We characterized the clinicopathologic manifestations of experimentally induced endotoxin-induced mastitis. Responses to hypertonic fluid therapy also were assessed. Eight cows received 1 mg of endotoxin by in infusion in the left forequarter. Four hours after endotoxin administration, cows received 0.9% NaCl, 5 ml/kg of body weight (n = 4) or 7.5% NaCl, 5 ml/kg (n = 4) IV. Endotoxin-infused cows had expanded plasma volume, hyponatremia, transient hyperchloremia and hypophosphatemia, increased serum glucose concentration, and decreased serum activities of liver- and muscle-specific enzymes. Calculated plasma volume increased at 6 hours in cows receiving hypertonic NaCl, and at 12, 24, and 48 hours after endotoxin infusion in both groups. Concurrent observations of decreased serum protein concentration, erythrocyte count, and hematocrit supported observations of increased plasma volume. Relative plasma volume was greater in cows receiving hypertonic NaCl (124.3%) than in cows receiving isotonic NaCl (106.6%) at 6 hours after endotoxin infusion. Cattle receiving hypertonic NaCl had increased voluntary water intake after IV fluid administration. Increased water consumption was not accompanied by increased body weight, indicating probable occurrence of offsetting body water loss. Serum sodium concentration in cows receiving hypertonic NaCl was increased 2 hours after fluid administration, but the magnitude of the change was minimal (< 4 mmol/L) and transient, indicating rapid equilibration with either interstitial or intracellular spaces. Serum sodium concentration was decreased in cows receiving isotonic NaCl at 12, 24, and 48 hours after endotoxin administration, compared with concentration prior to endotoxin administration, indicating selective loss of sodium.

Blood constituents and vascular volume indices were determined in 5 standing horses by use of 2-period crossover experimental design. Horses were either administered hypertonic (2,400 mosm/kg of body weight, IV) or isotonic (300 mosm/kg, IV) saline solution. Each solution was administered at a dosage of 5 ml/kg (infusion rate, 80 ml/min). Samples for determination of PCV, plasma volume, blood volume, plasma osmolality, total amount of plasma protein and plasma concentrations of protein, Na, K, and Cl were collected at 0 hour (baseline, before fluid infusion) and 0.5 hour (at the end of fluid infusion), and subsequently, at 0.25- or 0.5-hour intervals for 4.5 hours. All horses were given the predetermined dose of fluids by 0.5 hour after beginning the saline infusion. Values of P less than or equal to 0.05 were considered significant. Administration of hypertonic saline solution was associated with decreased mean body weight by 4.5 hours, but weight change after isotonic saline administration was not significant. Other than body weight and plasma protein concentration, between-trial difference (treatment effect) was not observed for any measured variable or index. The F values indicated that increasing the number of horses would have not changed these results. A time effect was evident across both trials, so that mean (+/- SD) plasma volume increased (12.3 +/- 1.07%) and mean plasma protein concentration (-12.1 +/- 1.03%) and PCV (-11.9 + 0.67%) decreased proportionately and transiently in association with administration of either fluid at that volume. Other time effects included increased plasma osmolality and Na and Cl concentrations. Blood volume estimates and total amount of plasma protein remained unchanged. These data indicate that in conscious clinically normal horses, changes in plasma protein concentration reflect changes in plasma volume and that blood volume may be regulated by alterations in plasma volume and red cell mass. These data also indicate that changes in plasma volume and constituent concentrations may be similar in response to administration of either 0.9% (300 mosm/kg) or 7.2% (2,400 mosm/kg) NaCl solutions (5 ml/kg) and that clinically normal horses can rapidly regulate variable Na loads.

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 < 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. The rapid administration of large-volume ISS appears superior to small-volume HSS for initial resuscitation of acutely endotoxemic, anesthetized calves. At this time, we do not advocate rapid infusion of ISS to septicemic calves because exacerbation of pulmonary hypertension may potentially depress respiratory function, and rapid increase in preload may hemodynamically compromise calves with depressed cardiac contractility.

Terminal renal dysfunction (TRD) was induced in 2 groups of dogs by partial surgical ablation of the kidney. Dogs of a control group and of 1 of the TRD groups were maintained on a diet containing normal phosphorus concentration, whereas dogs of the other TRD group were maintained on a low-phosphorus diet. Mild anemia developed in dogs of both TRD groups and could not be attributed to iron deficiency, increased erthrocyte concentration of 2,3-diphosphoglycerate, or absolute deficiency of erythropoietin (EP). Subsequently, all dogs were acutely depleted of approximately 25% of their blood volume. Erythropoietin concentration in dogs of the TRD groups was lower than that of controls, however, erythroid regenerative capacity was comparable with that of control dogs when plasma parathyroid hormone (PTH) concentration was lowered by reduced dietary intake of phosphorus. The PCV in dogs of the chronic TRD goups had a slight positive correlation with serum EP concentration, and a significant (P lesss than 0.05) negative correlation with plasma PTH and serum phosphorus and creatinine concentrations, using a correlation matrix. There was no longer a significant correlation between plasma PTH concentration and PCV after controlling for serum creatinine concentration by use of a multiple linear regression analysis. A significant (P less than 0.05) negative correlation also was observed between plasma PTH and serum EP concentrations, but not between serum EP and phosphorus or or creatinine concentrations. Significance of the EP and PTH association was reduced when analyzed, using a multiple linear regression analysis that included serum creatinine values. According to these data, PTH does have an independent effect on EP concentration, but the relationship between PTH and EP is not sufficiently strong to account for the genesis of the anemia of chronic TRD.

The effect of meal size and frequency on plasma volume, plasma aldosterone concentration and urinary Na and K clearances was determined in ponies. A daily maintenance ration of hay-grain pellets was provided either as a multiple feeding regimen, ie, 12 equal portions fed at 2-hour intervals, or as single large feedings, ie, half the ration fed every 12 hours at 0800 and 2000 hours. Only the effect of the single morning feeding was studied, using the latter regimen. Serial measurements of plasma volume were made by use of an indicator-dilution technique and indocyanine green (0.15 mg/kg of body weight, IV) that allowed repeated determinations at 2-hour intervals. Ingestion of the single large meal caused a 15% decrease in plasma volume by the end of a 1-hour feeding period. Feeding hypovolemia was confirmed by a coincident increase in plasma protein concentration (12%) and, in separate experiments, by analysis of postfeeding changes in the elimination of Evans blue dye. Plasma aldosterone concentration was significantly (P < 0.05) increased from 2 to 5 hours after feeding. Urinary Na clearance decreased in response to feeding and remained lower than the prefeeding value until 9 hours after feeding. Urinary K clearance increased from prefeeding and reached a peak value between 5 and 7 hours after feeding. Creatinine clearance was unaffected. In contrast, the aforementioned variables were unchanged during the multiple regimen. Results indicate that ingestion of a large concentrate meal by ponies causes periprandial hypovolemia, activation of the renin-angiotensin-aldosterone system, and a subsequent antinaturesis-kaluresis that lasts for several hours.