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

The collapsed left lungs of dogs were subjected to 1 hour of normothermic ischemia in situ followed by immediate ligation of the contralateral pulmonary artery. Adenosine in a dose of 50 mg/kg prolonged the survival of the dogs significantly. In the survivors only transient changes in the chest x-ray were seen, and no changes in arterial oxygenation were observed. The pulmonary architecture was well preserved on histological studies 14 days after operation. Animals whose ischemic lungs were not protected by adenosine showed an immediate drop in arterial oxygenation and a massive infiltrate of the ischemic lung. Histological study of the lungs showed a complete breakdown of the capillary-alveolar barrier. Allopurinol alone was ineffective by itself and was not able to improve the survival achieved with adenosine further. We conclude that it is possible to prolong the tolerance of a deflated lung to normothermic ischemia by pretreatment with adenosine.
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PMID:The effect of adenosine and allopurinol on the tolerance of the collapsed lung to warm ischemia. 34 12

In rats, cerebral perfusion pressure were altered abruptly by aortic transection to determine the production by ischemic brain of adenosine and its metabolites, inosine and hypoxanthine. Brain samples were obtained after 0, 5, 10, 15, 30, and 60 seconds of ischemia. Also measured were ATP, ADP, AMP, phosphocreatine (PCr), lactate, and pyruvate. Blood pressure was monitored continuously, and arterial PO2, PCO2, and pH were measured just prior to induction of ischemia. Adenosine was elevated t 2.30 +/- 0.31 (SE) nmol/g at 5 seconds from a control value of 0.96 +/- 0.07. A significant elevation of adenosine continued to 60 seconds (5.50 +/- 1.24). Furthermore, inosine showed a progressive upward trend during the entire 60 seconds of ischemia, whereas no change in hypoxanthine occurred between the moment of transection (31.81 +/- 2.01 nmol/g) and 60 seconds of ischemia (34.72 +/- 2.93). PCr decreased by 1.24 mumol/g within the first 5 seconds. After the onset of hypotension, significant changes did not occur in AMP and ADP until 30 seconds, and in ATP and pyruvate until 60 seconds after aortic transection; lactate was elevated by 10 seconds. The rapid rise of cerebral adenosine within 5 seconds after the onset of ischemia supports a role for adenosine in the regulation of cerebral blood flow.
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PMID:Brain adenosine production in the rat during 60 seconds of ischemia. 47 71

In contrast to the postocclusive hyperemia of brain, heart, and skeletal muscle, the hemodynamic response of the kidney following renal artery occlusion is highly variable in that both hyperemia and ischemia have been reported. The present study evaluates the factors influencing the renal response to complete renal artery occlusion (5-60 s) in the anesthetized cat. Marked postocclusive vasoconstriction could only be domonstrated in meclofenamate-treated (10 mg/kg) cats. The delta% renal blood flow (RBF) (30-s occlusion) was 16 +/- 4 in controls and 54 +/- 4 after meclofenamate (n= 10; P less than 0.001). Chronic denervation of the kidney, alpha-adrenergic receptor blockade, or infusion of [Sar1, Ile8]angiotensin II(2 microgram/min per kg) did not affect the postocclusive reduction of RBF, indicating that the vasoconstriction was independent of renal nerves, catecholamines, and circulating angiotesin II. Adenosine injected into the renal artery of five cats caused a dose-dependent transient fall of RBF. A dose of 100 nmol adenosine reduced RBF by 44 +/- 6% whereas after meclofenamate only 1 nmol produced the same degree of vasoconstriction. In summary, this study demonstrates a marked potentiation of the postocclusive vasoconstrictor response and the vasoconstrictive action of adenosine by meclofenamate in the anesthetized animal. No evidence was obtained to support a role for the sympathetic nervous system or circulating angiotensin II in mediating the postocclusive vasoconstriction.
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PMID:Characterization of the postocclusive response of renal blood flow in the cat. 69 69

Canine hindlimb muscles were perfused with arterial blood from a donor at a constant pressure or at a constant flow rate. Blood samples were analyzed for adenosine, oxygen and potassium during load-free twitch contractions (2 cps) and/or after 3-min ischemia. (1) During exercise hyperemia A-V oxygen (p smaller than 0.001) and V-A potassium (p smaller than 0.001) differences increased in both perfusion systems. Under the constant pressure total amount of adenosine and/or AMP released (TAAR) remained constant at 34.4 plus or minus 7.8 (mean plus or minus S.D.) nmoles/ml of blood compared with 31.0 plus or minus 5.6 at rest, whereas under the constant flow rate the value increased from 32.8 plus or minus 9.4 to 74.6 plus or minus 15.7 (p smaller than 0.001). (2) In reactive hyperemia A-V difference of oxygen increased (p smaller than 0.001) and TAAR remained at 33.0 plus or minus 8.3 under the constant pressure. Under the constant flow rate TAAR increased from 32.8 plus or minus 9.4 to 48.1 plus or minus 12.6 (p smaller than 0.001). (3) After ischemic contractions TAAR remained constant under the constant pressure perfusion. Under the constant flow rate, however, TAAR showed definite decrease compared with that during exercise hyperemia with intact flow (p smaller than 0.001). (4) The authors think that adenosine and/or AMP is the mediator of exercise hyperemia, supported by potassium ions and local hypoxia. Adenosine and/or AMP, and local hypoxia are responsible for reactive hyperemia. In ischemic contractions, no special circulatory mediator was found.
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PMID:Role of adenosine or AMP as a probable mediator of blood flow regulation in canine hindlimb muscles. 112 66

Adenosine diphosphate (8 mg per minute for five minutes) was infused into the carotid artery of 63 rabbits. The effects were twofold: systemic hypotension and platelet aggregation in the cerebral circulation. As a consequence of the last effect, platelet emboli were produced which occluded cerebral arteries in a number and size sufficient to cause cerebral ischemia. Areas of focal ischemia were observed through a cranial window, and documented with antipyrine autoradiography. Platelet thrombi were almost entirely transient, being fragmented and removed within a very short time of cessation of ADP infusion. Consequently, no permanent tissue damage ensued. This experimental model approaches the spontaneous transient ischemia attacks (TIAs) in man, demonstrating that these can be caused by pure platelet emboli. A high cholesterol diet administered for two months prior to ADP infusion did not enhance the effect of the procedure or make the platelet aggregation and the following ischemia longer in duration or more severe.
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PMID:Animal model of TIA: an experimental study with intracarotid ADP infusion in rabbits. 119 26

The prognosis of left bundle branch block is determined by associated cardiovascular disease. Exercise electrocardiography is not helpful in detecting ischemia in these patients. Exercise thallium-201 scintigraphy has been widely accepted for that purpose. The authors made an overview of several studies suggesting that exercise thallium-201 scintigraphy has low specificity regarding left anterior descending coronary artery disease. They also review the mechanisms of perfusion defects in patients with left bundle branch block without coronary artery disease. One important question to be clarified is weather small defects are unrelated to coronary artery disease. Finally the authors analyse a few methods to increase diagnostic accuracy of perfusion scintigraphy in left bundle branch block. First the employment of a new criterium that requires the apex to be abnormal to indicate left anterior descendent artery disease. Second Pharmacological Stress with Dipyridamole or Adenosine. Third imaging with Tc-99m-MIBI.
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PMID:[What is the value of myocardial perfusion studies with isotopes in patients with complete left bundle branch block?]. 129 Jun 46

In order to determine the effect of adenosine triphosphate (ATP) and adenosine in cardioplegic solutions, a comparative study has been undertaken in isolated guinea pig hearts using the Langendorff perfusion technique as a model of cardiopulmonary bypass. The hearts (n = 10 in each group) previously being perfused by Krebs-Henseleit solution, were arrested by one of the following cardioplegic solutions: 1) Potassium 20 mM/L (Plegisol), 2) Potassium 20 mM/L+ATP 10 mM/L, 3) Adenosine 10 mM/L, 4) Adenosine 10 mM/L+ATP 10 mM/L. After 45 min of hypothermic ischemia, postischemic recovery of heart rate, ventricular contractility, heart work and postischemic changes in tissue enzymes (LDH, SGOT, SGPT) were compared among the 4 different cardioplegic solutions. Arrest time and number of arrest beats were also recorded and compared among the groups. Although similar beneficial results on postischemic recovery were achieved with adenosine cardioplegia and with ATP supplemented potassium cardioplegia, ATP supplemented adenosine cardioplegia did not show any beneficial effects on postischemic recovery.
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PMID:Cardioplegia with adenosine and adenosine triphosphate in the isolated guinea pig heart. 129 45

The excitotoxic hypothesis suggests that cerebral ischemic damage results in part from the accumulation of the excitatory and potentially toxic neurotransmitters glutamate and aspartate. Adenosine, which also increases during cerebral ischemia, is proposed to inhibit neurotransmitter release. The purpose of this study was to determine if adenosine receptor blockade exacerbates the accumulation of glutamate and aspartate during cerebral ischemia. Microdialysis probes, implanted bilaterally in the caudate nucleus of halothane-anesthetized rats, were used to (1) assess changes in interstitial fluid (ISF) glutamate, aspartate, adenosine, and adenosine metabolites; (2) measure local cerebral blood flow (H2 clearance); and (3) deliver 8-(p-sulfophenyl)theophylline (SPT), an adenosine receptor antagonist, locally to the brain. The probe on one side of the brain was perfused with artificial cerebrospinal fluid (CSF) containing 10(-3) M SPT, while the probe on the opposite side received only artificial CSF. Animals were exposed to 20 min of ischemia (carotid occlusion+arterial blood pressure = 50 mm Hg) followed by 60 min of reperfusion. Dialysate glutamate and aspartate increased during and after cerebral ischemia, but were increased to a greater extent in the presence of adenosine receptor blockade. Likewise, the increase in dialysate adenosine and adenosine metabolites was enhanced on the side of locally administered SPT. These data suggest that endogenous adenosine attenuates the accumulation of glutamate and aspartate during cerebral ischemia.
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PMID:Adenosine receptor blockade augments interstitial fluid levels of excitatory amino acids during cerebral ischemia. 135 4

The rat hearts were subjected to 60-min ischemia by left coronary artery ligation followed by 60-min reperfusion, involving intravenous adenosine inosine or guanosine given in a dose of 1 mg/kg.min-1 in the first 30 minutes of reperfusion. Ischemia and subsequent reperfusion caused a progressive decrease in cardiac output and coronary blood flow. Adenosine was found to enhance coronary blood flow and increase cardiac and stroke outputs. Inosine produced nearly the same, but less pronounced effect. Guanosine increased cardiac output without changing coronary blood flow.
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PMID:[Hemodynamic effects of purine nucleosides in regional ischemia and reperfusion]. 140 75

The effects of adenosine in the nonischemic heart have been shown to be mediated via its binding to extracellular adenosine A1 and A2 receptors located predominantly on myocytes and endothelial cells, respectively. We tested the hypothesis that the beneficial effect of adenosine on postischemic myocardial function is mediated via an adenosine A1 receptor mechanism. Isolated rat hearts perfused at constant pressure (85 cmH2O) were subjected to 30 min of global no-flow ischemia (37 degrees C) and 45 min of reperfusion. Hearts treated with adenosine (100 microM) and the adenosine A1 receptor agonist N6-cyclohexyladenosine (CHA; 0.25 microM) recovered 72 +/- 4 and 70 +/- 4% of preischemic left ventricular developed pressures (LVDP), respectively, after 45 min of reperfusion compared with untreated hearts (54 +/- 3% of preischemic LVDP). Adenosine and CHA hearts exhibited greater myocardial ATP contents than control hearts after 10 min of ischemia, but there were no differences in tissue ATP levels after 30 min of ischemia. In contrast, hearts treated with the adenosine A2 receptor agonist phenylaminoadenosine (0.25 microM) failed to demonstrate improved postischemic function (52 +/- 5%). The addition of the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine blocked the cardioprotective effect of adenosine (57 +/- 4%). These results suggest that adenosine enhances postischemic myocardial function via an A1 receptor mechanism.
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PMID:Adenosine improves recovery of postischemic myocardial function via an adenosine A1 receptor mechanism. 144 99


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