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

We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 +/- 5 to 0.3 +/- 0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4 +/- 4.8 minutes) than either adenosine triphosphate (16.5 +/- 3.7 minutes) or intracellular pH (38.9 +/- 1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient.
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PMID:Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum. 200 87

Brain edema is a frequent complication of cerebral ischemia; however, its mechanism of formation is not well understood. Sodium is known to accumulate in brain during the early stages of partial ischemia. Therefore, the present studies were undertaken to determine the relation among BBB sodium transport, integrity of the BBB, and development of brain edema during the first 24 hr after the onset of cerebral ischemia. Partial cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. After recovery from the anesthetic, animals were scored for the presence of symptoms, and those with scores greater than 10 of 25 (n = 87) were chosen for this study. Measurements of tissue water, sodium, and potassium contents, and brain uptake of 22Na and 3H-mannitol were made in each group at 1.5, 3, 6, 12, and 24 hr after carotid ligation. Accumulation of sodium and water in the ischemic compared with the nonischemic cerebral cortex was progressive. This edema formation was not of the vasogenic type because the permeability of the BBB to mannitol was unchanged. Blood-to-brain sodium transport was reduced by 30% to 40% at all time points in the ischemic cortex. Nevertheless, the remaining sodium transport activity appeared to play a role in the development of brain edema because Na accumulated in the tissue at a rate that was approximately the same as the rate of 22Na uptake from blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood-to-brain sodium transport in ischemic brain edema. 216 71

Mitochondrial pyruvate-supported respiration was studied in vitro under conditions known to exist following ischemia, i.e., elevated extramitochondrial Ca2+, Na+, and peroxide. Ca2+ alone (7-10 nmol/mg) decreased state 3 and increased state 4 respiration to 81 and 141% of control values, respectively. Sodium (15 mM) and/or tert-butyl hydroperoxide (tBOOH; up to 2,000 nmol/mg protein) alone had no effect on respiration; however, Na+ or tBOOH in combination with Ca2+ dramatically altered respiration. Respiratory inhibition induced by Ca2+ and tBOOH does not involve pyruvate dehydrogenase (PDH) inhibition since PDH flux increased linearly with tBOOH concentration (R = 0.96). Calcium potentiated tBOOH-induced mitochondrial NAD(P)H oxidation and shifted the redox state of cytochrome b from 67 to 47% reduced. Calcium (5.5 nmol/mg) plus Na+ (15 mM) decreased state 3 and increased state 4 respiratory rates to 55 and 202% of control values, respectively. Sodium- as well as tBOOH-induced state 3 inhibition required mitochondrial Ca2+ uptake because ruthenium red addition before Ca2+ addition negated the effect. The increase in state 4 respiration involved Ca2+ cycling since ruthenium red immediately returned state 4 rates back to control values. The mechanisms for the observed Ca2(+)-, Na(+)-, and tBOOH-induced alterations in pyruvate-supported respiration in vitro are discussed and a multifactorial etiology for mitochondrial respiratory dysfunction following cerebral ischemia in vivo is proposed.
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PMID:Effect of peroxide, sodium, and calcium on brain mitochondrial respiration in vitro: potential role in cerebral ischemia and reperfusion. 231 94

The effect of pH of the reperfusion buffer on postischemic changes in tissue Ca and Na was examined in isolated Langendorff-perfused Sprague-Dawley rat hearts. Reperfusion began after 15-, 25-, or 60-min ischemia at 37 degrees C. After 60-min ischemia, reperfusion at pH 6.4 or 6.6 attenuated the reperfusion-induced Ca gain so long as the acidotic conditions were maintained (3.08 +/- 0.22, 1.37 +/- 0.41, and 16.96 +/- 1.18 mumol Ca gain/g dry wt for pH 6.4, 6.6, and 7.4, respectively after 15-min reperfusion). Conversely, reperfusion under alkalotic conditions (pH 7.9) after 60-min ischemia exacerbated the gain (27.45 +/- 4.75 and 8.92 +/- 1.53 mumol Ca gain/g dry wt during 5-min reperfusion at pH 7.9 and 7.4, respectively). Similar, but less pronounced Ca gains occurred during reperfusion after 15- or 25-min ischemia. Sodium content during reperfusion, but not during aerobic perfusion, was also found to be pH sensitive with acidosis causing a reduction and alkalosis an increase. These results could not be explained in terms of an effect of pH on recovery of high-energy phosphates, percentage "reflow" during reperfusion, or reperfusion-induced increases in tissue water or resting tension. The results are in agreement with the hypothesis that the "inhibitory" effect of acidosis on postischemic Ca overload could involve an effect of pH on the Na(+)-H+ exchanger and intracellular Ca storage.
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PMID:Effect of acidosis and alkalosis on postischemic Ca gain in isolated rat heart. 231 96

This study was designed to analyze the electrolytes changes in myocardial cells, and to clarify the effect of diltiazem, a calcium channel blocker on myocardial ischemia during open heart surgery. Thirty patients who underwent open heart surgery using cold glucose-insulin-potassium (GIK) cardioplegic solution were divided into following three groups. C group: diltiazem was not administered. CD group: cardioplegic solution containing diltiazem 7.5 mg/L was used. DP group: diltiazem 1.5 micrograms/kg/min was given continuously by intravenous administration from the day before operation to the day after operation. Atrial wall biopsies were performed before aortic cross clamp (non-ischemic status), after 60 minutes' ischemia, and 5 minutes after releasing aortic cross clamp (reperfusion). The specimens were freshly frozen and measured for various electrolytes by means of X-ray microprobe analysis. In C group, potassium level decreased during both ischemia and reperfusion, while calcium level increased during ischemia and significantly increased during reperfusion period. In DC and DP groups, calcium accumulation during reperfusion was suppressed, and potassium level which had been lowered during ischemia recovered to the level of non-ischemic status during reperfusion. Sodium and chlorine showed an increase during ischemia in each group. However, sodium accumulation in DC and DP groups tended to recover during reperfusion. DP and DC groups were considered to be superior to C group in terms of cardiac index and left ventricular work. This may be due to afterload reduction as evidenced by low systemic vascular resistance. Intracellular electrolytes environment during reperfusion and hemodynamics during early postoperative periods were excellent in DP group. CPK-MB was significantly lower in both CD and DP groups than in C group. These data suggested that diltiazem could suppress intracellular calcium accumulation and keep homeostasis of sodium-potassium pump mechanism in membrane during reperfusion. It is concluded that diltiazem is useful to protect myocardium from ischemia during open heart surgery.
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PMID:[The protective effect of diltiazem, a calcium channel blocker on myocardial ischemia during open heart surgery--an analysis of electrolyte changes in myocardial cells]. 234 17

Isolated guinea pig hearts subjected to global ischemia, were used to investigate whether lidocaine exerts an antiarrhythmic action against reperfusion-induced arrhythmias, and the effects of this drug upon myocardial ion contents during ischemia and reperfusion were studied. In the first series of experiments, the drug was administered 5 min prior to the induction of global ischemia and maintained during reperfusion. With 3.6 X 10(-6), 7.2 X 10(-6), 14.7 X 10(-6), and 29.5 X 10(-6) mol/L lidocaine, reperfusion-induced ventricular fibrillation and tachycardia were reduced from their control incidence of 83% and 100% to 41% and 58%, 33% (p less than 0.05) and 25% (p less than 0.001), 8% (p less than 0.01) and 8% (p less than 0.001), 0% (p less than 0.001) and 0% (p less than 0.001), respectively. The ion contents of myocardium were determined by atomic absorption spectrophotometer after washout of the ions from vasculature. Ischemia induced a marked accumulation of sodium and loss of potassium in the myocardial tissue. Both ischemia-induced sodium gain and potassium loss were significantly inhibited by lidocaine treatment. During reperfusion, sodium was further increased in the control group and this value was significantly lower in the lidocaine-treated group after 1 min of reperfusion. Sodium content remained at nearly constant level for the rest of reperfusion period. Potassium was suddenly increased during the first 5 min of reperfusion then continuously decreased until the end of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of lidocaine against ischemia and reperfusion-induced arrhythmias and shifts of myocardial sodium, potassium, and calcium content. 246 78

Sodium derived from the blood is known to accumulate in brain tissue during the early stages of incomplete ischemia. Our present studies were undertaken to determine the relation between blood-brain barrier sodium transport and the development of ischemic brain edema. Incomplete cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. Following recovery from the anesthetic, the gerbis were evaluated for the presence of neurologic symptoms and were divided into symptomatic (n = 77) and asymptomatic (n = 94) groups. Tissue water, sodium, and potassium contents, tissue plasma volume, and brain uptake of 22Na were measured in both groups 1.5, 3, 6, 12, and 24 hours after carotid ligation. There was a progressive accumulation of sodium and water in the ipsilateral cerebral cortex of the symptomatic group compared with either the corresponding contralateral cortex of the same gerbils or with the asymptomatic group. Net changes in brain sodium and potassium concentrations appeared to be the main determinants of fluid accumulation. Brain edema was not due to opening of the blood-brain barrier because the unidirectional transport of 22Na remained low and was even reduced by 35-55% in the ischemic cortex. Nevertheless, this sodium transport activity appeared to be rate-limiting in the development of brain edema during the first 3 hours of ischemia because the rate of sodium accumulation in the tissue was the same as the rate of 22Na transport from the blood to the brain. We conclude that blood-brain barrier sodium transport is an important factor in the formation of ischemic brain edema.
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PMID:Blood-brain barrier sodium transport limits development of brain edema during partial ischemia in gerbils. 277 85

To elucidate the mechanisms responsible for the increase in alpha 1-adrenergic receptors during ischemia in vivo, we developed a procedure for measuring alpha 1-adrenergic receptors in isolated, calcium-tolerant adult canine myocytes. Specific [3H]prazosin binding was rapid, saturable, reversible, and demonstrated the expected order of potency and stereospecificity for the alpha 1-adrenergic receptor. Myocytes exposed to 30 minutes of hypoxia at 25 degrees C or only 10 minutes at 37 degrees C exhibited a twofold to threefold increase in the number of alpha 1-adrenergic receptors with no significant change in receptor affinity. This hypoxia-induced increase in receptor number was reversible by 10 minutes of reoxygenation at 37 degrees C. In contrast, more prolonged hypoxia of 80 minutes or hypotonic shock actually decreased receptor number below normoxic, control values. The concentration of long-chain acylcarnitines in myocytes also increased threefold on exposure to 30 minutes of hypoxia. Sodium 2-[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (POCA, 10 microM), a potent inhibitor of carnitine acyltransferase I, not only abolished the accumulation of long-chain acylcarnitines but also the increase in alpha 1-adrenergic receptor number induced by 30 minutes of hypoxia. Likewise, incubation of normoxic cells with exogenous palmitoyl carnitine (1 microM) for 10 minutes also increased alpha 1-adrenergic receptor number in the presence or absence of POCA. Thus, hypoxia results in an increase in alpha 1-adrenergic receptors associated with an increase in endogenous long-chain acylcarnitines. Furthermore, inhibition of carnitine acyltransferase I prevents not only the sarcolemmal accumulation of long-chain acylcarnitines but also the exposure of the alpha 1-adrenergic receptor, indicating that accumulation of endogenous long-chain acylcarnitines is critical to the hypoxia-induced increase in alpha 1-adrenergic receptors on adult myocytes.
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PMID:Long-chain acylcarnitines mediate the hypoxia-induced increase in alpha 1-adrenergic receptors on adult canine myocytes. 282 80

Clinical studies have shown pulmonary and right ventricular hypertension to be important factors increasing the risk to patients during pulmonary angiography. This experiment was undertaken to define the hemodynamic changes induced by the administration of contrast material into the pulmonary arteries of dogs with embolic pulmonary hypertension, and to compare the effects of ionic and nonionic agents. Ten closed-chest dogs under light halothan anesthesia were subjected to pulmonary embolization with sephadex microspheres until severe pulmonary hypertension occurred and the cardiac output decreased to 50%-60% of the pre-embolization baseline. Intra-pulmonary injections of contrast material were performed in eight animals while hemodynamic indices were measured. Sodium methylglucamine diatrizoate induced severe, transient, hypotension associated with a large decrease in systemic vascular resistance and little change in the cardiac output. Hypotension is especially undesirable in the presence of pulmonary hypertension because it worsens the preexisting coronary ischemia and compromised right ventricular function. No elevation in mean pulmonary artery pressure was seen, and pulmonary vascular resistance decreased. Iohexol induced milder effects, perhaps because it exerts a less severe systemic vasodilatory effect and is not a negative inotrope. These findings suggest iohexol may be safer in the high risk patient, however, these data may not be directly applied to unanesthetized humans.
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PMID:The hemodynamic effects of the administration of ionic and nonionic contrast materials into the pulmonary arteries of a canine model of acute pulmonary hypertension. 337 76

Anterior ischemic optic neuropathy (A.I.O.N.) may cause optic disc edema in type-I diabetes. A.I.O.N. affects diabetic patients of all ages. Such optic neuropathy is more likely to become bilateral in diabetics than in the non-diabetic subjects. A 41-year-old diabetic insulin-dependent woman presented A.I.O.N. in RE; 5 years later, the same affection occurred in LE. The clinical course was relatively benign in both eyes, with good functional restitution. The patient was treated by high doses of Sodium Salicylate and Sulfinpyrazone. The pathogenesis of optic disc edema in type-I diabetes is, according to Hayreh (1981), ischemia of different grade in the district of the posterior ciliary arteries: microangiopathy, rheological anomalies and atherosclerotic added lesions produce a variability of clinical pictures of increasing seriousness. Our case has an intermediate position in such a continuous spectrum. The VEP supported the diagnosia of A.I.O.N.
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PMID:Anterior ischemic optic neuropathy in type I diabetes. 345 16


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