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.

We investigated small-volume (5 ml/kg) 7% NaCl in 6% dextran 70 (HS/D70) as an alternative to large-volume (60 ml/kg) 0.9% NaCl for treatment of experimentally induced canine gastric dilatation-volvulus (GDV) shock. The stomach was surgically displaced and then distended with an intragastric balloon in 11 dogs anesthetized with pentobarbital. All dogs were subjected to GDV for 180 minutes before partial decompression and resuscitation. Hemodynamic values, blood gas values, and plasma volume were measured during control, shock, and resuscitation periods. Resuscitation started with 1 group (n = 6) receiving 5 ml of HS/D70/kg, IV, over 5 minutes, and the other group (n = 5) receiving 60 ml of 0.9% NaCl/kg, IV, over 60 minutes. Both groups received a surgical maintenance dosage (20 ml/kg/h of 0.9% NaCl after initial resuscitation. Resuscitative effects of small-volume HS/D70 were similar to large-volume 0.9% NaCl during the first hour of treatment; however, cardiac output was significantly higher in the HS/D70 group for the last 2 hours of resuscitation. Changes in heart rate, left ventricular pressure change, and systemic vascular resistance appeared to be responsible for improved perfusion. Mixed venous oxygen partial pressure data supported improved perfusion in the HS/D70 group. Packed cell volume remained higher in the HS/D70 group, indicating less hemodilution and improved oxygen delivery. Resuscitation of this GDV-induced shock model was better sustained with small-volume HS/D70, compared with conventional large-volume 0.9% NaCl.

The respiratory, renal, hematologic, and serum biochemical effects of hypertonic saline solution (HSS) treatment were examined in 12 endotoxic, pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli endotoxin (055:B5) was infused IV at a rate of 0.1 microgram/kg of body weight over 30 minutes. Endotoxin induced severe respiratory effects, with marked hypoxemia and increases in arterial-alveolar O2 gradient (P[A-a]O2), physiologic shunt fraction (Qs/Qt), and physiologic dead space to tidal volume ratio (Vd/Vt). Oxygen consumption was decreased, despite an increase in the systemic O2 extraction ratio. Peak effects were observed at the end of endotoxin infusion. The renal response to endotoxemia was characterized by a decrease in free-water reabsorption and osmotic clearance, as well as a decrease in sodium and phosphorus excretion. Endotoxemia induced leukopenia, thrombocytopenia, hyperphosphatemia, hypoglycemia, acidemia, and increased serum alkaline phosphatase concentrations. Calves were treated with HSS (2,400 mosm/L of NaCl, 4 ml/kg, n = 4) or an equivalent sodium load of isotonic saline solution (ISS; 300 mosm/L of NaCl, 32 ml/kg, n = 4) 90 minutes after the end of endotoxin administration. Both solutions were infused over a 4- to 6-minute period. A control group (n = 4) was not treated. Infusion of HSS or ISS failed to induce a significant change in PaO2, P(A-a)O2, (Qs/Qt), (Vd/Vt), or oxygen consumption. Both solutions increased systemic oxygen delivery to above preendotoxin values. Hypertonic saline infusion induced significant (P < 0.05) increases in serum Na and Cl concentrations and osmolality, whereas ISS induced a significant increase in serum Cl concentration and a significant decrease in serum phosphorus concentration. Both HSS and ISS reversed the endotoxin-induced changes in renal function, with increases in free water reabsorption and osmotic clearance, as well as increases in sodium and phosphorus excretion. Sodium retention was greater following HSS administration. On the basis of these findings, hypertonic saline solutions can be rapidly and safely administered to endotoxic calves.