Effect of endotoxin administration on equine digital hemodynamics and starling forces

Using a pump-perfused extracorporeal isolated digital preparation, the effects of a 30-minute infusion of either saline solution (control) or endotoxin on equine digital hemodynamics and microvascular function were determined. Digital blood flow and arterial, venous, and capillary pressures were recorded at 15-minute intervals for 150 minutes. From these data, total vascular resistance and pre- and postcapillary resistances were calculated. Isogravimetric capillary filtration coefficient, vascular compliance, and the osmotic reflection coefficient were determined after the last hemodynamic measurements were taken. Changes in hemodynamic values of control equine digits were not observed. During the 120 minutes after infusion of endotoxin, digital blood flow decreased 43%, and total vascular resistance increased 89%. Precapillary resistance increased 122%, but postcapillary resistance did not change significantly. Changes in vascular compliance or the capillary filtration coefficient were not observed in response to either treatment. The osmotic reflection coefficient, an index of permeability, did not differ significantly between digits of the endotoxin-treated and control groups. These data indicate that the increase in vascular resistance during endotoxemia may have been attributable to arterial/arteriolar constriction and that neither the permeability nor the surface area of the exchange vasculature within the digit was significantly affected by endotoxin. Although marked alterations in vascular function are seen after administration of endotoxin, these changes do not parallel those documented in association with experimentally induced laminitis.     

Effects of slow infusion of a low dosage of endotoxin on systemic haemodynamics in conscious horses

The effects of intravenous (iv) infusion of endotoxin for 60 mins at a cumulative dosage of 0.03 micrograms/kg bodyweight on systemic arterial, right atrial and pulmonary arterial pressures, heart rate, cardiac output, and derived pulmonary vascular resistance and total peripheral vascular resistance were compared to the effects of iv infusion of saline solution in four healthy horses. Heart rate was increased significantly after endotoxin infusion, although diastolic arterial pressure, systolic arterial pressure, electronically averaged arterial pressure, cardiac output, total peripheral resistance, and right atrial pressure did not change significantly. Average pulmonary arterial pressure was increased significantly by endotoxin infusion. This was accompanied by a trend toward increased diastolic pulmonary arterial pressure (P = 0.1), systolic pulmonary arterial pressure (P = 0.08) and pulmonary vascular resistance (P = 0.07). These results suggest that low dosages of endotoxin produce pulmonary hypertension without causing hypotensive, hypodynamic shock.     

Hemodynamic responses of the equine digit to intravenous and digital arterial infusion of dopamine

In 6 adult horses anesthetized with pentobarbital, the hemodynamic responses of the equine digit to infusion of dopamine were evaluated by use of an isolated extra corporeal pump perfused digital preparation. Digital blood flow was maintained at a constant rate that was independent of systemic hemodynamic changes. Three sequential experiments were performed on each horse. In the first experiment (n = 6), dopamine was infused IV at rates of 1.0, 2.5, and 5.0 micrograms/kg/min. For the second experiment (n = 5), dopamine (400 micrograms/ml) was infused into the digital artery at the rates of 0.07, 0.7, and 1.2 ml/min. The third experiment (n = 5) consisted of a 5-minute intra-arterial infusion of phentolamine followed by the intra-arterial infusion of dopamine while continuing the infusion of phentolamine. Digital venous, arterial, and capillary pressures, total digital vascular resistance, and precapillary to postcapillary resistance ratios were determined in each experiment. Systemic infusion of dopamine did not induce changes in the hemodynamics of the digital vasculature. Digital arterial infusion of dopamine alone resulted in a dose-dependent increase in arterial pressure, total digital vascular resistance, and an increase in the precapillary to postcapillary resistance ratio. Phentolamine attenuated the vasoconstrictive response elicited by intra-arterial infusion of dopamine.     

Evaluation of equine digital Starling forces and hemodynamics during early laminitis

A carbohydrate overload model was used in 8 horses to evaluate Starling forces and hemodynamics of the digit during the prodromal stage of acute laminitis. A pump-perfused extracorporeal digital preparation was used to evaluate blood flow, arterial pressure, venous pressure, capillary pressure, isogravimetric capillary filtration coefficient, osmotic reflection coefficient, and vascular compliance. From these data, pre- and postcapillary resistances and pre- to postcapillary resistance ratios were determined. Vascular and tissue oncotic pressures were estimated from plasma and lymph protein concentrations, respectively. The osmotic reflection coefficient, an estimation of capillary permeability, was determined by means of the lymph protein wash-down technique. Using the collected data, tissue pressure in the digit was calculated by use of the Starling equation. In the isolated digit, mean isogravimetric capillary pressure was 55.13 mm of Hg, mean plasma and lymph oncotic pressures were 22.29 mm of Hg and 7.2 mm of Hg, respectively, the mean osmotic reflection coefficient was 0.66, the mean capillary filtration coefficient was 0.003 ml/min/mm of Hg/100 g, and mean interstitial fluid pressure was 44.82 mm of Hg. The high capillary pressure appeared to be caused by high vascular resistance from the venous side, predisposing to enhanced capillary filtration and interstitial fluid accumulation.     

Crystalloids versus colloids: implications in fluid therapy of dogs with intestinal obstruction

Responses of jejunal transcapillary and transmucosal fluid fluxes to IV infusion of crystalloid or colloid solutions were evaluated in 12 dogs. One isolated intestinal segment in each dog was used as the control segment, and 2 segments were distended to a intraluminal hydrostatic pressure of 10 cm of H2O. The artery supplying 1 of the 2 distended (autoperfused) segments was cannulated and perfused with blood from the femoral artery. One of the 2 distended segments was autoperfused from the femoral artery. Intraluminal pressure was increased in the autoperfused segment and in 1 other segment for three, 20-minute periods after administration of the crystalloid or colloid solution. Net transmucosal fluid flux was estimated, using a volume recovery method. In each autoperfused segment, blood flow, capillary pressure, lymph flow, and plasma protein and lymph protein concentrations were measured during each 20-minute distention period. Systemic arterial pressure was monitored throughout the procedure. Plasma and tissue oncotic pressures were calculated from the plasma protein and lymph protein concentrations. Total vascular resistance and precapillary and postcapillary resistances were determined. Capillary pressure increased after infusion with colloids and crystalloids, with the effects being more prolonged in the colloid group. Plasma oncotic pressure transiently increased after infusion with colloids and decreased after infusion with crystalloids. Lymph flow increased only in crystalloid-treated dogs. Due to alterations in transcapillary fluid filtration, crystalloids induced a net loss of fluid into the intestinal lumen, whereas the fluid absorptive capacity of the jejunum was unaltered by colloid treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic response of endotoxemic calves to treatment with small-volume hypertonic saline solution

The hemodynamic effects of hypertonic saline solution (HSS) resuscitation on endotoxic shock were examined in pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli (055:B5) endotoxin was infused IV at dosage of 0.1 microgram/kg of body weight for 30 minutes. Endotoxin induced large decreases in cardiac index, stroke volume, maximal rate of change of left ventricular pressure (+dP/dtmax), femoral and mesenteric arterial blood flow, glomerular filtration rate, urine production, and mean aortic pressure. Severe pulmonary arterial hypertension and increased pulmonary vascular resistance were evident at the end of endotoxin infusion. Treatment with HSS (2,400 mosm of NaCl/L, 4 ml/kg) or an equivalent sodium load of isotonic saline solution (ISS: 300 mosm of NaCl/L, 32 ml/kg) was administered 90 minutes after the end of endotoxin administration. Both solutions were infused IV over a 4- to 6-minute period. Administration of HSS induced immediate and significant (P less than 0.05) increase in stroke volume and central venous pressure, as well as significant decrease in pulmonary vascular resistance. These effects were sustained for 60 minutes, after which all variables returned toward preinfusion values. The hemodynamic response to HSS administration was suggestive of rapid plasma volume expansion and redistribution of cardiac output toward splanchnic circulation. Plasma volume expansion by HSS was minimal 60 minutes after resuscitation. Administration of ISS induced significant increase in cardiac index, stroke volume, femoral arterial blood flow, and urine production. These effects were sustained for 120 minutes, at which time, calves were euthanatized. Compared with HSS, ISS induced sustained increase in mean pulmonary arterial pressure and only a small increase in mesenteric arterial blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)     

Muscle hemodynamics in hereditary myopathy of Labrador retrievers

Morphologic lesions seen in six 8-month-old Labrador Retrievers with hereditary myopathy were predominantly small- and large-group atrophy of muscle cells of all fiber types. The dogs were intolerant of exercise and fatigued rapidly. An isolated gracilis muscle preparation was used to study the hemodynamic features of the microvasculature. Isogravimetric capillary pressure as well as arterial and venous pressures in the isolated gracilis muscle preparation obtained during maximal vasodilatation were within the range reported for healthy, mixed-breed dogs, as were precapillary, postcapillary, and total vascular resistances. Capillary filtration and osmotic reflection coefficients were not different from those reported in other studies on healthy dogs. All measurements and calculations were repeated during reperfusion, subsequent to a 4-hour period of global ischemia. Postischemic vascular responses were similar to the pattern previously reported in healthy dogs. These studies did not support the hypothesis of a vascular defect as a cause of hereditary myopathy in Labrador Retrievers.     

Effect of hypertonic vs isotonic saline solution on responses to sublethal Escherichia coli endotoxemia in horses

Cardiovascular responses to sublethal endotoxin infusion (Escherichia coli, 50 micrograms/ml in lactated Ringer solution at 100 ml/h until pulmonary arterial pressure increased by 10 mm of Hg) were measured 2 times in 5 standing horses. In a 2-period crossover experimental design, horses were either administered hypertonic (2,400 mosm/kg of body weight, IV) or isotonic (300 mosm/kg, IV) NaCl solution after endotoxin challenges. Each solution was administered at a dose of 5 ml/kg (infusion rate, 80 ml/min). Complete data sets (mean arterial, central venous, and pulmonary arterial pressures, pulmonary arterial blood temperature, cardiac output, total peripheral vascular resistance, heart rate, plasma osmolality, plasma concentration of Na, K, Cl, and total protein, blood lactate concentration, and PCV) were collected at 0 (baseline, before endotoxin infusion), 0.25, 1, 1.5, 2, 2.5, 3, 3.5, 4, and 4.5 hours after initiation of the endotoxin infusion. Blood constituents alone were measured at 0.5 hour and cardiovascular variables alone were evaluated at 0.75 hour. By 0.25 hour, endotoxin infusion was completed, a data set was collected, and saline infusion was initiated. By 0.75 hour, saline solutions had been completely administered. Mean (+/- SEM) cardiac output decreased (99.76 +/- 3.66 to 72.7 +/- 2.35 ml/min/kg) and total peripheral resistance (1.0 +/- 0.047 to 1.37 +/- 0.049 mm of Hg/ml/min/kg) and pulmonary arterial pressure (33.4 +/- 0.86 to 58.3 +/- 1.18 mm of Hg) increased for both trials by 0.25 hour after initiation of the endotoxin infusion and prior to fluid administration. For the remainder of the protocol, cardiac output was increased and total peripheral resistance was decreased during the hypertonic, compared with the isotonic, saline trial.(ABSTRACT TRUNCATED AT 250 WORDS)     

A comparison of the haemodynamic effects of propofol and isoflurane in pregnant ewes

The purpose of this study was to compare the effects of inhaled isoflurane and a constant infusion of propofol on maternal haemodynamics and uterine arterial and umbilical venous flows in pregnant ewes. Late term pregnant ewes ( n  = 5) were randomly assigned to receive either inhaled isoflurane or an intravenous infusion of propofol for 1 h, each on separate occasions. Maternal systemic arterial, right atrial and pulmonary arterial blood pressures, cardiac index, systemic vascular resistance index, stroke volume index, heart rate, and uterine arterial and umbilical venous flows were determined over the 1 h period of each treatment. Data were analysed using an univariate analysis of variance for repeated measures performed on the ranks of the data. Propofol anaesthetized ewes had significantly higher heart rate ( P  = 0.0040), mean arterial pressure ( P  = 0.0003) and cardiac index ( P  = 0.0475) compared to isoflurane anaesthetized ewes. There were no significant differences in uterine arterial flows, umbilical venous flows, or other measured variables. Continuous propofol infusions maintain maternal haemodynamics at significantly higher levels than does inhaled isoflurane, while uterine arterial and umbilical venous flows do not differ significantly.     

Cardiovascular Responses to Glibenclamide During Endotoxaemia in the Pig

Vanelli, G., Hussain, S.N.A., Dimori, M. and Aguggini, G., 1996. Cardiovascular responses to glibenclamide during endotoxaemia in the pig. Veterinary Research Communications, 21(3), 187-200The effects of blockading the ATP-sensitive potassium channel (K+ATP channels) on endotoxin-induced vascular derangements was studied. Escherichia coli endotoxin was infused (20 µg/kg per h) intravenously for 180 min into anaesthetized, mechanically ventilated, indomethacin-treated pigs. After 150 min of endotoxaemia, glibenclamide (a K+ATP channel blocker) was infused intravenously at 2 mg/kg per min for 5 min. The cardiovascular parameters were recorded before (control), every 30 min up to 150 min during endotoxaemia, and then at 5, 15 and 30 min after administration of glibenclamide. Infusion of endotoxin reduced the systemic arterial pressure to 60.6% ± 3.7% (p < 0.01) and increased the pulmonary arterial pressure by 75.9% ± 11.0% (p < 0.01) of the control values. Within 5 min, infusion of glibenclamide transiently but significantly reversed the systemic hypotension by raising the systemic vascular resistance, whereas the increased pulmonary arterial pressure was further augmented. Glibenclamide infusion did not influence the cardiac output. Within 30 min, the cardiovascular parameters had returned to the values induced by endotoxin, except for the systemic vascular resistance. Infusion of glibenclamide into normal pigs did not change the systemic pressure or resistance, but the pulmonary pressure and resistance were augmented transiently. These data suggest that, in pigs, the ATP-sensitive K+ channels may be one factor playing a role in the vascular changes due to endotoxaemia, especially in the systemic circulation.     

Effects of an endothelin receptor antagonist and nitroglycerin on digital vascular function in horses during the prodromal stages of carbohydrate overload-induced laminitis

OBJECTIVE: To evaluate changes in digital vascular function in horses with carbohydrate overload (CHO)-induced laminitis and determine the effects of an endothelin (ET) receptor antagonist and nitroglycerin on laminitis-associated vascular dysfunction. ANIMALS: 20 adult horses without abnormalities of the digit. PROCEDURES: Hemodynamic variables were recorded before (baseline) and hourly after all horses were administered a CHO ration via nasogastric tube. In 4 groups of 5 horses each, saline (0.9% NaCl) solution or ET receptor antagonist (10(5)M in digital blood) was administered into the digital arterial circulation according to 1 of 2 schedules. During anesthesia, blood flow; arterial, venous, and capillary pressures; and total, precapillary, and postcapillary resistances were measured in an isolated perfused digit of each horse. In all groups, nitroglycerin was infused (10(5)M in digital blood), and digital microvascular assessments were repeated. RESULTS: The CHO caused a significant decrease in right atrial pressure by 14 hours that was not affected by administration of saline solution or ET receptor antagonist. In isolated digits of anesthetized horses, CHO resulted in a significant decrease in digital blood flow associated with a significant increase in total and postcapillary resistances. Treatment with the ET receptor antagonist and nitroglycerin caused a significant decrease in total resistance. Postcapillary resistance was significantly decreased following treatment with the ET receptor antagonist but was not altered by treatment with nitroglycerin. CONCLUSIONS AND CLINICAL RELEVANCE: Treatment with an ET receptor antagonist and nitroglycerin resulted in significant improvement in vascular resistance in isolated perfused digits of anesthetized horses with CHO-induced laminitis.     

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.     

Hemodynamic Responses of Horses to Anesthesia and Surgery, Before and After Administration of a Low Dose of Endotoxin

Seven horses, which were part of an investigation of the effect of endotoxin administration on vascular reactivity, were anesthetized on two separate occasions for surgical excision of 4-cm sections of palmar digital artery and vein. On the first occasion, the horses were given an infusion of 1 L 0.9% NaCl solution intravenously (IV) just before induction of anesthesia (control); on the second occasion, the horses received an infusion of 1 L 0.9% NaCl containing Escherichia coli endotoxin, 0.1 μg/kg (endotoxin). On both occasions, anesthesia was induced with xylazine, guaifenesin, and ketamine, and maintained with halothane in oxygen. Hemodynamic measurements were made with the horses under anesthesia immediately before beginning surgery (period 1), during skin incision (period 2), during dissection and excision of the vessels (period 3), during skin suturing (period 4), and after completion of surgery during bandaging (period 5). Hemoglobin concentration and mixed venous oxygen content were greater at all periods in horses that received endotoxin. Otherwise, there were no significant differences in hemodynamic parameters between control horses and horses administered endotoxin before beginning surgery (period 1). During surgery and bandaging, horses administered endotoxin had significantly higher heart rate (periods 3, 4, and 5), cardiac index (periods 3, 4, and 5), and oxygen delivery (periods 2, 3, 4, and 5) than did control horses, and mean arterial blood pressure (period 2) and systemic vascular resistance (periods 2, 3, 4, and 5) were less than in control horses. Compared with period 1, surgical stimulation in control horses was associated with increased mean arterial blood pressure and systemic vascular resistance (periods 2, 3, 4, and 5), but cardiac index and oxygen delivery were decreased (periods 3, 4, and 5). In contrast, horses administered endotoxin responded to surgical stimulation with increased mean arterial blood pressure (periods 2, 3, 4, and 5) and vascular resistance (periods 4 and 5), as well as a heart rate-induced increase in cardiac index (periods 2, 3, 4, and 5) compared with period 1; oxygen delivery also increased (periods 2, 3, 4, and 5) during surgery in the endotoxin group. This study documents some of the differences in the response to anesthesia and surgery between normal horses and those that have received endotoxin.     

Effects of an infusion of dopamine on the cardiopulmonary effects of Escherichia coli endotoxin in anaesthetised horses

Horses with colic may be endotoxaemic and subsequently develop hypotension during anaesthesia for surgical operation. The aim of this study was to evaluate the efficacy of dopamine as a means to improve cardiovascular function in anaesthetised endotoxaemic horses. Nine horses (five in group 1 and four in group 2) were anaesthetised with thiopentone and guaifenesin and anaesthesia was maintained with halothane. After approximately one hour, facial artery pressure, heart rate, pulmonary artery pressure, cardiac output, temperature, pHa, PaCO2, PaO2, base excess, packed cell volume, plasma protein concentration and white cell count were measured (time 0). Escherichia coli endotoxin was infused intravenously over 15 minutes in both groups. Group 2 horses were given an intravenous infusion of dopamine (5 micrograms kg-1 min-1) starting five minutes after the start of the endotoxin infusion and continuing for 60 minutes. Measurements were made at 15 minute intervals for 120 minutes. In group 1, one horse died during the endotoxin infusion and in two other horses mean facial artery pressures decreased to 50 mm Hg. Total pulmonary vascular resistance and packed cell volume were significantly increased. Cardiac output, cardiac index and change in mean arterial pressure were significantly greater in group 2 horses than in group 1 horses. Conversely, diastolic pulmonary artery pressure, total vascular resistance and total pulmonary resistance were significantly less in group 2 than in group 1. PaO2, base excess and white blood cell count were significantly decreased in both groups. It was concluded that dopamine improved cardiovascular function in the presence of endotoxaemia and attenuated the rate of haemoconcentration, but had no effect on the development of decreased PaO2 or metabolic acidosis.     

The cardiopulmonary effects of dobutamine and norepinephrine in isoflurane-anesthetized foals

OBJECTIVE: To evaluate the cardiovascular effects of norepinephrine (NE) and dobutamine (DB) in isoflurane-anesthetized foals. STUDY DESIGN: Prospective laboratory study. METHODS: Norepinephrine (0.05, 0.10, 0.20, and 0.40 microg kg(-1) minute(-1)) and dobutamine (2.5, 5.0, and 10 microg kg(-1) minute(-1)) were alternately administered to seven healthy, 1- to 2-week-old isoflurane-anesthetized foals. Arterial and pulmonary arterial blood pressure, right atrial pressure, pulmonary artery occlusion pressure, heart rate, body temperature, cardiac output, arterial and mixed venous blood pH, partial pressure of carbon dioxide, partial pressure of oxygen [arterial partial pressure of oxygen (PaO(2)) and mixed venous partial pressure of oxygen (PvO(2))], and packed cell volume were measured. Standard base excess, bicarbonate concentration, systemic and pulmonary vascular resistance, cardiac index (CI), stroke volume, left and right stroke work indices, oxygen delivery (DO(2)), consumption, and extraction were calculated. Results Norepinephrine infusion resulted in significant increases in arterial and pulmonary arterial pressure, systemic and pulmonary vascular resistance indices, and PaO(2); heart rate was decreased. Dobutamine infusion resulted in significant increases in heart rate, stroke volume index, CI, and arterial and pulmonary arterial blood pressure. Systemic and pulmonary vascular resistance indices were decreased while the ventricular stroke work indices increased. The PaO(2) decreased while DO(2) and oxygen consumption increased. Oxygen extraction decreased and PvO(2) increased. CONCLUSIONS AND CLINICAL RELEVANCE: Norepinephrine primarily augments arterial blood pressure while decreasing CI. Dobutamine primarily augments CI with only modest increases in arterial blood pressure. Both NE and DB could be useful in the hemodynamic management of anesthetized foals.     

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.     

Equine endotoxemia: pathomorphological aspects of endotoxin-induced damage in equine mesenteric arteries

To evaluate the effects of endotoxin on the morphology of the equine mesenteric vasculature, each of two thoroughbred horses were given two intravenous injections (24 h apart) of a sublethal dose of endotoxin (10 microg/kg). Each injection produced results similar to those of clinical cases of equine colic with obstructive nature of the loop of bowel: diarrhoea within 2 h after administration, followed by cessation of both faecal excretion and sounds of intestinal peristalsis. The most prominent morphological change was the development of moniliform appearance of small mesenteric arteries, in which there were contracted and dilated segments of the small mesenteric arteries. This was accompanied by parietal hyalinization and intramural and extramural haemorrhage. These mesenteric vascular changes appear to reflect dynamic vasoconstriction in the living animal, resulting in reduction of mesenteric and intestinal blood flow and possibly inducing alterations of gastrointestinal function such as cessation of intestinal peristalsis.     

Endotoxic shock in the awake young pig: absence of beneficial effect of prednisolone sodium succinate treatment

In nonanesthetized young pigs, the influence of prednisolone sodium succinate therapy on a 65% lethal dose of Escherichia coli endotoxin was studied by evaluating clinical signs, several hemodynamic variables, survival rate, and changes seen at necropsy. Endotoxin infusion induced reproducible clinical signs characterized by nausea, vomiting, dyspnea, cyanosis, and moderate excitement followed by severe CNS depression. Among the hemodynamic variables, there were decreases in arterial blood pressure and cardiac output and increases in pulmonary arterial pressure, heart rate, and total peripheral and pulmonary vascular resistances. Core temperature and arterial pH did not change significantly. Survival rate at 30 hours after the start of the endotoxin infusion was 35%. According to the necropsy, marked edema and hemorrhages were in several organs. Treating the experimental animals with prednisolone sodium succinate (3 injections of 10 mg/kg of body weight after the start of the endotoxin infusion) did not influence any of the monitored hemodynamic variables, except for arterial blood pressure, which was higher at the end of the hemodynamic recording period (270 minutes after the start of the endotoxin infusion). Clinical signs, survival rate, and changes at necropsy were similar in both treated and nontreated pigs. This lack of effect can be due to an inappropriate dosage of the steroid or failure of steroid treatment to alleviate endotoxin-mediated effects.     

Hemodynamic Effects of Medetomidine in the Dog: A Dose Titration Study

Objective —To characterize the hemodynamic effects of medetomidine administered intravenously at doses ranging from 1 to 20 μg/kg, and to determine whether these effects are dose dependent. Study Design —Prospective randomized multidose trial. Animals —Twenty-five clinically normal male beagles (5 groups of 5), aged 1 to 4 years and weighing 13.5 ±1.7 kg. Methods —Medetomidine, at a dose of 1, 2, 5, 10, or 20 μg/kg, was administered intravenously at time 0. Heart rate, arterial pressure, central venous pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, body temperature, cardiac output, and packed cell volume were measured immediately before and at selected times after medetomidine administration (3, 7, 10, 20, 30, 40, 50, and 60 minutes in all groups, at 90 minutes for the 10 and 20 μg/kg groups, and at 120 minutes for the highest dose). Cardiac index, stroke index, rate-pressure product, systemic vascular resistance index, pulmonary vascular resistance index, and left and right ventricular stroke work indices were calculated. The degree of sedation was subjectively scored by an observer who was blinded to the treatment used. Results —Heart rate, rate-pressure product, cardiac index, and left and right ventricular stroke work indices decreased below baseline values. Central venous pressure and systemic vascular resistance index increased above baseline measurements. Except in the 2 μg/kg group, after an initial and short lasting increase, a prolonged decrease in arterial pressure was observed. Conclusions —Hemodynamic changes were observed with the intravenous (IV) administration of medetomidine, at any dose. However, the two lowest doses (1 and 2 μg/kg) produced less cardiovascular depression. Clinical Relevance —Medetomidine is an alpha-2 adrenoceptor agonist widely used in dogs, producing sedation, analgesia and cardiovascular depression. When using IV medetomidine, a reduction of the recommended dosage (ie, ±30 to 40 μg/kg) by up to 6 times did not significantly influence the cardiovascular effects.     

Pulmonary vascular pressures of strenuously exercising Thoroughbreds during intravenous infusion of nitroglycerin

OBJECTIVE: To determine whether intravenous infusion of nitroglycerin would modify pulmonary arterial, capillary, or venous hypertension in strenuously exercising Thoroughbreds. ANIMALS: 5 healthy Thoroughbred horses. PROCEDURE: Right atrial, right ventricular, and pulmonary vascular pressures were measured. Each horse was used in a control treatment (not medicated) and a nitroglycerin infusion (20 microg/kg of body weight/min) at rest and during exercise on a treadmill. Sequence of treatments was randomized for each horse, and treatments were separated by a 7-day interval. Galloping at 14.2 m/s on a 5% uphill grade elicited maximal heart rate (mean +/- SEM, 212 +/- 2 beats/min) and could not be sustained for > 90 seconds. Nitroglycerin dosage was selected, because maximal pulmonary and systemic hemodynamic effects of i.v. nitroglycerin were elicited at 5 microg/kg/min and increasing the dosage to 20 microg/kg/min did not cause adverse effects. RESULTS: In the control treatment, exercise performed at maximal heart rate resulted in a significant increase in right atrial as well as pulmonary arterial, capillary, and wedge pressures. Nitroglycerin infusion in standing horses significantly decreased right atrial and pulmonary vascular pressures, whereas heart rate increased. Exercise in nitroglycerin-infused horses also resulted in a significant increase in right atrial as well as pulmonary arterial, capillary, and wedge pressures, and these values were not significantly different from data for the control treatment. All horses experienced exercise-induced pulmonary hemorrhage for both treatments. CONCLUSIONS AND CLINICAL RELEVANCE: I.v. administration of nitroglycerin does not modify exercise-induced pulmonary hypertension and is unlikely to affect the incidence or severity of exercise-induced pulmonary hemorrhage in Thoroughbreds.