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

The changes in acetylcholine (ACh), monoamine and monoamine metabolite levels following cerebral ischemia in Mongolian gerbils were examined. In addition, the effects of Sho-saiko-to-go-keishi-ka-shakuyaku-to (TJ-960), which is a spray-dried mixture of 9 herbal drugs, on these changes were also examined. The dramatic decrement of ACh levels in ischemic gerbils was significantly inhibited by p.o. administration of TJ-960 at a daily dose of 3.5 g/kg or 700 mg/kg for one month. Norepinephrine (NE) was also reduced in all ischemic brain regions, and TJ-960 also recovered the level of NE. In ischemic gerbil brains, the dopamine (DA) levels decreased and its metabolites increased in the striatum, but DA and its metabolites in the thalamus + midbrain region increased. The serotonin (5HT) level was reduced in the cerebral cortex and hippocampus. TJ-960 inhibited these monoaminergic changes in ischemic gerbils. This suggests that TJ-960 may provide anti-ischemic action and beneficial effects on various symptoms induced by ischemia.
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PMID:The effects of sho-saiko-to-go-keishi-ka-shakuyaku-to (TJ-960) on ischemia-induced changes of brain acetylcholine and monoamine levels in gerbils. 237 Sep 41

The effects of a stable prostacyclin mimetic, iloprost (30 nmol/l), and of indomethacin (3 mumol/l) on ischemia-plus-reperfusion-induced changes in myocardial hemodynamics and sympathetic nerve function were examined in Langendorff-perfused rabbit heart isolated except for the postganglionic sympathetic cardiac nerves. Noradrenaline overflow was measured during an initial 1-min period of nerve stimulation (S1), compared with an identical stimulation (S2) made after 2 h of low-flow ischemia followed by a 30-min reperfusion period. Myocardial catecholamine content of left ventricular tissue was also measured. Pretreatment with iloprost, indomethacin, or vehicle began 10 min before ischemia. Global ischemia plus reperfusion reduced myocardial catecholamine content by 19% (vehicle), and the reduction was greater in indomethacin-pretreated hearts (37%, p less than 0.05), whereas iloprost increased tissue noradrenaline 18% above vehicle control (p less than 0.05). Initially, nerve stimulation-induced noradrenaline overflow ranged from 213 to 247 pmoles, and was significantly reduced after ischemia and reperfusion, the difference (S1-S2) being 198 pmoles (vehicle) and 117 pmoles (indomethacin), but only 44 pmoles after iloprost pretreatment (all groups p less than 0.01). In addition, iloprost improved the recovery of active systolic pressure development, coronary perfusion and left ventricular compliance on reperfusion, whereas a tendency toward further deterioration was observed in indomethacin-pretreated hearts. The results suggest that iloprost may protect both myocardial muscle and nerve cells from ischemia-plus-reperfusion injury. Preservation of myocardial catecholamine levels and sympathetic nerve responsiveness may contribute to improved recovery of reperfused ischemic myocardium.
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PMID:Prostaglandins and myocardial noradrenaline overflow after sympathetic nerve stimulation during ischemia and reperfusion. 241 Jul 36

Recently, this laboratory has demonstrated an enhanced susceptibility toward the development of ischemia-related lethal ventricular arrhythmias in the presence of therapeutic serum concentrations of digoxin in conscious dogs after myocardial infarction. The present study was performed to assess the effect of the interruption of cardiac sympathetic influences, via subacute left stellate ganglionectomy (LSGX), on digitalis-mediated ischemic ventricular arrhythmias. Commencing 4-5 days after anterior myocardial infarction, 11 dogs with LSGX and 14 sham controls were administered digoxin (0.0125 mg/kg/day i.v.) for 5-7 consecutive days. At baseline testing, programmed ventricular stimulation failed to initiate ventricular tachycardia in any postinfarction dog entered into this evaluation. After treatment, 11/11 digoxin + LSGX (1.33 +/- 0.10 ng/ml serum digoxin) and 14/14 digoxin-treated sham (1.23 +/- 0.14 ng/ml serum digoxin) dogs remained nonresponsive to programmed stimulation testing. The incidence of arrhythmic mortality in response to subsequent ischemia at a site remote from the infarcted anterior region was greater in the digoxin-treated sham group (1.22 +/- 0.21 ng/ml serum digoxin) than in the digoxin + LSGX group (1.33 +/- 0.10 ng/ml serum digoxin); mortality was 6/10 (60%) digoxin sham vs. 1/10 (10%) digoxin + LSGX, p less than 0.005. The underlying anterior myocardial infarct sizes (% of left ventricle: 6.8 +/- 2.3 vs. 6.6 +/- 1.1) did not differ between the digoxin sham and digoxin + LSGX groups. However, the digoxin sham controls developed larger posterolateral myocardial infarctions than did the digoxin + LSGX animals (% of left ventricle: 27.4 +/- 3.0 vs. 16.7 +/- 2.7, p less than 0.05). Norepinephrine concentrations in posterolateral through posteroseptal ventricular sections were not altered by LSGX in a separate group of digoxin-treated postinfarct dogs. The results suggest that left stellate ganglionectomy may reduce the incidence of digitalis-mediated malignant ventricular arrhythmias during ischemia, possibly due to a reduction in the severity of ischemic injury.
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PMID:Antiarrhythmic actions of left stellectomy in digitalis-mediated malignant ventricular arrhythmias in the postinfarcted canine heart. 245 51

The aim of this study was to examine the electrophysiological effects of isoprenaline, phenylephrine, and noradrenaline on sheep Purkinje fibers in vitro, superfused either with a normal or with a modified physiological salt solution (PSS) designed to mimic some of the conditions occurring during mild myocardial ischemia (hyperkalemia, hypoxia, and acidosis). Intracellular microelectrode recording techniques were used to record resting and action potentials. Noradrenaline (10(-7) to 10(-5) M) and phenylephrine (10(-7) to 10(-5) M) prolonged the action potential of normal fibers in a concentration-dependent manner, the effect of phenylephrine being greater than that of noradrenaline. The only effect of isoprenaline (10(-7) to 10(-5) M) was a slight hyperpolarization. The modified PSS caused marked reductions in resting membrane potential, upstroke, and duration of the action potential. On these depressed fibers isoprenaline, noradrenaline, and phenylephrine all prolonged the action potential, and in the case of noradrenaline the duration of the abbreviated action potential was restored beyond control. This effect of noradrenaline and isoprenaline was more marked under ischemic than normal conditions, whereas the opposite was true of phenylephrine. In the presence of effective alpha- or beta-adrenoceptor blockade, the noradrenaline-induced prolongation of the "ischemia"-abbreviated action potential was attenuated. In some of the preparations exposed to simulated ischemia, noradrenaline caused inexcitability. In conclusion, isoprenaline, phenylephrine, and noradrenaline exhibited different electrophysiological effects on mildly "ischemic" sheep Purkinje fibers compared to their effects on normal fibers.
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PMID:Cardiac electrophysiological effects of isoprenaline, phenylephrine, and noradrenaline on normal and mildly "ischaemic" sheep Purkinje fibers. 246 60

Noradrenaline (NA) metabolism in the neocortex and hippocampus was examined in rats at 1, 24, and 48 h following 15 min of reversible forebrain ischemia. As assessed by the ratio of accumulated 3,4-dihydroxyphenylalanine (DOPA) to the tissue NA level after inhibition of DOPA decarboxylase, the NA turnover rates were markedly increased (120-148% above the control) at 1 h postischemia in both the neocortex and hippocampal formation (CA1 and CA3 plus dentate gyrus). The DOPA:NA ratio went back to control levels after longer postischemic survival times. The ratio between levels of the deaminated NA metabolite, 3,4-dihydroxyphenylethyleneglycol (DOPEG), and NA, which gives another measure of NA turnover rate, showed similar changes. In the neocortex and the CA3 plus dentate gyrus, the DOPEG:NA ratio was markedly increased (89-118%) 1 h after the ischemia, but this change had disappeared at 24 and 48 h. Thus, both the DOPA accumulation experiments and the NA and DOPEG measurements indicate that following transient forebrain ischemia, there is an increased NA turnover in the hippocampus and cortex only in the early recirculation period and not after longer postischemic survival times. The degree of neuronal necrosis in the CA1 region was examined light microscopically on celestine blue-acid fuchsin-stained sections at 24, 48, and 96 h following the ischemic insult. The neuronal damage in CA1 was sparse after 24 h of recovery, had increased markedly after 48 h, and was very pronounced at 96 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Noradrenaline metabolism in neocortex and hippocampus following transient forebrain ischemia in rats: relation to development of selective neuronal necrosis. 250 51

The present study was carried out to examine the effect of potassium depletion in rat kidneys subjected to a temporary ischemic event produced by clamping of left renal artery. The postischemic kidneys of rats on a normal diet with adequate potassium intake showed an increase in H2O, Na and K excretion, with no change in inulin clearance whereas significant differences were found in potassium-deprived rats. Potassium depletion was brought about by dietary K deprivation for 10 days. K-depleted rats (serum K = 2.5 +/- 0.1 mEq/l) had a decrease in inulin clearance of the postischemic kidney from 1.01 +/- 0.10 to 0.43 +/- 0.05 ml/min (p less than 0.01), and a greater increase in fractional excretion of H2O, Na and K when compared to normal rats. The postischemic kidney from both normal and hypokalemic rats showed a decrease in Na-K-ATPase of the inner stripe of the outer medulla. These data indicate that short-term ischemia produces polyuria, increases natriuresis and kaliuresis, associated, at least in part, with a decrease in Na-K-ATPase in the inner stripe of the outer medulla (probably the thick ascending limb of Henle) and that K depletion potentiates ischemic renal failure.
Nephron 1989
PMID:Effect of potassium depletion on ischemic renal failure. 253 74

Two cases of renal segmental infarction and 1 case of renal patchy ischemia demonstrated by magnetic resonance imaging (MRI) are reported. MRI of renal infarction in two renal grafts following surgical ligation revealed an area of noncorticomedullary differentiation and an area with a low signal intensity. Renal ischemia in 1 patient with acute renal dysfunction with severe loin pain and patchy renal vasoconstriction was visualized as an ill-defined focus of low signal intensity in the renal cortex, indicating a long T1 relaxation time. Delayed wedge-shaped contrast enhancement was demonstrated on CT scan in the same area. The common finding in renal infarction and ischemia in our cases was the area of low signal intensity on MRI.
Nephron 1989
PMID:Magnetic resonance imaging in renal infarction and ischemia. 264 69

Circulatory and metabolic skin-flap events were studied prior to and up to 6 hours after elevation of buttock island flaps in pigs. During the elevation, significant reductions in superficial skin blood flow, measured by laser Doppler flowmetry (LDF) and dermal flap temperature, were seen. Significant correlations were found between blood flow and temperature. Total flap blood flow, measured as venous outflow, also showed an initial transient decrease, but 2 hours after flap construction, venous outflow had returned to preoperative values. A significant increase in lactate release, together with increased oxygen consumption and glucose uptake, was seen 4 hours after the surgical intervention. Hypoxanthine release, indicating ischemia, was seen only during the first hour after flap elevation. Noradrenaline outflow was noted after 4 and 6 hours, but there was no parallel reduction in flap blood flow. A great deal of the flow reduction in acutely elevated island flaps may thus be due to primary hypothermia rather than to the degenerative release of noradrenaline, which seems to have no early effect on skin flap blood flow. On the other hand, the noradrenaline release may be linked to an increased metabolic activity in the skin flaps.
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PMID:Early circulatory and metabolic events in island skin flaps of the pig. 266 81

Three healthy adult males developed acute renal failure following cocaine abuse. Muscle pain, tenderness, elevated levels of serum muscle enzymes, heme-positive urine and the presence of pigmented granular casts in urine all indicated occurrence of rhabdomyolysis. One of them developed acute compartmental syndrome of the left leg and required emergency fasciotomy. The course of renal failure and fast recovery were suggestive of acute tubular necrosis in all 3 patients. A possible role of cocaine in the aggravation of renal and/or muscle ischemia has been speculated.
Nephron 1989
PMID:Acute renal failure following cocaine abuse. 231 44

The aim of this study was to assess the direct effects of norepinephrine on mechanisms of arrhythmia induced by conditions of ischemia followed by reperfusion. Isolated canine Purkinje fiber-papillary muscle preparations were studied using standard microelectrode techniques. Tissues were superfused for 40 min with a solution simulating "ischemia" (i.e., hypoxic, acidotic, elevated lactate, and zero substrate) and then "reperfused" for 60 min. Ischemia produced a moderate loss of membrane potential in both tissues. Reperfusion resulted in rapid polarization of the tissues, which was accompanied by oscillatory afterpotentials and aftercontractions in 6 of 12 and 4 of 12 Purkinje fibers, respectively. This was followed by a progressive loss of membrane potential and inexcitability in Purkinje fibers. Recovery was associated with activity resembling depolarization-induced automaticity in 4 of 12 fibers. Addition of norepinephrine (0.5 microM) to the ischemic and reperfusion solutions altered primarily the reperfusion responses. Oscillatory afterpotentials and aftercontractions were larger and occurred in 8 of 8 and 6 of 8 Purkinje fibers, respectively. Norepinephrine also prevented or blunted the progressive depolarization to inexcitability in Purkinje tissues and increased automaticity occurring at low (depolarization-induced automaticity) and more polarized membrane potentials (enhanced normal pacemaker activity). This study demonstrates that norepinephrine exacerbates several potential mechanisms of arrhythmia elicited by reperfusion in canine Purkinje tissues.
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PMID:Arrhythmic effects of norepinephrine in a model of cardiac ischemia and reperfusion. 276 8


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