Effect of dehydration on cardiovascular responses and electrolytes after hypertonic saline/dextran treatment for moderate hemorrhage.

STUDY OBJECTIVE: To determine if hypertonic saline/dextran (HSD) is effective in treating hemorrhage in the presence of dehydration. DESIGN: After surgical preparation, swine were euhydrated or dehydrated for 24 or 48 hours. Animals were bled 25 mL/kg over 60 minutes and treated with HSD. SETTING: Laboratory. PARTICIPANTS: Seventeen immature Yorkshire pigs. INTERVENTIONS: 4 mL/kg HSD (7.5% NaCl in 6% dextran-70) administered over one minute. MEASUREMENTS AND MAIN RESULTS: All euhydrated animals survived; 100% of the pigs survived 180 minutes after treatment. Two animals dehydrated for 24 hours and three animals dehydrated for 48 hours died within three hours of HSD treatment. In all groups, plasma potassium was reduced significantly and equally; cardiac output was increased; mean arterial pressure rose rapidly within first five minutes, but was sustained only in euhydrated animals; hematocrit, hemoglobin, and plasma total protein levels were reduced; and plasma glucose increased with persistent between-group differences. RESULTS: HSD immediately rectified the decreases in mean arterial pressure and cardiac output incurred during hemorrhage; over time, however, the improvement in pressure was not sustained in dehydrated pigs. Parallel increases in plasma osmolality and sodium concentrations were offset by the initial group differences resulting from dehydration. CONCLUSION: Dehydration does not compromise the efficacy of HSD as a resuscitation treatment for hemorrhagic shock.

Neuroendocrine responses to hypertonic saline/dextran resuscitation following hemorrhage.

The neuroendocrine responses to resuscitation with 7.5% hypertonic saline/6% Dextran-70 (HSD) following hemorrhagic hypotension were evaluated in conscious swine. Following hemorrhage (37.5 ml/kg/60 min) animals received 4 ml/kg of HSD (n = 6) or 0.9% saline (n = 8). Administration of normal saline did not alter cardiovascular function nor attenuate an increase in hormones. HSD rapidly improved cardiovascular function and acutely decreased ACTH, plasma renin activity (PRA), cortisol, norepinephrine (NE), epinephrine (E), aldosterone, and lysine vasopressin levels (LVP). The initial decreased in ACTH, cortisol, and aldosterone levels was due primarily to hemodilution associated with the expansion of plasma volume. The reductions in NE, E, LVP, and PRA were greater than those attributed to hemodilution alone. Values for LVP, NE, and E remained at values below those at the end of hemorrhage, but greater than basal levels, while PRA returned to values similar to these at the end of hemorrhage. The decrease in LVP, NE, and E following HSD resuscitation for the treatment of hemorrhagic hypotension may result from and contribute to the rectification of cardiovascular and metabolic function.

Hypertonic saline/dextran improves renal function after hemorrhage in conscious swine.

This study was performed to determine whether resuscitation with a single bolus of 7.5% NaCl/6% Dextran 70 (hypertonic saline/Dextran, HSD) could restore renal function following hemorrhage. Chronically instrumented, conscious pigs were hemorrhaged 28 ml/kg. This level of hemorrhage reduced mean arterial pressure (MAP) and cardiac output (CO) to nearly half, renal blood flow (RBF) to approximately 25%, and glomerular filtration rate (GFR) and urine flow (V) to less than 10% of their initial values. A single, 4 ml/kg bolus injection of HSD increased MAP and RBF to approximately 80% of baseline values and restored CO and GFR to levels which were significantly different from control values. These improvements were sustained for 2 h with no further treatment. Urine flow transiently increased although not to pre-hemorrhage values, and then subsided. Plasma osmolality increased from 275 to 282 mOsm/kg H2O, and plasma sodium increased from 141 to 149 mEq/l. Recovery following administration of an equal volume of normal saline was significantly less for all variables. Euvolemic animals showed no response in MAP, CO, RBF, or GFR when treated with HSD although V, osmotic and sodium excretion increased. These results demonstrate that resuscitation with HSD following hemorrhage not only restores MAP and CO, but maintains renal function as well.

Blood gas and acid-base status of conscious pigs subjected to fixed-volume hemorrhage and resuscitated with hypertonic saline dextran.

Conscious, chronically instrumented pigs were subjected to a progressive, fixed-volume hemorrhage (37.5 ml/kg over 1 h) and subsequent resuscitation with 7.5% hemorrhage (37.5 ml/kg over 1 h) and subsequent resuscitation with 7.5% NaCl/6% Dextran 70 (4 ml/kg). Hemorrhage led to increases in arterial PO2, HbO2, plasma lactate, base deficit, and mixed venous PCO2. It led to decreases in arterial PCO2, plasma bicarbonate, and buffer base, as well as mixed venous PO2, HbO2, and pH. These effects were attributable to reduced O2 delivery, lactacidemia, hyperventilation, and hemodilution. Resuscitation with hypertonic saline/dextran produced a transient increase in arterial PCO2 and base deficit and a transient decrease in pH, effects that were attributable to a transfer of venous blood attributes to the arterial circulation. Resuscitation also produced an immediate decrease in arterial buffer base, an effect attributable to hemodilution. Subsequently, over 4 h, most cardiopulmonary and metabolic variables gradually reverted toward control levels, thereby ameliorating the deleterious blood gas and acid-base disturbances produced by severe hemorrhage.

Renal responses to graded hemorrhage in conscious pig.

We developed a conscious pig model with a chronically instrumented kidney to measure renal blood flow (RBF), glomerular filtration rate (GFR), and excretory functions during hemorrhage. Seven to 10 days before experimentation, pigs were splenectomized, arterial and venous catheters were implanted, an ultrasonic flow probe was placed on the renal artery, and a pyelostomy was performed for nonocclusively placing a ureteral catheter. Measurements were taken before hemorrhage, and at hemorrhage volumes of 7, 14, 21, and 28 ml/kg (equivalent to 10.5, 21, 31, and 42% of the estimated blood volume), or at corresponding time points for controls. RBF was decreased by 30% when 21% of the blood (14 mg/kg) was removed, before arterial pressure, GFR, or urine flow or excretion was changed. At volumes of hemorrhage greater than 14 ml/kg, there were progressive decreases in RBF, GFR, urine flow rate, osmotic and electrolyte excretion, and arterial pressure. Thus pigs, like humans, respond to hypovolemia with an early redistribution of blood flow away from the kidney.

Resuscitation of conscious pigs following hemorrhage: comparative efficacy of small-volume resuscitation.

Efficacy of small-volume resuscitation (4 ml/kg) with 7.5% NaCl in 6% Dextran 70 (HSD), 7.5% NaCl (HS), dextran (D), and 0.9% NaCl (NS) was evaluated in conscious swine bled 37.5 ml/kg over 60 min. Hemorrhage reduced cardiac index (CI), stroke volume (SV), and mean arterial pressure (MAP). Four-hour survival after HSD (67%) was significantly (P less than 0.05) greater than after HS (25%), D (17%), or NS (0%). The superior performance of HSD, and to a lesser extent HS, was associated with rapid plasma volume expansion, improved CI and SV, and decreased heart rate. The acute increases in cardiac index and stroke volume were greater following treatment with HSD and the improvement persisted for 4 hr. HSD also produced a transient increase in MAP. Plasma Na+ concentration and osmolality were increased to a similar extent with HSD and HS, while plasma K+ levels were initially decreased, returning to control levels within 60 min. HSD appears to be a superior small-volume resuscitation solution compared to the other treatments with no detrimental effects.

Oxygen delivery and demand in conscious pigs subjected to fixed-volume hemorrhage and resuscitated with 7.5% NaCl in 6% Dextran.

A conscious porcine model was used to investigate the adequacy of O2 delivery relative to O2 demand, initially during a fixed-volume hemorrhage (37.5 ml/kg over 1 hr) and subsequently after resuscitation with 7.5% NaCl/6% Dextran 70 (4 ml/kg). Hemorrhage produced a small increase in O2 consumption, severe lactacidemia, and a doubling of apparent O2 demand. These effects were attributable to a behavioral compensation (periodic bouts of muscle activity) which presumably served to improve venous return. Despite enhanced ventilatory function, arterial O2 delivery was markedly reduced by hemorrhage, an effect that was due entirely to decrements in cardiac output and hemoglobin level. The disparity between O2 delivery and O2 demand was lessened following resuscitation with 7.5% NaCl/6% Dextran 70, primarily by suppression of demand and secondarily by an augmentation of delivery.