Reduced oxygen consumption precedes the drop in body core temperature caused by hemorrhage in rats.

This study examines the early time course in core temperature change and oxygen consumption at 4 levels of hemorrhage. Chronically instrumented rats were acclimatized to a respirometry chamber for 30 min. The rats were briefly (10 min) removed from the chamber for a fixed volume hemorrhage of 0 mL/kg (sham), 8 mL/kg, 16 mL/kg, 24 mL/kg, or 32 mL/kg. Rats were then returned to the chamber, and oxygen consumption and body core temperature were monitored for the next 2 h. Oxygen consumption (control 1.26 mL O2/g/h) fell significantly 5 min after hemorrhage in all but the sham and 8 mL/kg hemorrhage groups, with the decrease proportional to the hemorrhage volume. The 32 mL/kg hemorrhage group showed the greatest decrease, to 0.47 mL O2/g/h. Body core temperature (control 37.5 degrees C) fell more gradually, declining to 35.6 degrees C 110 min after the 24 mL/kg hemorrhage, and to 33.2 degrees C at 6 h after the 32 mL/kg hemorrhage. In the 16 mL/kg hemorrhage group, oxygen consumption fell significantly by 5 min after hemorrhage, but a drop in body temperature was not seen until 25 min after hemorrhage. The data from this study indicate that the drop in core temperature does not cause the observed decrease in oxygen consumption. In fact, the timing and magnitude of the drop in oxygen consumption indicate that the reduced metabolic rate may mediate the hemorrhage-induced drop in body core temperature in conscious rats.

Reduced metabolic rate accompanies the hemorrhage-induced hypothermia in conscious rats.

The mechanism for the hemorrhage-induced drop in body temperature is unknown. This study determined the alterations in cutaneous heat exchange and metabolic heat production caused by a moderate hemorrhage in conscious rats. Chronically instrumented rats were subjected to a 16 ml/kg hemorrhage, followed by a 4-h recovery period, while monitoring body core temperature and cutaneous temperature. Cutaneous heat transfer was disrupted by housing the animals at an elevated (28 degrees C) ambient temperature. A separate group of experiments measured the change in oxygen consumption in the post-hemorrhage period. Moderate hemorrhage caused a drop in body core temperature which stabilized at 0.7+/-0.3 degrees C below control in the second hour following hemorrhage. Disruption of cutaneous heat exchange by reducing the thermal gradient did not diminish the hemorrhage-induced hypothermia. Hemorrhage caused a significant decline of oxygen consumption (-0. 21+/-0.05 ml O(2)/g per h). This 16% drop in resting oxygen consumption was prevented by immediately retransfusing the aspirated blood back into the rat. These data indicate that a decrease in metabolic heat production mediates the drop in body core temperature caused by moderate hemorrhage in conscious rats.

A comparison of demand-valve and bag-valve ventilations in a swine pneumothorax model.

OBJECTIVE: Two means of delivering artificial ventilation readily available to out-of-hospital personnel are the bag-valve (BV) and the O2-powered demand-valve (OPDV). However, use of the OPDV has been limited because of concerns that it may worsen an underlying pneumothorax. This study compared the changes in size of pneumothorax in swine ventilated with the 2 devices. METHODS: Three swine were anesthetized, intubated, and instrumented with a femoral arterial line and a pediatric Swan-Ganz catheter. A chest tube was placed, the chest was opened, and the lung parenchyma was visualized. The lung was disrupted by a single stab with a #10 scalpel; the chest was then sealed; and a pneumothorax was created by injecting 30 mL of air through the chest tube. The animals were ventilated by 12 emergency medical technicians using either BV or OPDV. After 10 minutes of ventilation, the pneumothorax volume was measured. RESULTS: When comparing final pneumothorax volumes after 10 minutes of ventilation with the 2 devices, there was no significant difference (mean +/- SD = 40.8 +/- 28.2 mL vs 52.3 +/- 23.1 mL, p = 0.286). CONCLUSION: There is no difference in final pneumothorax volumes after OPDV or BV ventilation.

Ventilatory strategies affect gas exchange in a pig model of closed-chest cardiac compression.

STUDY OBJECTIVE: To identify the arterial and mixed venous blood gas changes caused by different ventilatory strategies during resuscitation from ventricular fibrillation in a pig model of closed-chest cardiac compression. METHODS: A prospective randomized animal study was performed using 27 domestic pigs (body weight, 30 to 35 kg). Pentobarbital-anesthetized pigs were assigned to receive one of three treatments: (1) chest compression without assisted ventilation (n = 8), (2) assisted ventilation with room air (n = 8), and (3) assisted ventilation with 100% oxygen (n = 8). A fourth group, with the airway completely blocked, was added at the end of the experiment (n = 3). After instrumentation, the ventricles were fibrillated, and chest compression was begun 30 seconds after fibrillation with the use of the Thumper Mechanical CPR system (Michigan Instruments). Arterial and mixed venous blood gas samples were collected at 1, 3, 10, and 20 minutes of resuscitation. Defibrillation was attempted after the 20-minute sample was taken. RESULTS: Fibrillation followed by chest compression alone caused a significant drop in arterial and mixed venous partial pressure of oxygen (PO2) and a significant increase in arterial and mixed venous partial pressure of carbon dioxide (PCO2). Compared with the chest compression only, ventilation with room air significantly increased arterial and mixed venous PO2 and decreased arterial and mixed venous PCO2. Ventilation with 100% oxygen further increased arterial and mixed venous PO2 but did not affect PCO2, when compared with room air ventilation. The only successful defibrillations (3 animals) occurred in the group receiving 100% oxygen. CONCLUSION: This study indicates that passive air movement during chest compression does not allow physiologically significant pulmonary gas exchange and that room air ventilation alone is not sufficient to maintain mixed venous PO2.

Transient increase in plasma catecholamines following hypertonic/hyperosmotic fluid administration in conscious rats.

Plasma norepinephrine and epinephrine levels were monitored to determine possible alterations of the sympathetic nervous system caused by hypertonic fluid administration. Iv infusion (3.5 ml/kg, 1 min) of 7.5% NaCl/6% Hespan transiently increased both plasma norepinephrine and epinephrine levels to 197 +/- 28% and 220 +/- 30% of control, respectively, at 1 min. These increases were no longer significant 5 or 15 min following infusion. A brief hypotension was also observed immediately following hypertonic fluid administration. Thus, prolonged sympathetic activation does not occur following hypertonic fluid infusion in normovolemic conscious rats.

Transient increase in plasma catecholamines following hypertonic/hyperosmotic fluid administration in conscious rats

Plasma norepinephrine and epinephrine levels were monitored to determine possible alterations of the sympathetic nervous system caused by hypertonic fluid adeministration. Iv infusion (3.5 ml/Kg, 1 min) of 7.5% NaCl/6% Hespan transiently increased both plasma norepinephrine and epinehrine levels to 197 ñ 28% and 220 ñ 30% of control, respectively, at 1 min. These increases were no longer significant 5 or 15 min following infusion. A brief hypotension was also observed immediately following hypertonic fluid administration. This, prolonged sympathetic activation does not occur following hypertonic fluid infusion in normovolemic conscious rats

Verapamil prevents isoproterenol-induced cardiac failure in the rat.

Virgin, male Sprague-Dawley rats were used to study the production of cardiac failure by a single subcutaneous injection of 85 mg/kg dl-isoproterenol (ISO) and the possible preservation of cardiac function by a pre-treatment of 50 mg/kg verapamil (VER) 5 min prior to 85 mg/kg ISO. At 24 hrs after drug injections cardiac function was assessed in anesthetized, open-chest rats by the measurement of cardiac output and by a volume loading of the heart with a 2 min, 15.3 ml/min jugular vein infusion of Tyrode's solution. Peak cardiac index and peak stroke index were depressed by ISO. VER completely prevented these signs of ISO-induced cardiac failure. A second group of rats was sacrificed 24 hrs after ISO and VER-ISO and their left ventricular calcium contents were determined. ISO caused a significant increase in left ventricular calcium content. VER attenuated the ISO-induced increase in myocardial calcium content, but did not prevent it. This data raises questions as to whether VER's property as a transarcolemmal calcium flux inhibitor was the mechanism of preservation of cardiac function following ISO administration. It is possible that VER may have preserved cardiac function by altering ISO-induced hemodynamic changes in the rat.