phosphocreatine and Hemorrhage

Topics: Adenosine Diphosphate; Adenosine Triphosphate; Animals; Arterioles; Arteriosclerosis; Blood Platelets; Creatine Kinase; Hemorrhage; Hemostasis; Humans; Phosphocreatine; Platelet Adhesiveness; Platelet Aggregation; Thrombosis; Venules

Sequential 31P nuclear magnetic resonance (NMR) spectra were measured in adult dogs to determine the relationship between cardiac function and myocardial intracellular pH (pHi) and phosphorylated energy metabolites during 2 h of hemorrhagic shock. Simultaneous measurements of coronary blood flow (radioactive microspheres), arterial and coronary sinus pH, blood gases, and oxygen content were performed. In addition, changes in brain NMR spectra were correlated with changes in cerebral blood flow during shock. Two hurs of hypovolemic shock resulted in significant decreases in phosphocreatine (PCr), PCr-to-ATP ratio, and pHi, whereas Pi rose significantly relative to baseline values. Return of shed blood and crystalloid fluid resuscitation improved cerebral and coronary perfusion and returned cardiac contractile function to near baseline values. We conclude that severe and sustained hemorrhagic shock produced significant alterations in brain and heart phosphorylated metabolites as well as significant intracellular acidosis; however, these changes in energy metabolites were reversible with adequate fluid resuscitation from shock.

Topics: Adenosine Triphosphate; Animals; Blood Volume; Brain; Cerebrovascular Circulation; Coronary Circulation; Dogs; Energy Metabolism; Hemorrhage; Hypotension; Male; Myocardium; Nucleotides; Phosphocreatine; Phosphorus; Resuscitation; Shock

Experiments on dogs with long-term hypotony caused by blood loss have demonstrated irreversible lesions in the majority of cardiomyocytes and hypodynamic condition of the heart with a high content of macroergic phosphates in the myocardium. Intravenous injection of sodium hydroxybutyrate in a dose of 180-200 mg/kg after 60 min of hypotony seems to improve energy transport and utilization in the ischemic myocardium. It increases the working capacity and power of the heart muscle, pump function of the heart and makes longer the period of ultrastructural changes in cardiomyocytes.

Topics: Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Animals; Creatine; Dogs; Energy Metabolism; Heart; Hemodynamics; Hemorrhage; Hydroxybutyrates; Hypotension; Myocardium; Phosphocreatine; Sodium Oxybate

The present report is a review of recent experimental studies in a canine model of acute coronary occlusion. The questions addressed were: (1) Does coronary reperfusion reduce myocardial infarct size? (2) What is the relationship between microvascular damage and hemorrhage and the development of myocardial necrosis? (3) What are the biochemical, functional and ultrastructural characteristics of reperfused tissue salvaged from necrosis? Coronary occlusion followed by reperfusion in the dog resulted in significant subepicardial salvage of myocardium if reperfusion was instituted before 6 hours of ischemia. Because ultrastructural evidence of microvascular damage was found only after irreversible damage to myocytes, and because gross hemorrhage after coronary reperfusion was confined to zones of myocardium that were already necrotic, it does not appear that hemorrhage should serve as a deterrent to reperfusing reversibly injured myocytes. Severely ischemic myocardium that had been salvaged by coronary reperfusion required several days before it returned to normal from biochemical, functional and ultrastructural standpoints.

Topics: Adenosine Triphosphate; Animals; Cardiomyopathies; Coronary Circulation; Dogs; Heart; Hemorrhage; Humans; Microcirculation; Myocardial Contraction; Myocardial Infarction; Myocardium; Phosphocreatine

A dog model was used to measure the hemodynamic changes occurring during acute pancreatitis induced by intraductal injection of fresh trypsin-bile-blood mixture. Pancreatic blood flow was measured with 15-micrometer radioactive microspheres. Measurements of pancreatic adenosine triphosphate (ATP) and creatine phosphate (CP) were made under normal conditions and during acute hemorrhagic pancreatitis. Basal ATP and CP concentrations were 5.82 +/- 0.25 and 5.30 +/- 0.31 mmol/g wet tissue, respectively. Hemorrhagic pancreatitis was characterized by a severe reduction in pancreatic blood flow, followed by a 45% fall of ATP and a 70% lowering of CP. These results suggest that inadequate pancreatic tissue perfusion during acute pancreatitis results in a marked depletion of high-energy phosphate stores. We suspect this energy depletion reflects the progression of the disease from edematous to hemorrhagic pancreatitis and causes irreversible damage of pancreatic tissue.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Dogs; Hemodynamics; Hemorrhage; Pancreas; Pancreatitis; Phosphocreatine; Regional Blood Flow

In 62 dogs, hypotension to a mean arterial pressure of either 40 or 50 torr (equivalent to a cerebral perfusion pressure of 30 or 40 torr, respectively) for one hour was induced by hemorrhage (oligemia), trimethaphan, halothane, or sodium nitroprusside. Before and during the period of hypotension, the following were measured: mean arterial blood pressure, cardiac output, whole-body O2 consumption, cerebral blood flow, cerebral O2 consumption, arterial blood gases, blood O2 content, and lactate, pyruvate, glucose, epinephrine, and norepinephrine concentrations. At the end of the period of hypotension, brain biopsies were taken for determination of adenosine triphosphate, phosphocreatine, lactate, and pyruvate concentrations. In an additional eight dogs following one hour of hypotension (at 40 torr) induced by one of the four techniques, the brains were perfused with carbon black, removed, and examined. In another ten dogs following hypotension (at 40 torr) induced with either halothane or trimethaphan, the animals were observed for three days and then killed for examination of the brain. Dogs maintained at a mean arterial pressure of 40 torr, despite differences in cerebral blood flow, demonstrated metabolic disturbances compatible with systemic and cerebral hypoxia. These were greatest in those dogs given nitroprusside in excess of 1.0 mg/kg, presumably due to cyanide toxicity. In dogs maintained at 50 torr, metabolic disturbances were minimal or absent in the halothane- and nitroprusside-treated dogs but were still apparent in the oligemic and trimethaphan-treated dogs. Carbon black infusions revealed no evidence of non-homogeneous flow. Three of the ten dogs observed for three days had persistent post-hypotension neurologic dysfunction. Two of these were given trimethaphan. The results suggest that the systemic and cerebral effects of halothane and nitroprusside (at doses less than 1.0 mg/kg) are similar and at a mean arterial pressure of 50 torr are of little consequence. By contrast, hypotension induced by trimethaphan or oligemia results in detectable metabolic alterations even at a pressure of 50 torr.

Topics: Adenosine Triphosphate; Animals; Brain Chemistry; Cerebrovascular Circulation; Dogs; Ferricyanides; Halothane; Hemodynamics; Hemoglobins; Hemorrhage; Hypotension; Lactates; Nitroprusside; Phosphocreatine; Trimethaphan

Topics: Adenosine Triphosphate; Adipose Tissue; Animals; Biopsy; Blood Pressure; Blood Volume; Body Water; Cats; Female; Hematocrit; Hemorrhage; Lactates; Male; Muscles; Phosphocreatine; Time Factors

Topics: Adenosine Triphosphatases; Adenosine Triphosphate; Animals; Burns; Dogs; Hemorrhage; Liver; Male; Phosphocreatine; Resuscitation

Topics: Adenosine; Animals; Ascorbic Acid; Brain; Carbohydrate Metabolism; Coenzymes; Hemorrhage; Nucleosides; Nucleotides; Phosphocreatine; Polyphosphates; Rats