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

The effects of increased acidity and of lactate at acid pH values on the ultrastruct of normal dog myocardium were investigated using a simple in vitro system. Thin tissue slices incubated in isotonic, phosphate-buffered sodium chloride at pH 6.5, 6.8, or 7.0 developed within 10 minutes electron-dense mitochondrial inclusions resembling those seen in dog heart muscle after 40 or more minutes of ischemia. Mitochondria of tissue incubated in a comparable medium incorporating 3000 mu g. of lactate per ml. showed similar electron-dense inclusions, together with marked swelling. These results indicate that lowered tissue pH alone is not responsible for the mitochondrial changes typical of ischemic heart muscle. Since an earlier study has shown that marked mitochondrial swelling without dense granule formation can be produced by incubation of tissue in lactate at physiologic pH, it seems likely that the swelling of mitochondria in ischemic myocardium is due to the accumulation of lactate anions, whereas the development of the mitochondrial inclusions is associated with decreased pH.
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PMID:Mitochondrial changes in dog myocardium induced by lowered pH in vitro. 23 54

With the author's own observations and literature sources as a background the key issues concerned with increasing the viability of the myocardium in acute ischemia are considered. The possibility of a material enlargement of the collateral coronary circulation through administration of mesatonemonoaminoxidase inhibitors, diprazine, preparations of the metabolites type and of other agents is shown. Under consideration are data on the membranes-stabilizing effect in acute ischemia of the myocardium of dimedrol, diprazine and prednisolone, as well as possible ways of increasing the survival of the myocardium by activating the redox-processes and through an adequate supply of energy to ensure the vital functions of the myocardial cell at rest by using pertinent pharmacological agents (cytochrome C, NADP, ubiquinone, hexose-phosphate, monoaminodicarboxylic amino acids).
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PMID:[Problem of increasing the viability of the ischemic myocardium in the light of experimental studies]. 23 63

A stable free-radical polymeric derivative of prostaglandin B1 (PGBx) has been synthesized that exhibits regenerative effects on oxidative phosphorylation in aged mitochondria. The molecular weights of the most active preparations fall between 2000 and 2600. PGBx is characterized by a single-line electron spin resonance spectrum that is stable at room temperature. PGBx restores phosphorylating ability and net ATP synthesis in isolated mitochondria aged for 4 days at 0 degrees C and protects against further degradation of phosphorylating activity when such aged mitochondria are preincubated at 28 degrees C in the absence of adenine nucleotide phosphate acceptors. This compound has been reported to exert beneficial effects in vivo in experimental pathological conditions, such as regional ischemia, in which the mitochondria of the ischemic region may have been damaged.
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PMID:Protection and reactivation of oxidative phosphorylation in mitochondria by a stable free-radical prostaglandin polymer (PGBx). 28

31P NMR was used to continuously monitor ATP and inorganic phosphate levels in perfused mouse liver. Under "optimal" conditions, the time resolution of the technique was approximately 1 min. In the absence of any metabolic perturbations the ATP level remained constant for at least 2 hr and decreased by only approximately 20% in 18 hr. Both ATP and inorganic phosphate levels responded to alterations in the oxygen supply to the liver. The half-time for this response was approximately 1 min, and the response to short periods of hypoxia or ischemia was partially reversible. The addition of insulin caused only a minor decrease in the ATP level but significantly decreased the rate of response of ATP and phosphate levels to hypoxia and ischemia.
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PMID:Rapid ATP assays in perfused mouse liver by 31P NMR. 29 54

Mitochondria isolated from rat kidney subject to in vitro ischemia at various time intervals demonstrated a continuous decline of the ability to accumulate calcium following a high initial stable phase of accumulation of calcium which is dependent both on ATP and respiration. This decline occurs during the reversible phase of cell injury and appears to be a sensitive indicator of membrane changes in a binding and/or transport protein or of other membrane permeability characteristics. The morphology of mitochondrial densities related to calcium accumulation in mitochondria varied. Any form of calcium accumulation, resulted in marked swelling of mitochondria. Control renal mitochondria in sucrose were highly condensed. Partially inhibited calcium accumulation in the presence of phosphate was also associated with numerous small spheric or punctate deposits in close relationship to the inner membrane. Uninhibited calcium accumulation resulted in the formation of needle-like structures radiating from such inner membrane associated sites.
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PMID:Studies on the pathogenesis of ischemic cell injury. VI. Accumulation of calcium by isolated mitochondria of ischemic rat kidney cortex. 41 33

Acute mesenteric ischemia is extremely difficult to diagnose because peritoneal signs are absent until the bowel becomes necrotic and irretrievably damaged. So far the only reliable diagnostic procedure has been mesenteric angiography. The present study verifies that significant elevations of serum inorganic phosphate concentrations occur in dogs after mesenteric occlusion; the authors' initial clinical studies in humans support these experimental findings. Detailed analysis of body fluid and soft tissue phosphate content shows that the high phosphate load originates in the sloughing intestinal mucosa; if this phosphate escapes filtration by the liver it enters the systemic circulation. Simple measurement of the inorganic phosphate concentrations of the serum and peritoneal fluid may lead to earlier diagnosis of acute intestinal ischemia and a successful revascularization procedure to prevent its progression to infarction.
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PMID:Preinfarction diagnosis of acute mesenteric ischemia by simple measurement of inorganic phosphate in body fluids. 44 38

Brief periods of ischemia have been shown to produce marked reactive hyperemia in both red (slow) and white (fast) skeletal muscle. However, evidence is lacking for specific vasodilator metabolites which are rapidly produced in ischemic skeletal muscle. The present study examined the effects of 1 and 3 minutes of ischemia on creatine phosphate (CrP), adenine nucleotide metabolism, and anaerobic glycolysis in red anterior (ALD) and white posterior latissimus dorsi (PLD) muscles of the chicken. Tissue metabolite concentrations were determined from perchloric acid or trichloroacetic acid extracts using enzymatic assay or high pressure liquid chromatography. CrP or adenine nucleotides were not significantly altered in either muscle following 1 or 3 minutes of ischemia. However, adenosine increased by 611% in the ALD at 1 minute. Following 3 minutes of ischemia, adenosine concentrations were elevated by 439% and 201% in the ALD and PLD, respectively. The PLD showed the greatest increases in inosine and IMP. Inorganic phosphate increased by 67% and lactate increased by 142% in the ALD at 3 minutes. The PLD, which is reported to have a high anaerobic glycolytic capacity, showed no increase in lactate. These results support the hypothesis that adenosine may be a mediator of akeletal muscle reactive hyperemia following short periods of ischemia.
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PMID:Effects of ischemia on tissue metabolites in red (slow) and white (fast) skeletal muscle of the chicken. 45 3

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

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

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


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