horses.     

Cardiovascular effects of tramadol in dogs anesthetized with sevoflurane

Cardiovascular effects of tramadol were evaluated in dogs anesthetized with sevoflurane. Six beagle dogs were anesthetized twice at 7 days interval. The minimum alveolar concentration (MAC) of sevoflurane was earlier determined in each dog. The dogs were then anesthetized with sevoflurane at 1.3 times of predetermined individual MAC and cardiovascular parameters were evaluated before (baseline) and after an intravenous injection of tramadol (4 mg/kg). The administration of tramadol produced a transient and mild increase in arterial blood pressure (ABP) (P=0.004) with prolonged increase in systemic vascular resistance (SVR) (P<0.0001). Compared with baseline value, mean ABP increased significantly at 5 min (119% of baseline value, P=0.003), 10 min (113%, P=0.027), and 15 min (111%, P=0.022). SVR also increased significantly at 5 min (128%, P<0.0001), 10 min (121%, P=0.026), 30 min (114%, P=0.025), 45 min (113%, P=0.025) and 60 min (112%, P=0.048). Plasma concentrations of tramadol were weakly correlated with the percentage changes in mean ABP (r=0.642, P<0.0001) and SVR (r=0.646, P<0.0001). There was no significant change in heart rate, cardiac output, cardiac index, stroke volume, pulmonary arterial pressure, right atrial pressure and pulmonary capillary wedge pressure. In conclusion, the administration of tramadol produces a prolonged peripheral vascular constriction in dogs anesthetized with sevoflurane, which is accompanied with a transient and mild increase in arterial blood pressure. It also indicated that the degree of vasoconstriction might depend on the plasma concentration of tramadol.     

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.     

Cardiovascular effects of pancuronium bromide in mongrel dogs.

The cardiovascular effects of a new nondepolarizing muscle relaxant, pancuronium bromide, were studied in mongrel dogs. Small, but significant, increases in mean arterial blood pressure were observed after each of 2 intravenous doses (0.01 mg/kg and 0.1 mg/kg) were given. Heart rate increased significantly in dogs administered the larger dosage, and indexes of ventricular functions demonstrated a trend toward positive cardiac inotrophy after either the large or the small dose.