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

The precise mechanism responsible for early contractile failure after the onset of myocardial anoxia or ischemia has attracted speculation and controversy. The simple and attractive hypothesis that adenosine triphosphate (ATP) deficiency is responsible for this failure has often been dismissed on the basis of claims that there is only a small reduction in cell ATP content at a time when contractile activity is severely reduced. The premise of this article is that the changes in cell ATP content and distribution that theoretically should occur after oxygen depletion may not have been adequately considered and that previous measurements of cell ATP content may not have been carried out at the correct time. Using an isolated rat heart preparation and high speed freeze-clamping techniques it has been possible to demonstrate that a substantial decrease in myocardial ATP and creatine phosphate content occurs after the onset of anoxia but before the onset of contractile failure. Thus, during the first 5 seconds of anoxia contractile activity remains constant whereas ATP decreases by 25 percent and creatine phosphate by 50 percent. Thereafter, contractile failure occurs and the rate of utilization of high energy phosphates declines with the cell content at a plateau or possibly increasing. These results are assessed in the light of the dynamic changes in energy metabolism occurring in early anoxia and suggest that ATP depletion in a specific cell compartment may be the primary trigger for early contractile failure.
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PMID:Oxygen deprivation and early myocardial contractile failure: a reassessment of the possible role of adenosine triphosphate. 49 6

We compared the effectiveness of three pharmacologically and chemically dissimilar vasodilators (histamine, glucagon, and perhexiline) in reversing the hemodynamic and metabolic deficits of intestinal ischemia produced by hemorrhage. With intraarterial infusion into the superior mesenteric artery of anesthetized control dogs, all three agents increased mesenteric blood flow and oxygen consumption without altering systemic arterial blood pressure. Similarly, in the ischemic gut following moderate hemorrhage all three vasodilators increased mesenteric flow and oxygen consumption while reducing vascular resistance and not affecting systemic arterial blood pressure. On a molar basis glucagon was the most potent dilator drug. In severely hemorrhaged dogs whose intestinal blood flow had been reduced nearly 80%, glucagon restored oxygen uptake and vascular resistance to control levels. These findings demonstrate the efficacy of three different vasodilators in reversing the mesenteric ischemia and hypoxia produced by hemorrhage.
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PMID:Effects of vasodilators on mesenteric ischemia and hypoxia induced by hemorrhage. 49 29

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.
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PMID:Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia. 50 72

The histochemical investigation of the oxidizing-reducing enzymes in the gastrocnemius muscle was carried out on the material of 42 patients with atherosclerotic lesions of the abdominal aorta and the extremity arteries. The results obtained were compared with the muscle blood flow value and the level of the partial strain of oxygen in the gastrocnemius muscle. A conclusion is made that it is expedient to investigate the level of metabolic activity of muscles of the injured extremity for the estimation of the vitability of muscles which is very important for solving the question about the possible revascularization of the extremity in severe ischemia due to chronic occlusing process in the extremity arteries.
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PMID:[Metabolic activity of the gastrocnemius muscles in atherosclerotic lesion of the abdominal aorta and arteries of the extremities]. 50 10

The relationship of changes in regional coronary flow to the nature and degree of biochemical disturbances during occlusion of branches of the left anterior descending coronary artery and following reestablishment of flow was investigated in two groups of dogs: group I, moderate ischemia before reflow, and group II, severe ischemia prior to reflow. Regional coronary blood flow was determined before ligation, after 60 min of ischemia and after 15 min of reflow using labelled microspheres. Hearts made ischemic for 60 min but not reperfused served as controls. Groups I and II were distinguished by the following features. Group II showed a marked exacerbation of biochemical damage on reperfusion of the ischemic region (reduced levels of ATP, impairment of mitochondrial oxygen consumption and mitochondrial calcium binding). This was accompanied by significant subendocaridial hyperemia. Reperfusion in group I, on the otherhand, partially reversed these changes (increased level of ATP in the ischemic-reperfused region, improved mitochondrial oxygen consumption and calcium binding). Mitochondrial calcium uptake and oxidative phosphorylation (ADP/O ratio) were not affected in any group. These data illustrate that the degree of biochemical damage following reperfusion of the ischemic myocardium is determined by the degree of ischemia, and suggest that interference with ATP production by the mitochondria is not responsible for the damage.
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PMID:The relationship of regional coronary blood flow to mitochondrial function during reperfusion of the ischemic myocardium. 50 23

Bilateral ligation of common carotid arteries sharply decreases volume blood flow and oxygen consumption in the cortex, in diencephalon and midbrain whereas inducing no changes in the cerebellum and medulla oblongata. The same is true for intensity of metabolism of both total and separate fractions of phospholipids. This suggests that the changes of phospholipid metabolism in neural tissue depend on the degree of its blood supply disturbance and duration of the ischemia.
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PMID:[Effect of cerebral blood supply disorders on certain aspects of metabolism]. 51 Jun

It has been reported that incomplete cerebral ischemia with cerebral blood flow less than 10% of control may be more damaging than an equal period of complete ischemia. In this study, the effects of severe, incomplete cerebral ischemia on neurological outcome and cerebral metabolism were studied in dogs anesthetized with nitrous oxide. The results were compared with those of a previous study concerned with the effects of complete ischemia. Dogs could sustain only 8 to 9 minutes of complete ischemia with return of normal neurological function, whereas maintenance of a cerebral blood flow rate less than 10% of control extended this limit to 10 6o 12 minutes. Following a 10-minute exposure, only dogs undergoing incomplete ischemia regained a normal cerebral oxygen consumption within 90 minutes; similarly, animals subjected to incomplete ischemia enjoyed a faster return of EEG activity than dogs exposed to complete ischemia of the same duration. Cerebral metabolite levels did not prove to be a good index of return of neurological function. Within periods of cerebral ischemia in which meaningful neurological recovery might be expected, we conclude that some blood flow is better than no flow.
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PMID:Incomplete versus complete cerebral ischemia: improved outcome with a minimal blood flow. 51 35

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.
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PMID:Cold blood as the vehicle for potassium cardioplegia. 51 80

The effect of two dopaminergic agonists (apomorphine and bromocriptine) on electrical activity and oxygen supply of the brain was investigated in cats submitted to hypovolemic oligemia (mean arterial blood pressure: 45 mmHg). While both drugs stimulated the brain by prolonging the oligemia-induced seizures in the caudate nucleus and in the cerebral cortex, only apomorphine improved the pO2 distribution in the cortical tissue after 120 min oligemia. Bromocriptine, in contrast, had a beneficial effect of shorter duration. These data show that under conditions of incomplete ischemia the brain can still be activated. Furthermore, these results provide additional support for the biochemically founded hypothesis of different dopamine receptors in the brain.
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PMID:Dopaminergic agonists and their influence on the oxygenation and function activity of underperfused brain tissue. 52 54

We measured ventilatory responses to CO2 (delta VI/delta PCO2) and transient hypoxia (delta VI/delta SaO2) during reductions of brain blood flow (BBF) to 70% and 50% of control in unanesthetized goats. Increase in inspiratory volume per change in CO2 tension (delta VI/delta PCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial oxygen saturation (delta VI/delta SaO2) was assessed by the transient N2 inhalation method. Delta VI/delta SaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. Delta VI/delta PCO2 increased (0.94 +/- 0.18 to 1.29 +/- 0.24 l . min-1 . Torr-1) at 70% BBF if arterial CO2 tension were used to represent the CO2 stimulus but was unchanged if venous CO2 tension were used. At 50% BBF, delta VI/delta PCO2 was depressed (0.38 +/- 0.13 l . min-1 . Torr-1) for both representations of the CO2 stimulus. Brain ischemia increased blood pressure and heart rate but blunted the increase in BBF caused by hypercapnia. We conclude that 1) moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2, 2) delta VI/delta PCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed, and 3) severe brain ischemia (50% BBF) blunts delta VI/delta SaO2 and delta VI/delta PCO2, probably as a consequence of hypoxic depression of the respiratory neurons.
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PMID:Effects of graded reduction of brain blood flow on chemical control of breathing. 53


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