Anesthetic influence on response to hemorrhage in rats.
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Biomedical subjects
Publications and source records attributed to W R Drucker.
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Many mechanisms, including alterations in muscle metabolism, cellular damage, decreased blood volume, and hepatic disfunction, are influential in producing the observed progressive rise in the concentration of amino acids in arterial and venous blood during persisting hypovolemic shock. The rapid rise of venous and arterial concentrations of amino acids and the increase in venoarterial concentration difference suggest that hypovolemia causes a net release from muscle of a potential substrate for energy metabolism. The blood flow through peripheral tissues, however, is reduced to such an extent during hypovolemic shock that the net rate of release of amino acids is not greater than preshock release and may be less. Therefore, the homeostatic advantages served by the alteration in protein metabolism during the more chronic stresses of starvation or after injury may not obtain during acute hypovolemia.
Normal rats subjected to hypovolemic shock (Wiggers model) exhibited the characteristic rise in blood glucose as well as the initial fall in hematocrit indicative of plasma refill. Concurrently there was a rise in osmolality. Late in shock these animals became hypoglycemic and the hematocrit rose despite a persisting hyperosmolality. Rats which had been deprived of food for 24 hours in order to deplete the liver glycogen did not become hyperglycemic after hemorrhage and had a less marked fall in hematocrit. The plasma osmolality rose to the same high level as that of the fed rats but the rise was slower. From this we conclude that glucose may be largely responsibile for the rise in osmolality early in shock in fed animals but it is not responsible for the continuing hyperosmolality in fed or fasted animals. Nor is it responsible for the initial rise in fasted animals. Hyperosmolality may delay but does not prevent fluid loss from the capillaries late in shock.
This study was done to determine why the plasma insulin remained elevated during shock. Mongrel Female dogs (12-15 kg) were depancreatized and maintained on a constant intraportal infusion of porcine insulin while they were bled to reduce and maintain the mean arterial blood pressure at 50 mm Hg for 165 min. Blood samples were taken for glucose and plasma insulin at 15 min intervals. The data show that there was a progressive rise of plasma insulin during the course of hemorrhagic shock. This occurred despite a constant infusion of insulin, the sole source of insulin available to these depancreatized dogs. Since removal of plasma insulin is largely due to insulin utilization, our findings imply that the rise of plasma insulin in hemorrhagic shock is caused by decreased utilization.
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Prior nutrition is known to influence tolerance to hypovolemic shock. This study was undertaken to determine the influence of dietary composition on the response of animals subjected to hypovolemic shock. Particular attention was directed to the role of high and low protein diet content with a proportionate change in carbohydrate content to yield isocaloric diets. Rats were placed on one of three diets and were subsequently subjected to shock either by 1) hemorrhage to a pre-determined mean arterial blood pressure, or by 2) hemorrhage of a pre-determined volume of blood based on per cent of body weight. Serial measurements were made of blood pressure, blood volume removed, survival time,hematocrit, blood glucose, pH and blood gases. The results indicate that a high protein diet does not prolong tolerance to recurrent blood loss but there is a greatly reduced tolerance to hemorrhage shock in rats whose body weight was maintained on a low protein/high carbohydrate diet. The latter animals also exhibited impaired refill of plasma volume and a paradoxical, continuing hyperglycemic response during hypovolemia. This study suggests that although an abundant supply of blood glucose is available as an energy source, glucose uptake in the peripheral tissues is inhibited during hypovolemia by unknown mechanisms and thus homeostasis is curtailed. The protein content of the diet may be a critical factor in carbohydrate use during shock.
In dogs subjected to hypovolemic shock (modified Wiggers model) severe enough to decrease the arterial flow in an isolated hind limb by two-thirds, a marked hyperglycemia (three times control) and an increase in blood glucose AV difference (ten times control) occur. Despite the decreased arterial flow, glucose uptake by peripheral tissues increased by a factor of three within one-half hour of hemorrhage and remained elevated for several hours. Presumably, the increased glucose uptake reflects the need for more energy substrate during the hypoxic conditions of the decreased peripheral blood flow.
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