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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To avoid the compensatory hemodynamic responses, which have limited interpretation of hemoglobin-oxygen affinity modifications in animal experimentation, an isolated blood-perfused rabbit heart model providing metabolic, functional, and vectorcardiographic measurements has been developed. Fixed-flow perfusions of unchanged or affinity-modified red blood cell suspensions were carried out to assess the benefits of high affinity during hypoxic hypoxia and of low affinity during posthypoxic recovery. Using fully saturated suspensions, the influence of affinity level during restricted flow and reperfusion was also studied. Higher myocardial oxygen consumption (MVO2) was associated with high-affinity blood during mild hypoxia and low-affinity blood during posthypoxic recovery. At low flows, heart rate and MVO2 tended to be lower in high-affinity perfusions, and to recover more completely during low-affinity reperfusions. Ventricular function, vectorcardiographic patterns, and lactate levels were affected by hypoxia and ischemia, but not by level of affinity. The relevance of these observations to the therapeutic potential of hemoglobin-oxygen affinity modification is discussed.
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PMID:Application of an isolated heart model to investigate blood-oxygen delivery. 47 72

This study was conducted to determine whether low level exposure to carbon monoxide would increase myocardial ischemia associated with acute myocardial infarction. An hour after coronary artery ligation, eleven anesthetized dogs underwent five sequential respiratory exposures to 5,000 ppm carbon monoxide, producing mean blood carboxyhemoglobin levels of 4.9% to 17.0%. Ischemia, as indicated by the amount of S-T segment elevation in epicardial electrocardiograms, increased significantly at the lowest carboxyhemoglobin level and increased further with increasing carbon monoxide exposure. These changes occurred in the absence of altered heart rate, blood pressure, left atrial pressure, cardiac output, or blood flow to ischemic myocardium. Flow to non-ischemic myocardium increased with carbon monoxide exposure, the percentage increase being approximately double the increase in carboxyhemoglobin level. Thus, low level exposure to carbon monoxide can significantly augment ischemia in acute myocardial infarction, apparently through a reduction in oxygen supplied to ischemic tissue. The data suggest that hypoxia induced by carbon monoxide exposure is more severe than can be accounted for by a simple reduction in oxygenated hemoglobin.
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PMID:Augmentation of myocardial ischemia by low level carbon monoxide exposure in dogs. 47 72

Shock was induced in 537 rats by exteriorization of the intestines and occlusion of the superior mesenteric circulation for 1 hour. After 1 hour of this intestinal ischemia shock, oxygen consumption (VO2) decreased to half of the preexperimental values. When no infusion was given, the survival rate at 24 hours was 22%; this was correlated with the degree of restoration of VO2 at 1 hour after shock. VO2 and survival rate improved with infusion of albumin, dextran 40, and dextran 40, and dextran 70. With increasing doses of colloids, both VO2 and survival rate increased; the optimal effect was at the dose of 2 g/kg body weight. When no other therapy was given, colloids at concentrations of 3.5 or 6% solutions had a better effect on survival than the 10% solution. Colloids were more effective than Ringer's acetate when the latter was given in the same volume and up to three times the volume of the colloids.
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PMID:Oxygen consumption and recovery from surgical shock in rats: a comparison of the efficacy of different plasma substitutes. 47 54

Twenty-four pigs were studied to assess the effect of potassium in a cardioplegic solution on the ability of the swine myocardium to maintain functional and metabolic integrity following induced ischemia. The pigs were evaluated on total and right heart bypass with measurement at normothermia and after a one-hour intervention of stroke volume (SV), coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and lactate extraction. Myocardial tissue gases (PmO2 and PmCO2) were continuously monitored and, at the conclusion of the procedure tissues were analyzed for adenosine triphosphate (ATP). There were five interventions: (1) hypothermic perfusion (28 degrees C) (Group 1); (2) hypothermic ischemia (28 degrees C) (Group 2); and hypothermic ischemia with a cardioplegic solution (nonlactated Ringer's solution, pH 7.4, 4 degrees C) using (3) normokalemia (4 mEq of potassium chloride/L, 300 mOsm/L (Group 3), (4) hyperkalemia (43 mEq of KCl/L, 390 mOsm/L) (Group 4), and (5) normokalemia with increased osmolarity (3.6 mEq of KCl/L, 400 mOsm/L) (Groups 5). A significant decrease in SV and elevation in peak PmCO2 were seen in all groups subjected to ischemia except those protected with hyperkalemic solution. We conclude that the presence of hyperkalemia in a cold root perfusion solution provides better myocardial protection than cold root perfusion alone. Furthermore, potassium arrest appears to be more protective than coronary perfusion at 28 degrees C.
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PMID:The importance of hyperkalemia in a cold perfusion solution: a correlative study examining myocardial function, metabolism, tissue gases, and substrates. 48 29

The levels of the adenine nucleotides ATP, ADP, and AMP in the stria vascularis were measured under normal conditions, and following various durations of ischemia. The concentrations of these compounds were used for the calculation of the adenylate energy charge, the energy status and the phosphorylation state of the stria. Following 10 min of ischemia the adenylate energy charge had decreased three fold, the energy status seven fold and the phosphorylation state 14 fold. To study the potential for recovery of strial function following various brief and prolonged ischemic intervals, a method for the perfusion of the ear via the anterior inferior cerebellar artery was developed. For various reasons it was found advantageous to use "artifical blood" as perfusate, relying upon fluorocarbons as oxygen carriers. The endolymphatic potential was used as electrical indicator of strial function. Recovery of the endolymphatic potential following brief periods of ischemia was paralleled by a corresponding increase of the ATP levels and a drastic decrease of the AMP levels of the stria vascularis. Preliminary results on the effects of substrate-free perfusion are presented.
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PMID:Adenine nucleotides of the stria vascularis. 48 54

Effects of chronic denervation upon in vivo forearm metabolism were studied in six patients and six controls. The diagnosis was amyotrophic lateral sclerosis in four patients, the neuronal form of Charcot-Marie Tooth disease in one patient, and an unclassified chronic disease of the lower motor neurons in one patient. In all cases the forearm muscles showed clinical weakness and electrical evidence of denervation, while muscle biopsy from a proximal muscle of the upper limb showed typical denervation atrophy. At rest there was increased oxygen utilization and lactate output as well as a tendency for increased uptake of glucose and long chain fatty acids from arterial blood per 100 ml of forearm tissue. During exercise the abnormally high lactate output increased further. An increased arterial lactate concentration was present during rest and exercise. Oxidation of fatty acids was not impaired. It is suggested that these abnormalities are consistent with an augmented utilization of blood borne fuels at rest by denervated muscles. A concurrent regional ischemia of muscles during rest and exercise, possibly due to defective autoregulation of skeletal muscle blood flow, may explain the abnormally high lactate generation.
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PMID:The effects of partial chronic denervation on forearm metabolism. 48 96

Earlier results are reviewed suggesting that transient pronounced, incomplete cerebral ischemia could be more deleterious for the recovery of brain tissue energy state than a complete interruption of the blood flow. Measurements of respiratory function of brain mitochondria, isolated after 30 min of either complete or incomplete ischemia, demonstrated a similar inhibition of respiratory activity and maximal phosphorylation rates in both situations. This inhibition was totally normalized during recirculation after complete ischemia while a further deterioration was found after incomplete ischemia. The in vivo alterations of the cortical tissue distribution of redox states during transient, incomplete ischemia (15--60 min) were measured using a flying spot fluorometer, which gives a real-time and on-line display of the tissue distribution of NADH and oxidized flavoprotein. A reoxidation in both systems was demonstrated during the recirculation period and the distribution of redox states showed no further heterogeneity in the postischemic period as compared to the preischemic distribution. It is concluded that reoxygenation of the brain tissue is possible even after long periods of incomplete ischemia. The normal distribution of redox states during recirculation suggests that mechanisms other than an impaired or inhomogeneous oxygen delivery during the postischemic period are responsible for the failure in recovery of mitochondrial function and tissue energy state.
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PMID:Cerebral energy state, mitochondrial function, and redox state measurements in transient ischemia. 48 72

Failure of microvascular re-perfusion, no reflow, of the brain after a period of ischemia has been proposed as the etiology of the cerebral dysfunction frequently seen in patients after resuscitation from hemorrhagic shock. For this investigation rats were stressed by subjecting them to a period of combined hypoxia and hypotension followed by resuscitation. Micro-oxygen electrodes measured brain oxygen tension, thus allowing an assessment of the distribution of cerebral blood flow, during stress and after resuscitation. After resuscitation, a hyperemic response was noted, followed by gradual return of some areas of the brain to normal perfusion, while other areas remained hyperemic for at least 2 hours post-resuscitation. On the basis of these results there appears to be no support for the no-reflow hypothesis. These data imply that therapeutic modalities aimed at increasing cerebral blood flow and oxygenation in the post-resuscitation period are insufficient in themselves for improved survival of patients sustaining a hypotensive, hypoxic episode.
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PMID:Effects of hypoxia and hypotension on oxygen delivery in the brain. 49 Jul 43

N-dimethyl propranolol (UM-272) has been shown to protect the heart from injury produced by ischemia. In the present study we examined the effects of UM-272 on the function of isolated rabbit cardiac mitochondria and microsomes. Concentrations of 13 micrometers or below were without effect on these organelles. UM-272 (130 micrometers) significantly decreased respiratory control of mitochondria utilizing glutamate plus malate, or succinate, as substrates. At 1.3 mM, UM-272 increased the initial rate of basal oxygen consumption, and decreased the rate of ADP-stimulated respiration. UM-272 was slightly more potent than d,1-propranolol. At a concentration of 1.3 mM, UM-272 significantly decreased the rate and maximum amount of 45CaCl2 accumulated by microsomes in the presence of ATP and oxalate. Concentrations of drug that suppress cellular metabolism are close to those required to prevent ischemic injury. We suggest that sarcolemmal and intracellular actions of the drug which help to depress oxygen demand and ATP utilization may account for part of the drug's protective effects.
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PMID:Effects of N-dimethyl propranolol (UM-272) on isolated cardiac mitochondria and microsomes. 49 13

In an isolated rat liver perfusion system the effects of normothermal ischemia on hepatic functions were investigated. After 30 minutes of anoxy bile production and BSP elimination capacity of the liver are significantly reduced. The quantity of secreted "ascites" from the surface of the liver several times high after anoxic damage, while oxygen consumption, portal venous pressure and ammonia elimination do not differ significantly from the controls. Pretreatment with insulin plus glucose, isoproterenol, hypoxanthine, chlorpromazine and glucagon (5 micrograms/100 g i.v., or 0.2 mg/100 g s.c.) does not reduce noticeably the normothermal anoxic lesion of the liver Glucagon (50 micrograms/100 g i.v.), allopurinol, dibenzyline, ATP-MgCl2 and aspartic acid enhance significantly the ischemia-tolerance of liver in vitro.
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PMID:Ischemic damage of the liver. Part I: In vitro investigation of the prevention of the ischemic lesion of the liver. 49 24


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