adenosine triphosphate/hemorrhage

Cardiac dysfunction during hemorrhagic shock (HS) is associated with myocardial ischemia, during which adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channels can be activated. We investigated the role of K(ATP) channels in HS-induced myocardial ischemia. Canine HS was induced using an

OBJECTIVE Recent experimental evidence suggests that activation of adenosine triphosphate (ATP)-sensitive potassium channels contributes to vascular failure and early mortality after hemorrhagic shock. The present investigation evaluated the effects of the water-soluble sodium salt of glipizide, an

Complex formation between salicylic acid and adenosine or adenosine triphosphate in 0.2m phosphate buffer at pH=7 was investigated as a potential factor contributing to the prolongation of acetylsalicylic acid-induced GI blood loss. Spectrophotemetric techniques were used to evalute the

The findings of decreased adenosine triphosphate (ATP) levels in liver, kidney, and other tissues of animals in hemorrhagic shock were the rationale for previous experimental attempts to improve cell function by administration of fluids that contained high concentrations of ATP. The beneficial

The beneficial effects of adenosine triphosphate (ATP)-MgCl2 administered as a bolus following fluid infusion or in combination with the infusion fluid were investigated in rabbits subjected to severe but reversible haemorrhagic shock. ATP-MgCl2 treatment led to a significant improvement of the

BACKGROUND This is a review of studies with two agents, glutamine and crocetin, which have been found to enhance recovery of cellular adenosine triphosphate (ATP) and adenosine diphosphate after hemorrhagic shock. METHODS The studies used a sublethal (30 minutes) reservoir shock model in 300- to

BACKGROUND To determine the role of nitric oxide and adenosine triphosphate-sensitive potassium (KATP) vascular channels in vascular decompensation during controlled hemorrhagic shock in swine. METHODS Thirty instrumented, anesthetized adolescent Yorkshire swine were subjected to controlled isobaric

BACKGROUND The purpose of this study was to determine whether a decrease in macrophage energetics contributes to the profound immune dysfunction that occurs after hemorrhage and, if so, whether adenosine triphosphate (ATP)-MgCl2 treatment has any beneficial effects on the above

BACKGROUND Lumi-aggregometry quantification of platelet dense granule adenosine triphosphate (ATP) release is commonly used for diagnosing platelet function disorders. As the test findings show considerable variability for healthy controls, we postulated that patient findings might also be variable

The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3

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

The effect of intravenous (iv) infusion of 6.25 mumol of ATP-MgCl2 on survival and tissue ATP levels in hemorrhagic shock was investigated using a rat model. Mortality in ATP-MgCl2-treated shocked rats was 50% compared with 53% in saline-treated controls. Tissue ATP levels in ATP-MgCl2-treated

The effect of experimental anaemia induced by phlebotomy and the effect of infusion of various fluids on the 2,3-DPG, ATP and total organic phosphate (Porg) concentration were examined in the red cells of beagles made anaemic by withdrawal of 30% of the circulating blood. Particular groups of dogs

Topical application or intraperitoneal injection of heparin and heparin oligosaccharides produces a potent inhibition of skin hemostasis. Studies conducted with disaccharides derived from heparin, heparan sulfate, and chondroitin sulfates have shown that delta-4,5-uronyl-(1----4)-glucosamine,