Tissue hypoxia and ischemia - Info and Reading Options

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This monograph was held at the Annenberg Center of the University of Pennsylvania on August 13 and 14, 1976. The symposium was jointly sponsored by the following groups at the University of Pennsylvania: the Respiratory Physiology Group of the Department of Physiology, the Cardiopulmonary Section of the Department of Medicine, the Johnson Research Foundation, the Cerebrovascular Research Center of the Department of Neurology, the Head Injury Center of the Department of Neurosurgery, the Institute for Environmental Medicine, and the International Society on Oxygen Transport to Tissues. Its purpose was to promote an interdisciplinary discussion of oxygen sensors in various tissues and their mechanism of action as well as to examine the deleterious effects of hypoxia and ischemia with special reference to the brain. There were four sessions, one on the biochemistry of physiologic oxygen sensors, two on the mechanism of oxygen sensing in tissues and one on the circulatory and metabolic aspects of cerebral hypoxia and ischemia. In the first session, conceptual problems concerning what constitutes a molecular oxygen sensor and the transduction process were considered. In addition, the oxygen sensing characteristics of microsomal enzymes were discussed as well as microsomal oxygenase reactions, in particular those in which cytochrome P-450 plays a central role. The role of hydrogen peroxide formation in oxidation-reduction reactions involving the microsomes was explored. Other molecules which were considered as possible oxygen sensors were monoxygenases, myoglobin and hemoglobin. The reactions and kinetics of these oxygenated hemeproteins were examined. There was also discussion of the peroxisomal enzymes; catalase and three oxidases (urate, L-a-hydroxyacid and D-aminoacid oxidases) with emphasis on their properties which are important under physiologic conditions. Mitochondrial production of superoxide radicals and hydrogen peroxide, the oxygen dependence of this production and the physiologic relevance of these substances at the cellular level were considered. The second session dealt with the mechanism of oxygen sensing. Data concerning the bioelectric activity of chetnoreceptors and the effect of acetylcholine release on chemoreceptor function was presented. Oxygen tension sensors of vascular smooth muscle were examined and a hypothesis to explain the production of oxygen dependent mechanical tension in vascular smooth muscle was put forth. Evidence was presented that the effect of hypoxia may be mediated by a mechanism other than inhibition of aerobic energy production. The mechanism of oxygen induced contraction of the ductus arteriosus and the roles of ATP, calcium ion and prostaglandins in this system were discussed. The sensing of oxygen tension in the pulmonary circulation and the circulatory effects of tissue oxygen sensors, particularly in regard to coronary blood flow, were considered. The adenosine hypothesis for the regulation of blood flow in cardiac and skeletal muscle was critically examined. In the third session the examination of the mechanism of oxygen sensing in tissues was continued. The oxygen linked response of the carotid chemoreceptors and the interaction of hypoxic and hypercapnic stimuli were discussed. Data from microelectrode studies of the effects of changes in oxygen and carbon dioxide tension, temperature and osmolarity on carotid body cells were presented and the mechanism by which the chemoreceptors sense changes in arterial oxygen and carbon dioxide tension were examined. The role of catecholamines and cyclic AMP in the chemoreception process of the carotid body was considered. The fourth session was concerned with the circulatory and metabolic aspects of cerebral hypoxia and ischemia. The characteristic metabolic features of hypoxic hypoxia both at normal and reduced perfusion pressures as well as of incomplete and complete ischemia and how these metabolic changes relate to irreversible neuronal damage was discussed. Data demonstrating the presence of increased energy consumption and glucose metabolism in the brain following ischemia of transient duration was presented. Regional changes in energy metabolism and glycolysis in incomplete ischemia were also considered. The effects of ischemia of the cerebral cortex on other regions of the brain and spinal cord were examined in regard to cyclic nucleotide levels. The changes in tissue P02, ion fluxes and redox state produced by cerebral hypoxia and ischemia were discussed. Consideration was given to intracellular events possibly marking irreversible level jury following ischemia. The cerebral hemodynamic and metabolic alterations that occur in patients with cerebrovascular accidents in animal models of strokes were examined. The effects of hypovolemic shock on cerebral blood flow and its regulation as well as on brain metabolism and mitochondrial function were discussed.

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