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F J Pearce

Publications and source records attributed to F J Pearce.

26 records · Page 2Linked to original sources
PubMed1983

Effect of hemorrhage and anoxia on hepatic gluconeogenesis and potassium balance in the rat.

Previous investigations have demonstrated impairment of hepatic gluconeogenic activity during both hypovolemia and sepsis, but the mechanisms responsible remain unclear. The present study was designed to determine the influence of lack of oxygen on gluconeogenesis independent of humoral factors, products of ischemic peripheral tissues or pH changes. Livers obtained from Sprague-Dawley rats fasted 24 hours were perfused with Krebs-Henseleit buffer containing 5 mM lactate for 30 minutes. In the control group (n = 8) perfusion was continued; in others, anoxia was induced by perfusing with buffer equilibrated with 95% N2 and 5% CO2 for periods of 15, 30, or 60 minutes (n = 4, 5, and 5, respectively). The initial conditions were then reinstituted for an additional 45 minutes. Anoxia caused hepatic release of K+, indicative of disordered hepatic cellular ionic gradients and an abrupt cessation of gluconeogenesis. Reoxygenation partially reversed these alterations but some impairment of gluconeogenesis persisted and the degree of uptake of K+ from the perfusion media was decreased as the duration of anoxia increased. The degree of restoration of gluconeogenesis after a period of anoxia was closely associated with restoration of cellular uptake of K+. By comparison, livers taken from hypovolemic animals maintained at a mean arterial blood pressure of 40 mm Hg until the beginning of the decompensatory stage of shock exhibited a gluconeogenic capacity of only 41% of control animals and was comparable to the compromise induced by between 30 and 60 minutes of anoxia. These results suggest that the abilities to restore hepatic electrolyte balance and gluconeogenesis after oxygen deprivation are affected in parallel and may reflect a common dependence on the restoration of ATP stores after the insult.

Animals↗
PubMed1982

The role of blood glucose in defense of plasma volume during hemorrhage.

The purpose of this study was to assess the importance of the hyperglycemic response in defense of plasma volume during hemorrhagic shock. Normal well-fed white rats were divided into four groups of 10 each. Two shock models were used each containing rats fasted for 24 hr and control rats maintained on a standard diet. All rats had free access to water. Hemorrhage was produced either by bleeding to a constant mean arterial blood pressure of 40 mm Hg or by removing a fixed per cent of blood volume at 30-min intervals. All control animals withstood a larger volume of blood loss and survived longer than fasted animals, regardless of which shock model was used. They also manifested a significantly greater mean maximum per cent rise in blood glucose and decline in hematocrit during hypovolemia. A change in blood glucose was correlated with change in hematocrit, and to the extent that the latter is a reflection of plasma refill, fed animals demonstrated a greater ability to refill lost plasma volume. The strong correlation between glucose levels and hematocrit during all phases of hypovolemic shock indicates that blood glucose may be an important determinant of plasma refill. The mechanisms whereby glucose exerts these effects may involve its role as an osmotic agent and as a substrate for energy metabolism.

Animals↗
PubMed1982

Liver adenosine triphosphate (ATP) in hypoxia and hemorrhagic shock.

Reduction of liver ATP in proportion to the severity of shock and hypoxia is well known. We have studied the interrelationships among arterial oxygenation, arterial pH, and liver ATP in experimental hypoxia and in hemorrhagic shock in rats. No significant correlation was found between liver ATP and arterial pH in both hemorrhagic shock and hypoxia and between liver ATP and arterial PO2 in hypoxia. Induction of experimental observations suggest that in this form of hemorrhagic shock, arterial pH may be a sensitive indicator of decreased hepatic perfusion and impaired liver ATP production.

Acidosis, Respiratory↗
PubMed1981

Insulin effectiveness in hypovolemic dogs.

The question addressed in this study was whether exogenous insulin can enhance the rate of assimilation of blood glucose after prolonged hypovolemia when homeostasis is waning. Twenty-three well-fed mongrel dogs were maintained at a mean arterial blood pressure of 50 mm Hg by bleeding. Periodic analyses were made of arterial and venous plasma concentration of glucose, femoral blood flow, arterial plasma concentration of insulin, and hematocrit. At the onset of physiologic deterioration signaled by the need to reinfuse 50 ml of shed blood to maintain 50 mm Hg blood pressure, dogs received either 10 ml saline (control; n=15) or 10 ml saline containing 2 units insulin (treated; n=8). Administration of 2 units of insulin to eight of the dogs caused a significantly faster decline of blood glucose than that observed in saline-treated animals. Despite the more rapid decline in plasma concentration of glucose in animals that received insulin, there was no significant difference in glucose uptake between the two groups of animals. The hemoconcentration reflected by a rising hematocrit that develops when hypovolemia persists was accentuated by the administration of insulin without supplementary fluids. The absence of any effect of insulin on glucose uptake in the hindlimb in the late phase of hypovolemic shock suggests that the accelerated decline in arterial glucose levels may be due to inhibitory effects of insulin on hepatic glucose release. These results are not consistent with the resistance of plasma glucose to insulin in the late phases of hypovolemic shock.

Animals↗
PubMed1980

Effect of lactate and palmitate on substrate utilization of isolated rat soleus.

The effects of exogenous lactate and palmitate on the metabolism of rat soleus muscle were studied. In the presence of glucose and insulin, the addition of 8 mM lactate resulted in a decrease in the oxidation of both glucose and other substrates. Lactate accounted for 70% of the oxygen consumption under these conditions. Glycogen accumulation and the incorporation of exogenous palmitate into triglycerides were stimulated by lactate addition, whereas the utilization of exogenous glycerol was depressed. The addition of 1 mM palmitate in either the presence or absence of lactate resulted in an inhibition of both glycolysis and the utilization of exogenous glucose. The results are discussed in terms of the effect of lactate levels on recovery from exercise.

Animals↗