Ronald F. Kotrc
DOI: http://dx.doi.org/10.1016/0735-6757(83)90078-5
Published in issue: September 1983
Blaine C. White
DOI: http://dx.doi.org/10.1016/0735-6757(83)90079-7
Published in issue: September 1983
Blaine C White, Carl D Winegar, Raymond E Jackson, Kathleen M Joyce, David N Vigor, Thomas J Hoehner, Gary S Krause, Robert F Wilson
DOI: http://dx.doi.org/10.1016/0735-6757(83)90080-3
Published in issue: September 1983
xPerfusion of the cerebral cortex during closed chest CPR in dogs, generating systolic pressures of 60 to 70 mmHg, is only 10% of pre-arrest blood flow. In contrast, internal cardiac massage produces normal cortical perfusion rates. Following a 20-min perfusion arrest, during pressure controlled reperfusion, cortical flow rates decay to less than 20% normal after 90 min of reperfusion. This appears to be due to increasing cerebral vascular resistance, and is not due to rising intracranial pressure.
Adelbert Ames III
DOI: http://dx.doi.org/10.1016/0735-6757(83)90081-5
Published in issue: September 1983
xThe ability to synthesize new protein was used as a marker of irreversible neuronal injury in experiments with isolated rabbit retinas exposed to various types of ischemic insult. The retinal neurons were able to fully recover their protein synthetic capacity after 20 min of complete ischemic anoxia, but not after 30 min. There was better toleration to either isolated substrate deprivation or complete anoxia than to both together. Increasing extracellular Mg2+ prolonged toleration to complete ischemic-anoxia.
Gary Fiskum
DOI: http://dx.doi.org/10.1016/0735-6757(83)90082-7
Published in issue: September 1983
xIschemia causes a pathological drop in the cellular energy state due to inhibition of mitochondrial oxidative phosphorylation. The reversibility of this condition depends on the damage to mitochondrial membrane-linked activities during the period of ischemia or during reoxygenation of the tissue. It is likely that the ischemia-induced damage is due to a combination of factors including an increase in the cytosolic free Ca2+ concentration, a triggering of phospholipase and protease activities, an increase in cellular free fatty acids, and a decrease in pH.
Marcel Borgers, Fred Thoné, Jos Van Reempts, Fons Verheyen
DOI: http://dx.doi.org/10.1016/0735-6757(83)90083-9
Published in issue: September 1983
xIn order to study the effects of substances with selective Ca2+ entry blocking properties which enhance the tolerance to ischemia by preventing a toxic calcium overload, attempts are made to localize calcium ultrastructurally. Under normoxic conditions, a mobile pool of Ca2+ is localized in synaptic vesicles and in mitochondria of brain cells; in mitochondria of cardiac, skeletal and vascular smooth muscle; and in the junctional SR of fast skeletal muscle. A plasmalemmabound pool of Ca2+ is present in cardiac and slow skeletal muscle.
Frank C. Messineo
DOI: http://dx.doi.org/10.1016/0735-6757(83)90084-0
Published in issue: September 1983
xCalcium entry into cardiac cells is believed to be controlled by transmembrane-voltage dependent, protein regulated “channels”. The sarcoplasmic reticulum participates in the regulation of cytosolic calcium by ATP dependent Ca2+ sequestration during diastole, and by action potential stimulated calcium release. Massive calcium overloading occurs during reperfusion following myocardial ischemia. Calcium overloading activates phospholipases, which may activate another mechanism involved in lethal cellular injury, that is, the accumulation of long chain fatty acids and their derivatives.
Stig Rehncrona, Erik Kågström
DOI: http://dx.doi.org/10.1016/0735-6757(83)90085-2
Published in issue: September 1983
xCurrent evidence suggests that the brain has considerable potential to tolerate prolonged periods of complete ischemic anoxia. Moreover, the brain may be less damaged by complete ischemic anoxia than by severe incomplete ischemia. The accumulation of lactic acid in the brain during severe incomplete ischemia approaches three times the levels seen with complete ischemic anoxia, and this phenomenon is implicated in exacerbated biochemical and structural injury.
Edwin M. Nemoto, Gerald K. Shiu, Joseph P. Nemmer, Achiel L. Bleyaert
DOI: http://dx.doi.org/10.1016/0735-6757(83)90086-4
Published in issue: September 1983
xEnergy depletion and lactate are at plateau levels within five minutes of complete ischemic-anoxia in the brain; however, irreversible brain injury has not occurred in this time. Brain free fatty acids (FFA) rise sharply during the first five minutes of ischemic-anoxia, but then continue to rise during the following hour without plateauing. Barbiturate anesthesia preischemia attenuates the FFA rise. Other agents which also attenuate the FFA increase include, among others, phenytoin and Innovar. The Ca2+ antagonists flunarizine and gallopamil also attenuated FFA rise, but were not as effective as pentobarbital during ischemia.
Burton M. Altura, Bella T. Altura
DOI: http://dx.doi.org/10.1016/0735-6757(83)90087-6
Published in issue: September 1983
xExperiments indicate that several different calcium antagonists have vasodilatory properties which may be expressed selectively on different organ vascular beds. Verapamil was most active as a vasodilator in muscular microvasculature. Cerebral venules are most sensitive to nimodipine. Nisoldipine is inactive in cerebral vascular dilation. We have also studied the vasodilatory effects of several barbiturates. Pentobarbital is the most active cerebrovasodilator in this class of anesthetics. This agent inhibits the vasospastic activity of potassium, serotonin, and prostaglandins, and appears to be a calcium entry antagonist in vasculature.
K.-A. Hossmann
DOI: http://dx.doi.org/10.1016/0735-6757(83)90088-8
Published in issue: September 1983
xFactors influencing survival of neurons during ischemia and neuronal revival after ischemia are reviewed. During ischemia, biochemical and electrophysiological changes depend on residual blood flow rate: below 30 to 40 ml/100 g/min EEG amplitude decreases, below 18 ml/100 g/min spontaneous neuronal activity ceases, and below 10 ml/100 g/min cell membranes depolarize. Attempts to improve blood flow after middle cerebral artery occlusion with vasoactive drugs were not successful but there was an indication that the calcium antagonist nimodipine reduced ischemia-induced disturbances of ion homeostasis.
Peter Safar
DOI: http://dx.doi.org/10.1016/0735-6757(83)90089-X
Published in issue: September 1983
Daniel M. Goodenberger, Stanley Podlasek, J.Douglas White, Claude Cadoux
DOI: http://dx.doi.org/10.1016/0735-6757(83)90090-6
Published in issue: September 1983
Roy A.M. Myers, Lawrence D. Messier, Dennis W. Jones, R Adams Cowley
DOI: http://dx.doi.org/10.1016/0735-6757(83)90091-8
Published in issue: September 1983
Norman Rosenberg
DOI: http://dx.doi.org/10.1016/0735-6757(83)90092-X
Published in issue: September 1983
Robert Askenasi, Jean-Louis Vincent
DOI: http://dx.doi.org/10.1016/0735-6757(83)90093-1
Published in issue: September 1983
J.Douglas White
DOI: http://dx.doi.org/10.1016/0735-6757(83)90094-3
Published in issue: September 1983
Michael J. Bresler
DOI: http://dx.doi.org/10.1016/0735-6757(83)90095-5
Published in issue: September 1983
Toby L. Litovitz
DOI: http://dx.doi.org/10.1016/0735-6757(83)90096-7
Published in issue: September 1983
Toby L. Litovitz
DOI: http://dx.doi.org/10.1016/0735-6757(83)90097-9
Published in issue: September 1983
Glenn C. Hamilton
DOI: http://dx.doi.org/10.1016/0735-6757(83)90098-0
Published in issue: September 1983
Glenn C. Hamilton
DOI: http://dx.doi.org/10.1016/0735-6757(83)90099-2
Published in issue: September 1983
DOI: http://dx.doi.org/10.1016/0735-6757(83)90100-6
Published in issue: September 1983
