Over a 54-hour period, blood was removed from 8 adult sheep (body weight, 38.1 +/- 0.5 kg mean +/- SEM) in 9 episodes, 5 on day 1, 3 on day 2, and 1 on day 3. Cumulative blood loss was 1,630 +/- 63, 2,380 +/- 71, and 2,693 +/- 69 ml on days 1, 2, and 3, respectively. Blood samples (20 ml) were collected from 5 control ewes (33.8 +/- 2.8 kg) at equivalent times. Over the first day, mean arterial blood pressure decreased in the hemorrhaged sheep from 101 +/- 2 mm of Hg to 76 +/- 5 mm of Hg, but returned to control values by the beginning of the second day and, thereafter, was not different from control values. Heart rate was increased after the first hemorrhage episode and remained high throughout the entire protocol. Over the entire period, there were statistically significant decreases in hematocrit, plasma osmolality, sodium, total calcium (P < 0.001), potassium, and chloride values (P < 0.05). There was no change in plasma phosphate, bicarbonate, creatinine, or magnesium concentrations and an increase in plasma urea nitrogen (P < 0.001) concentrations. Plasma arginine vasopressin concentration was increased significantly (P < 0.001) over the entire period. Plasma ACTH concentration was significantly (P < 0.05) increased over time, but only some values on day 1 were significantly outside the normal range of the control group data. Because of wide variation between sheep, the group data for aldosterone were not significantly different from control values. Blood volume was restored on day 1 with fluid of osmolality, Na, and Cl composition equivalent to that of plasma. The effects of arginine vasopressin were apparent by day 2, when the major decrease in osmolality and Na and Cl concentrations were observed The sheep has good capacity to withstand severe, prolonged hemorrhage, most likely because of a large reserve of RBC in the spleen; hematocrit remained at 31% of control values when an estimated 100% of initial circulating blood volume had been removed.

During growth, central venous, right ventricular, pulmonary arterial, Pulmonary capillary wedge, and systemic arterial pressures, heart rate, and cardiac Output were repeatedly measured in 41 Friesian calves, considered as having conventional muscular conformation, and in 19 Belgian White and Blue double-muscled calves. A total of 123 and 70 recordings were collected in conventional and double-muscled calves, respectively. These circulatory indices were calculated: stroke volume, cardiac and stroke indices, pulmonary and systemic pulse pressures, pulmonary and systemic vascular resistance indices, and right and left ventricular work indices. Results indicated that systemic arterial and pulse pressures, as well as cardiac output, stroke volume, cardiac and stroke indices, and right and left ventricular work indices were significantly (P less than or equal to 0.05 to 0.001) lower but, in contrast, pulmonary and systemic vascular resistance indices were significantly (P less than or equal to 0.001) higher in double-muscled than in conventional calves. Right-sided vascular pressures and heart rate were similar in the 2 groups. These results indicated that global cardiac performance may be considerably poorer in double-muscled calves. Diminished cardiac performance of double-muscled calves appears to be related neither to relative bradycardia nor to reduced ventricular preload. The potential role of increased ventricular afterload or of reduced myocardial contractility in double-muscled cattle should be determined by direct measurements.

The uterine hemodynamic response to maternal positioning in dorsal recumbency was evaluated in 7 conscious pregnant cows during the third trimester. Anesthetic or sedative drugs were not administered. Uterine artery flow was measured, using a previously implanted ultrasonic flow probe. Catheters implanted in the uterine artery and vein were used for measurement of blood pressure and for blood sample collections. Heart rate, systemic arterial pressure, uterine arterial blood flow, arterial and venous oxygen and carbon dioxide tensions, and pH were measured in cows in standing position. Cows were cast with ropes and positioned in dorsal recumbency, then measurements were repeated at 15 and 30 minutes. Compared with standing measurements, dorsal recumbency caused 50% increase in heart rate and 44% increase in arterial blood pressure. Uterine artery flow did not change significantly. Despite increased ventilation, arterial oxygenation was reduced during dorsal recumbency. There were minimal differences between measurements at 15 and 30 minutes of dorsal recumbency.

We evaluated the biochemical and hemodynamic response to hypertonic saline solution plus dextran in isoflurane-anesthetized pigs infused IV with Escherichia coli endotoxin (5 micrograms/kg of body weight for 0 to 1 hour + 2 micrograms/kg for 1 to 4 hours). After 120 minutes of endotoxemia, pigs were treated with a bolus (4 ml/kg over 3 minutes) of either normal saline solution (NSS; 0.9% NaCl), or hypertonic saline solution plus dextran (HSSD; 7.5% NaCl + 6% dextran-70). Administration of HSSD significantly (P < 0.05) increased serum osmolality and concentrations of sodium and chloride for approximately 2 hours during endotoxemia. Plasma total protein concentration decreased significantly (P < 0.05) for 2 hours after treatment with HSSD, indicating hemodilution and increased plasma volume. Although HSSD transiently increased cardiac index (CI) for approximately 15 minutes, this effect was not sustained; however, the endotoxin-induced decrease in CI was ameliorated from 120 to 180 minutes. In pigs of the endotoxin + NSS group from 180 to 240 minutes, CI decreased significantly (P < 0.05), compared with baseline and control values. The endotoxin-induced increases in mean pulmonary arterial pressure and pulmonary vascular resistance were not attenuated by HSSD. At 135 minutes, total peripheral vascular resistance was transiently lower (for approx 15 minutes) in pigs treated with HSSD, compared with control pigs. The endotoxin-induced increase in plasma lactate concentration was not attenuated by HSSD, indicating continued peripheral O2 debt. We conclude that, despite sustained increases in serum osmolality and concentrations of sodium and chloride, HSSD has only transiently beneficial cardiopulmonary effects during endotoxemia in pigs.

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (BL) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of BL. All horses were monitored for 6 hours after BL data were collected. Blood samples were collected from the colonic vein and main pulmonary artery (systemic venous (SV) for measurement of plasma endotoxin, 6-keto prostaglandin F1alpha (6-kPG), thromboxane B2 (TXB2), and prostaglandin E2 (PGE2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (CV) serum samples. Data were analyzed, using two-was ANOVA, and post-hoc comparisons were made, using Dunnett's and Tukey's tests. Statistical significance was set at P < 0.05 Endotoxin was not detected in CV or SV plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at BL among groups for CV or SV 6-kPG, PGE2, or TXB2 concentrations, nor were there any changes across time in group-1 horses. Colonic venous 6-kPG concentration increased during ischemia in horses of groups 2 and 3; CV 6-kPG concentration peaked at 3 hours in group-3 horses, then decreased during reperfusion, but remained increased through 6 hours in group-2 horses. Systemic venous 6-kPG concentration increased during reperfusion in group-3 horses, but there were no changes in group-2 horses. Colonic venous PGE2 concentration increased during ischemia in horses of groups 2 and 3, and remained increased for the first hour of reperfusion in group-3 horses and for the 6-hour duration of ischemia in group-2 hors.

Prothrombotic changes occurring in the prodromal stages of carbohydrate-induced laminitis were investigated. Hemostatic alterations were evaluated by determining platelet counts, platelet survival, activated partial thromboplastin time, one-stage prothrombin time, and monocyte procoagulant activity. Thrombosis of vessels in the hoof wall was evaluated by contrast arteriography and histologic examination. Of 5 horses, 4 became lame between 28 and 52 hours after carbohydrate administration. Mean platelet count in laminitis-affected horses was lower throughout the prodromal stages of laminitis, compared with that in control horses, but differences were not statistically significant. However, survival of indium-111-labeled platelets was less than the value in control horses by 6 hours after carbohydrate administration. Arteriography of disarticulated feet revealed marked reduction in blood supply to hooves in laminitis-affected horses. Histologic examination of the laminar dermis disclosed microthrombi in venules of the laminar dermis in 2 of 4 affected horses. Statistically significant changes in prothrombin time were not observed, and changes in activated partial thromboplastin time were slight and occurred only at the onset of lameness. Statistically significant changes in monocyte procoagulant activity were not observed. Plasma endotoxin-like activity was not detected in laminitis-affected horses. These data indicate that platelet survival was decreased within the first 6 hours after induction of carbohydrate-induced laminitis, but systemic activation of the coagulation system was not detected.

In an effort to better understand the role of vasodilators in the management of pulmonary hypertension associated with chronic heartworm disease (HWD), pulmonary hemodynamic measurements were obtained from 7 experimentally infected, anesthetized dogs before and after hydralazine administration (mean dose, 1.96 mg/kg of body weight). Five dogs were maintained on room air, while 2 were maintained on 100% oxygen during the hydralazine study. The hemodynamic effect of hydralazine in dogs with HWD was evaluated, using heart rate, cardiac index, mean pulmonary artery pressure, mean arterial pressure, total pulmonary resistance, total systemic resistance, total systemic resistance/total pulmonary resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, and left and right ventricular double products ([mean arterial pressure X heart rate] and [mean pulmonary artery pressure X heart rate], respectively). Responders were defined as those in which total pulmonary resistance decreased greater than or equal to 20% without an increase in mean pulmonary arterial pressure and in which heart rate increase was less than or equal to 10%. Comparison was also made between maximal hemodynamic effect of hydralazine with that after 100% oxygen administration for 15 minutes to previously normoxemic dogs (n = 5). Significance was determined if P < 0.05, using the paired t-test. Hydralazine induced significant reductions in mean pulmonary and systemic arterial pressures and total pulmonary resistance, with no significant change in heart rate, cardiac index, total systemic resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, or right and left ventricular double products. Four (57%) of the 7 dogs studied were considered responders. Pretreatment cardiac index, mean pulmonary artery pressure, and total pulmonary resistance did not allow differentiation of responders from nonresponders.

Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only PAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.