Kinetics of endotoxin concentration and tumor necrosis factor-alpha,interleukin-1beta,and interleukin-6 activities in the systemic and portal circulation during small intestinal ischemia and reperfusion in dogs

OBJECTIVE: To determine whether small intestinal ischemia and reperfusion induces bacterial translocation and proinflammatory cytokine response in either the systemic or portal circulation in dogs. ANIMALS: 17 healthy adult Beagles. PROCEDURE: The superior mesenteric artery (SMA) was occluded for 0 (group-3 dogs), 30 (group-1 dogs), or 60 (group-2 dogs) minutes, followed by reperfusion for 180 minutes; serum lactate and endotoxin concentrations and tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 activities in the systemic and portal circulation and intramucosal pH were measured at various time points. RESULTS: In group-2 dogs, TNFalpha activity was found to be significantly increased in the portal circulation, peaking at 60 minutes of reperfusion; TNF-alpha activity, in the systemic circulation, gradually increased from 60 minutes of reperfusion to the end of the experiment; however, the increase was not significant. In group-1 and -2 dogs, IL-6 activities significantly and gradually increased in the systemic and portal circulation during the reperfusion phase, and the magnitude of these increases was dependent on the duration of the ischemic phase. There were no significant changes in IL-1beta activity or endotoxin concentration in any dog group. CONCLUSIONS AND CLINICAL RELEVANCE: Results of the our study indicate that intestinal ischemia and reperfusion leads to significant increases of the circulating TNF-alpha and IL-6 activities, depending on the duration of the ischemia phase, in the absence of detectable endotoxin in the circulation. This finding suggests that intestinal ischemia and reperfusion induces a systemic proinflammatory cytokine response in dogs.     

Assessment of acid-base status and plasma lactate concentrations in arterial,mixed venous,and portal blood from dogs during experimental hepatic blood inflow occlusion

OBJECTIVE: To determine the effects of extended experimental hepatic blood flow occlusion (ie, portal triad clamping [PTC]) in dogs by measuring acid-base status and plasma lactate concentrations in arterial, mixed venous, and portal blood and evaluating the relationship between metabolic and concurrent hemodynamic changes. ANIMALS: 6 healthy Beagles. PROCEDURE: During anesthesia with isoflurane, cardiac output and arterial blood pressure were measured. Arterial, mixed venous, and portal blood samples were collected simultaneously for blood gas analyses and plasma lactate measurements before PTC and at 8-minute intervals thereafter. RESULTS: PTC resulted in severe hemodynamic and metabolic alterations. Eight minutes after PTC, significant decreases in cardiac index from a baseline value of 3.40 +/- 0.27 to 1.54 +/- 0.26 L/min/m2 and in mean arterial blood pressure from a baseline value of 74 +/- 6 to 43 +/- 6 mm Hg were recorded. After PTC, results indicative of lactic acidosis were found in portal blood at 16 minutes, in mixed venous at 32 minutes, and in arterial blood at 48 minutes. Significant differences in measured variables were also found between arterial and portal blood samples, between mixed venous and portal blood samples, and between arterial and mixed venous blood samples after PTC, compared with differences at baseline. CONCLUSIONS AND CLINICAL RELEVANCE: Analysis of mixed venous blood is preferable to analysis of arterial blood in the assessment of metabolic derangement. In a clinical setting, occluded portal blood is released to the systemic circulation, and the degree of reperfusion injury may depend on the metabolic status of pooled portal blood.     

Effects of small intestinal ischemia and reperfusion on expression of tumor necrosis factor-alpha and interleukin-6 messenger RNAs in the jejunum, liver, and lungs of dogs

OBJECTIVE: To determine the effects of intestinal ischemia and reperfusion on the expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mRNAs in the jejunum, liver, and lungs of dogs. ANIMALS: 8 healthy adult Beagles. PROCEDURES: In each dog, the cranial mesenteric artery was occluded for 0 (control group; n=4) or 60 (I-R group; 4) minutes, followed by reperfusion for 480 minutes; serum TNF-alpha and IL-6 activities and expression levels of TNF-alpha and IL-6 mRNAs in jejunal, hepatic, and lung tissues were measured before and at the end of the ischemic period and at intervals during reperfusion. For each variable, values were compared between the control and I-R groups at each time point. RESULTS: Compared with the control group, serum IL-6 activity increased significantly after 180 minutes of reperfusion in the I-R group; also, jejunal TNF-alpha mRNA expression increased significantly after 60 (peak) and 180 minutes of reperfusion. In the I-R group, expressions of IL-6 mRNA in the liver and TNF-alpha and IL-6 mRNAs in the lungs increased significantly at 480 minutes of reperfusion, compared with the control group. Serum TNF-alpha activity, expression of IL-6 mRNA in the jejunum, and expression of TNF-alpha mRNA in the liver in the control and I-R groups did not differ. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that the liver, lungs, and jejunum contributed to the production of TNF-alpha and IL-6 after intestinal ischemia and reperfusion in dogs, suggesting that intestinal ischemia and reperfusion induce a systemic proinflammatory cytokine response in dogs.     

Evaluation of hepatosplanchnic circulation and intestinal oxygenation in dogs with a condition that mimicked septic shock induced by continuous infusion of a low dose of lipopolysaccharide

OBJECTIVE: To determine whether continuous infusion of a low dose of lipopolysaccharide (LPS) to induce a condition mimicking septic shock in dogs would affect systemic and hepatosplanchnic circulation and oxygenation. ANIMALS: 12 healthy adult Beagles. PROCEDURE: Dogs received a low dose of LPS (Escherichia coli O55:B5) by continuous IV infusion at a rate of 1 microg/kg/h for 8 hours. Systemic hemodynamics; systemic oxygenation; blood flow in the cranial mesenteric artery, common hepatic artery, and portal vein; intestinal and hepatic tissue blood flow; mesenteric oxygenation; and intramucosal Pco2 were examined before and at selected time points after onset of the LPS infusion. RESULTS: After onset of the LPS infusion, cardiac index increased and mean arterial pressure (MAP) and systemic vascular resistance decreased, which is characteristic of the hyperdynamic state in septic patients. Hepatosplanchnic blood flow increased during the hyperdynamic state. Intestinal Pco2 was increased even when blood flows increased. During the latter half of the experimental period, MAP was maintained but hepatosplanchnic blood flows decreased and intestinal Pco2 increased further. CONCLUSIONS AND CLINICAL RELEVANCE: Analysis of the results suggested that hepatosplanchnic blood flow enters the hyperdynamic state during the early stages of sepsis and that intestinal tissue oxygenation is threatened even when hepatosplanchnic blood flow is increased or maintained. Hence, improvement of hepatosplanchnic circulation and intestinal tissue oxygenation is important in dogs with clinical evidence of a septic condition.     

Evaluation of splanchnic oxygen extraction ratio as an index of portal vein pressure in dogs

OBJECTIVE: To determine changes in splanchnic oxygen extraction ratio during experimentally induced portal hypertension in dogs. ANIMALS: 6 clinically normal dogs. PROCEDURE: Standard midline laparotomy and median sternotomy were performed in anesthetized dogs. Baseline measurements of arterial blood pressure, aortic blood flow, portal vein blood flow, and portal vein pressure were acquired, and arterial, venous, and portal vein blood samples were obtained to determine systemic and splanchnic oxygen extraction ratios. The portal vein was gradually occluded until a pressure of 18 cm of H2O was reached; this pressure was maintained for 30 minutes, and measurements and collection of blood samples were repeated. RESULTS: Portal vein blood flow decreased significantly from 457 +/- 136 ml/min before to 266 +/- 83 ml/min after induction of portal hypertension. Oxygen content in the portal vein significantly decreased from 12.3 +/- 1.85 to 8.2 +/- 2.31%, and splanchnic oxygen extraction ratio significantly increased from 15.8 +/- 6.2 to 37.4 +/- 10.9% during portal hypertension. There was a significant inverse correlation between portal vein blood flow and splanchnic oxygen extraction ratio at baseline and during portal hypertension. CONCLUSIONS AND CLINICAL RELEVANCE: An increase in splanchnic oxygen extraction ratio is evident with partial attenuation of the portal vein and the concurrent decrease in portal vein blood flow. Correlation of oxygen extraction ratio with portal vein blood flow may be a more important indicator for determination of an endpoint to prevent congestion and ischemia of the gastrointestinal tract and pancreas during ligation of portosystemic shunts.     

The Cardiopulmonary Effects of Oxymorphone in Hypovolemic Dogs

Blood was withdrawn from 15 dogs over the course of about 1 hour until the mean arterial blood pressure was reduced to 60 mm Hg. Small aliquots of additional blood were withdrawn in order to maintain the mean arterial blood pressure near 60 mm Hg for an additional hour. Oxymorphone (0.4 mg/kg) was then administered intravenously to ten dogs, and all measurements were repeated in 5, 15, 30, and 60 minutes. Five dogs served as controls.
Heart rate, tidal volume, arterial oxygen, oxygen extraction, and pH significantly decreased after oxymorphone administration, while systemic and pulmonary arterial blood pressures, systemic vascular resistance (transiently), breathing rate, minute ventilation, physiologic dead space, venous admixture, venous oxygen, arterial and venous carbon dioxide, and bicarbonate concentration increased significantly. Cardiac output was also increased, but the change was not statistically significant. Oxymorphone was associated with significantly lower heart rate, tidal volume, arterial oxygen, and pH, and higher systemic and pulmonary arterial pressure, cardiac output, venous oxygen, and arterial and venous carbon dioxide, compared to the control group, which did not receive oxymorphone.
Oxymorphone significantly improved cardiovascular performance and tissue perfusion in these hypovolemic dogs. Oxymorphone did cause a significant increase in arterial carbon dioxide and a decrease in arterial oxygenation. Oxymorphone is an opioid agonist that may represent a reasonable alternative for the induction of anesthesia in patients who are candidates for induction hypotension.     

Effects of a peripheral alpha2 adrenergic-receptor antagonist on the hemodynamic changes induced by medetomidine administration in conscious dogs

OBJECTIVE: To evaluate the effects of administration of a peripheral alpha(2)-adrenergic receptor antagonist (L-659,066), with and without concurrent administration of glycopyrrolate, on cardiopulmonary effects of medetomidine administration in dogs. ANIMALS: 6 healthy adult dogs. PROCEDURES: Dogs received saline (0.9% NaCl) solution (saline group), L-659,066 (group L), or L-659,066 with glycopyrrolate (group LG). These pretreatments were followed 10 minutes later by administration of medetomidine in a randomized crossover study. Hemodynamic measurements and arterial and mixed-venous blood samples for blood gas analysis were obtained prior to pretreatment, 5 minutes after pretreatment, and after medetomidine administration at intervals up to 60 minutes. RESULTS: After pretreatment in the L and LG groups, heart rate, cardiac index, and partial pressure of oxygen in mixed-venous blood (PvO2) values were higher than those in the saline group. After medetomidine administration, heart rate, cardiac index, and PvO2 were higher and systemic vascular resistance, mean arterial blood pressure, and central venous pressure were lower in the L and LG groups than in the saline group. When the L and LG groups were compared, heart rate was greater at 5 minutes after medetomidine administration, mean arterial blood pressure was greater at 5 and 15 minutes after medetomidine administration, and central venous pressure was lower during the 60-minute period after medetomidine administration in the LG group. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of L-659,066 prior to administration of medetomidine reduced medetomidine-induced cardiovascular changes in healthy dogs. No advantage was detected with concurrent administration of L-659,066 and glycopyrrolate.     

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.     

Effect of Platelet-Activating Factor Antagonist L-691,880 on Low-Flow Ischemia-Reperfusion Injury of the Large Colon in Horses

Objective—To determine the effect of platelet-activating factor (PAF) antagonist L-691,880 on low-flow ischemia and reperfusion (I-R) of the large colon in horses. Animals —12 adult horses. Experimental Design—Horses were anesthetized, and the large colon was exteriorized through a ventral median celiotomy and instrumented. Colonic arterial blood flow was reduced to 20% of baseline (BL) and maintained for 3 hours; flow was then restored, and the colon was reperfused for 3 hours. One of two solutions was administered intravenously 30 minutes before reperfusion: group 1, 10 mL/kg 0.9% NaCl; and group 2, 5 mg/kg PAF antagonist L-691,880 in 0.9% NaCl. Hemodynamic variables were monitored and recorded at 30-minute intervals. Systemic arterial and colonic venous blood were collected for measurement of blood gas tensions, oximetry analyses, packed cell volume, and total plasma protein concentrations. Colonic venous blood was collected for determination of lactate, 6-keto prostaglandin F_1α (6-kPG), prostaglandin E₂ (PGE₂), and thromboxane B₂ (TXB₂) concentrations. Full-thickness biopsy specimens were harvested from the left ventral colon for histological evaluation. Results—There were no significant differences between the two groups for any hemodynamic or metabolic variables. Colonic venous pH decreased, and carbon dioxide tension and lactate concentration increased during ischemia but returned to BL values during reperfusion. Colonic venous 6-kPG concentration was significantly increased above BL value at 2 hours and remained increased through 6 hours in horses of both groups. Colonic venous PGE₂ concentration was significantly greater in group 2 compared with group 1 throughout the study. Colonic venous PGE₂ concentration was increased above BL value from 3 to 6 hours in horses of both groups. Colonic venous TXB₂ concentration was not different between groups but was significantly increased above the BL value for the first hour of reperfusion. Low-flow I-R of the large colon caused significant mucosal necrosis, hemorrhage, edema, and neutrophil infiltration; however, there were no differences in histological variables between vehicle-control and PAF antagonist-treated horses. Conclusion—No protective effects of PAF antagonist L-691,880 were observed on colonic mucosa associated with low-flow I-R. Additionally, deleterious drug-induced effects on hemodynamic and metabolic variables and colonic mucosal injury were not observed.     

Effects of atracurium on intraocular pressure, eye position, and blood pressure in eucapnic and hypocapnic isoflurane-anesthetized dogs

OBJECTIVE: To determine effects of atracurium on intraocular pressure (IOP), eye position, and arterial blood pressure in eucapnic and hypocapnic dogs anesthetized with isoflurane. ANIMALS: 16 dogs. PROCEDURE: Ventilation during anesthesia was controlled to maintain Paco2 at 38 to 44 mm Hg in group- I dogs (n = 8) and 26 to 32 mm Hg in group-II dogs (8). Baseline measurements for IOP, systolic, diastolic, and mean arterial blood pressure, central venous pressure (CVP), and heart rate (HR) were recorded. Responses to peroneal nerve stimulation were monitored by use of a force-displacement transducer. Atracurium (0.2 mg/kg) was administered i.v. and measurements were repeated at 1, 2, 3, and 5 minutes and at 5-minute intervals thereafter for 60 minutes. RESULTS: Atracurium did not affect IOP, HR, or CVP Group II had higher CVP than group I, but IOP was not different. There was no immediate effect of atracurium on arterial blood pressure. Arterial blood pressure increased gradually over time in both groups. Thirty seconds after administration of atracurium, the eye rotated from a ventromedial position to a central position and remained centrally positioned until 100% recovery of a train-of-four twitch response. The time to 100% recovery was 53.1 +/- 5.3 minutes for group I and 46.3 +/- 9.2 minutes for group II. CONCLUSIONS AND CLINICAL RELEVANCE: Atracurium did not affect IOP or arterial blood pressure in isoflurane-anesthetized dogs. Hyperventilation did not affect IOP or the duration of effect of atracurium.     

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.     

Use of an isolated intestinal circuit to evaluate the effect of ischemia and reperfusion on mucosal permeability of the equine jejunum

OBJECTIVES: To evaluate the efficacy of an isolated perfusion circuit and the effect of ischemia-reperfusion on mucosal permeability of the jejunum. STUDY DESIGN: In vitro study of intestinal mucosal permeability. ANIMALS: Twelve healthy adult horses. METHODS: A control segment of jejunum was placed in an isolated perfusion circuit for 240 minutes and mucosal permeability was measured. After detecting no deleterious effects of the isolated system on the control intestine, low flow ischemia was created in experimental segments for 20, 40, 60 and 90 minutes followed by 60 minutes of reperfusion and mucosal permeability was evaluated. At the completion of the studies, histologic evaluation was used to determine mucosal grades, surface area, and volume. RESULTS: Control tissue was maintained in the isolated circuit for 240 minutes without effect on mucosal grade, surface area, or volume relative to intact tissue. After ischemia-reperfusion, mucosal grade increased, and volume and surface area decreased progressively with longer periods of ischemia. Mucosal clearance of albumin remained constant during 240 minutes of perfusion in control tissue and was elevated after ischemia-reperfusion. CONCLUSIONS: No deleterious changes were noted in jejunum perfused with this isolated circuit, whereas alterations in mucosal permeability were present after ischemia-reperfusion. CLINICAL RELEVANCE: The isolated perfusion circuit successfully maintained an isolated segment of jejunum within physiologic limits, and can be used to evaluate the effects of injury and the efficacy of pharmaceuticals to attenuate these changes.     

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.     

Changes in clinical, hematologic and biochemical indicators in controlled respiration during anesthesia in dogs]

Some clinico-biochemical parameters were investigated in fifty clinically healthy dogs in the course of controlled breathing in halothane inhalation anaesthesia to evaluate in a complex manner the dynamics of metabolic processes in the dog organism. The test dogs were divided into three groups. In the first test group, ECG and values of acid-base balance parameters in venous blood were followed in ten dogs. In the second test group, the values of blood gases were followed in addition to the above-mentioned parameters in twenty anesthetized dogs. In the third test group comprising twenty animals, acid-base parameters in arterial blood and blood gas tension were evaluated. Greatest divergences were recorded in pH values, blood gas tension and acid-base balance values. Partly compensated respiration acidosis was observed already in 30 minutes from the start of anaesthesia, as shown by complex evaluation. The results indicate that also in optimum ventilation programme it is necessary to apply infusion solutions to the internal environment of organism which will secure metabolic rebalancing in the course of artificial pulmonary ventilation.     

Cardiovascular and respiratory effects of thiopental administration in hypovolemic dogs

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. 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, 8 mg of thiopental/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.     

Agreement between arterial and central venous blood pH and its contributing variables in anaesthetized dogs with respiratory acidosis

ObjectiveTo determine the accuracy of variables that influence blood pH, obtained from central venous (jugular vein) blood samples compared with arterial (dorsal pedal artery) samples in anaesthetized dogs with respiratory acidosis.Study designProspective, comparative, observational study.AnimalsA group of 15 adult male dogs of various breeds weighing 17 (11-42) kg [median (range)].MethodsDogs were premedicated with buprenorphine (0.03 mg kg^–1) and medetomidine (0.01 mg kg^–1) administered intramuscularly by separate injections, anaesthetized with propofol intravenously to effect and maintained with isoflurane in 50% air-oxygen. Arterial and central venous catheters were placed. After 15 minutes of spontaneous breathing, arterial and central venous blood samples were obtained and analysed within 5 minutes, using a bench-top gas analyser. Differences between arterial and central venous pH and measured variables were assessed using Wilcoxon rank sum test and effect size (r: matched-pairs rank-biserial correlation) was calculated for each comparison. The agreement (bias and limits of agreement: LoAs) between arterial and central venous pH and measured variables were assessed using Bland-Altman; p < 0.05. Data are reported as median and 95% confidence interval.ResultsArterial blood pH was 7.23 (7.19-7.25), and it was significantly greater than central venous samples 7.21 (7.18-7.22; r = 0.41). Agreement between arterial and venous pH was acceptable with a bias of 0.01 (0.002-0.02) and narrow LoAs. PCO₂ [arterial 54 (53-58) mmHg, 7.2 (7.1-7.7) kPa; venous 57 (54-62) mmHg, 7.6 (7.2-8.3) kPa], bicarbonate ion concentration and base excess did not differ between samples; however, agreement between arterial and venous PCO₂ was not acceptable with a bias of –2 (–5 to 0) mmHg and wide LoAs.Conclusions and clinical relevanceBlood pH measured from central venous (jugular vein) blood is an acceptable clinical alternative to arterial blood (dorsal pedal artery) in normovolaemic anaesthetized dogs with respiratory acidosis.     

Effects of ischemia and dimethyl sulfoxide on equine jejunal vascular resistance, oxygen consumption, intraluminal pressure, and potassium loss

Physiologic effects of 1 hour of ischemia and 1 hour of reperfusion on equine jejunum and protective effects of systemic administration of dimethyl sulfoxide (DMSO, 1 g/kg of body weight) were investigated in 18 ponies, using neurally intact segments of jejunum perfused at constant flow with heparinized blood. Ponies were allotted to 4 groups: group 1, saline solution administered (control, n = 3); group 2, DMSO administered (DMSO, n = 3); group 3, ischemia induced and saline solution administered (ischemia, n = 6); and group 4, ischemia induced and DMSO administered (ischemia-DMSO, n = 6). Intestinal vascular resistance (R, mm of Hg/ml/min/100 g), oxygen consumption (VO2, ml/min/100 g), frequency and amplitude of rhythmic changes in intraluminal pressure, intestinal compliance (C, ml/mm of Hg), and arteriovenous potassium concentration difference (delta AV [K+], mEq/L) were determined and compared with stable preischemic values within groups. There were no significant changes in any variable in ponies of groups 1 or 2. In ponies of group 3, significant (P less than or equal to 0.05) changes included: an initial increase in R during reperfusion, followed by a decrease to values below preischemic values by 15 minutes of reperfusion; decreased VO2 during the entire reperfusion period; increased amplitude of rhythmic contractions during initial reperfusion; decreased frequency of rhythmic contractions during ischemia; and increased delta AV [K+] during initial reperfusion. Changes in ponies of group 4 were identical to changes in ponies of group 3, with the exception that DMSO administration prevented the decrease in R during reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of atropine to reduce mucosal eversion during intestinal resection and anastomosis in the dog

OBJECTIVE: To determine whether atropine altered the degree of mucosal eversion during jejunal resection and anastomosis in the dog. STUDY DESIGN: Part I: Prospective, blinded, randomized, controlled study using a therapeutic dose (0.04 mg/kg systemic) of atropine. Part II: Prospective, unblinded, assigned, controlled study using a pharmacologic (0.04 mg/kg local arterial) dose of atropine. ANIMALS: Part I: Twenty-two young adult female Beagle dogs used during a nonsurvival third-year veterinary student surgical laboratory (small intestinal resection and anastomosis). Part II: Ten young adult female Beagle dogs used immediately after completion of a nonsurvival third-year veterinary student orthopedic surgical laboratory. METHODS: Part I: Dogs were randomly assigned to receive either atropine (0.04 mg/kg), or an equal volume of saline, given intramuscularly (premedication) and again intravenously prior to intestinal resection. Part II: In each dog, atropine (0.04 mg/kg)/saline was alternately given in the proximal/distal jejunum. RESULTS: Part I: There was no clinically or statistically significant difference between systemic atropine and saline solution on the degree of jejunal mucosal eversion after resection. Part II: There was a statistically significant decrease in jejunal mucosal eversion with atropine compared with saline solution when injected into a local jejunal artery. CONCLUSION: Systemic atropine (0.04 mg/kg) does not alter the degree of jejunal mucosal eversion during resection and anastomosis. Jejunal intraarterial atropine (0.04 mg/kg) reduced jejunal mucosal eversion during resection and anastomosis. CLINICAL RELEVANCE: The clinical usefulness and consequences of jejunal arterial atropine administration to reduce mucosal eversion remain to be determined.     

Effects of lactated Ringer solution and prednisolone sodium succinate on dogs with induced hemorrhagic shock.

Hemorrhagic shock was induced in nonsplenectomized dogs by removing 41% of their blood volume over a 15-minute period. Hemodynamic and metabolic variables were determined prior to and for 3 hours after completion of hemorrhage. One group of 5 dogs was not treated. After the 30-minute sample was collected, a second group of 5 dogs was given lactated Ringer solution (LRS) at 88 ml/kg of body weight, IV. A third group of 5 dogs was given LRS (88 ml/kg, IV) and prednisolone sodium succinate (11 mg/kg, IV) 30 minutes after hemorrhage. The IV administration of LRS was completed within 15 minutes. The glucocorticoid was administered as an IV bolus after 500 ml of LRS had been given. The large volume and administration of LRS significantly (P = 0.05) improved many of the hemodynamic and metabolic effects of acute hemorrhage and hemorrhagic shock. At one time or another during the 2.5-hour observation period after the initiation of treatment, mean arterial pressure, cardiac index, systemic vascular resistance, heart rate, respiratory rate, lactate, glucose, and arterial and venous blood gas values were significantly (P = 0.05) improved, compared with baseline values. The addition of prednisolone sodium succinate to the treatment regimen improved the effectiveness of LRS alone only in some dogs at random sampling times. Significant trends were not observed except, possibly, the improvement of venous pH and A-V pH and PCO2 differences.     

Comparison of measured oxyhemoglobin saturation and oxygen content with analyzer-calculated values and hand-calculated values obtained in unsedated healthy dogs

OBJECTIVE: To compare direct measurements of canine oxyhemoglobin (HbO2) saturation and blood oxygen content (ContO2) in healthy dogs with analyzer-calculated values derived by use of a human HbO2 relationship and with hand-calculated values derived by use of a canine HbO2 relationship. ANIMALS: 17 healthy dogs. PROCEDURE: 3-mL samples of heparinized arterial and jugular venous blood were collected from each dog. The pH, Pco2, Po2, hemoglobin, HbO2, carboxyhemoglobin, methemoglobin, and ContO2 were measured; HbO2 and ContO2 were calculated automatically by analyzers and also hand-calculated. Blood gas analyzer-calculated and hand-calculated HbO2 values were compared with co-oximeter-measured HbO2 values. Analyzer-calculated and hand-calculated ContO2 values were compared with oxygen content analyzer-measured values. RESULTS: Hand-calculated HbO2 values for arterial and jugular venous samples were slightly but significantly lower than those calculated by a blood gas analyzer or obtained from a co-oximeter. Hand-calculated and analyzer-calculated arterial and venous ContO2 were similar to measured values. CONCLUSIONS AND CLINICAL RELEVANCE: Although certain HbO2 and ContO2 values generated by use of the different methods were significantly different, these differences are unlikely to be clinically important in healthy dogs.