diaphorase/infarction

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[Histochemical studies on succinic and malic acid dehydrogenases and DPN and TPN diaphorases in experimental myocardial infarction].

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Coronary artery ligation in anesthetized rats as a method for the production of experimental dysrhythmias and for the determination of infarct size.

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Coronary artery ligation in anesthetized rats was assessed as a method for the production of experimental dysrhythmias and for the determination of infarct size. Following occlusion of the left main coronary artery, very marked ventricular dysrhythmias occurred in two distinct phases, an early and a

Altered number of diaphorase (NOS) positive neurons in the hypothalamus of rats with heart failure.

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Recently, we have demonstrated a decreased neuronal isoform of nitric oxide synthase (nNOS) message in the hypothalamus of rats with heart failure (HF). The purpose of this study was to determine the changes in NADPH-diaphorase (a commonly used marker for neuronal NOS activity) positive neurons in

Induction of NADPH-diaphorase activity in the rat forebrain after middle cerebral artery occlusion.

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Induction of NADPH-diaphorase (NDP) following ischemic infarction was studied by means of histochemistry in the rat cerebral cortex 1,2,7, and 14 days after distal occlusion of the right middle cerebral artery (MCA). The fine structure of cells in the penumbra region of the necrotic center was also

[Morphologo-histochemical characteristics of ischemic cerebral infarcts in the acute stage of the stroke in patients with atherosclerosis].

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Morphological and histochemical investigations of the activity of succinate, malate, lactate, isocitrate, and glucoso-6-phosphate dehydrogenases, and NAD-diaphorase in the central, marginal, borderline and perifocal zones of ischemic brain infarctions were carried out. Deep changes in the activity

Macroscopic enzyme histochemistry in myocardial infarction: artefactual nature of the creatine phosphokinase reaction.

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The histochemical creatine phosphokinase (CPK) tetrazolium test has been evaluated to detect recent human myocardial infarction in gross slices of the heart at necropsy. The demonstration of the lesion with this method has been assumed to result from local loss of CPK from the damaged myocardium.

The effects of TRH analogues on cerebral ischaemia produced by middle cerebral artery occlusion in the rat.

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This study examined the effects of two stabilised analogues of TRH, RX 77368 and CG 3509, in a rat cerebral ischaemia model produced by unilateral occlusion of the middle cerebral artery. The analogues were given intraventricularly after artery occlusion. The extent of the cortical ischaemia was

Induction of protein inhibitor of neuronal nitric oxide synthase/cytoplasmic dynein light chain following cerebral ischemia.

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Administration of inhibitors of neuronal nitric oxide synthase or deletion of the encoding gene in rodents provided evidence that neuronal nitric oxide synthase activity may contribute to neuronal cell death following global and focal cerebral ischemia. In the present study, we investigated by in

Permanent occlusion of the middle cerebral artery upregulates expression of cytokines and neuronal nitric oxide synthase in the spinal cord and urinary bladder in the adult rat.

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The expression pattern of proinflammatory cytokines, neuronal nitric oxide synthase (nNOS), substance P (SP) and calcitonin gene related peptide (CGRP) in the spinal cord and the bladder in response to permanent middle cerebral artery occlusion (MCAO) was investigated. In this connection, the gene

Marked induction of calcium-independent nitric oxide synthase activity after focal cerebral ischemia.

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We studied the effect of focal cerebral ischemia on inducible (iNOS) and constitutive (cNOS) nitric oxide synthase enzymatic activities in the affected brain. The middle cerebral artery (MCA) was occluded in spontaneously hypertensive rats. Animals were killed 1, 2, 4, and 7 days later. cNOS and

Assessment of induction of biliverdin reductase in a mouse model of middle cerebral artery occlusion.

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Reproducible animal models of stroke are indispensable for investigation of pathogenesis and treatment of ischemic brain injury. Defined location and size of infarction as well as consistent production of neurological deficits make it possible to evaluate therapeutic potential of neuroprotective

Upregulation of neuronal nitric oxide synthase and mRNA, and selective sparing of nitric oxide synthase-containing neurons after focal cerebral ischemia in rat.

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Nitric oxide synthase-containing neurons are presumed to be resistant to neurodegeneration and neurotoxicity, however this resistance has not been demonstrated after focal cerebral ischemia. We therefore measured the temporal profile of neuronal nitric oxide synthase (NOS-I) mRNA and

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