Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transient ischemia of the extremities was applied in compression or traumatic neuropathies affecting radial nerve (17 cases), ulnar nerve (3 cases), upper brachial plexus (4 cases) or peroneal nerve (10 cases). The limb opposite to that displaying paresis was submitted repeatedly to a 15-minute-period of ischemia every other day for two weeks. The procedure induced in most patients (27 out of 34 cases) a motor improvement of variable degree. In some patients (13 cases) the motor recovery occurred two days or more after starting the procedures, while in others (14 cases) during the very day in which the initial session of ischemia was made or even during the first hour of procedure application. The most beneficial effects of peripheral ischemia were noted in compression neuropathy of peroneal nerve palsy, 9 out of 10 patients with such a disorder being improved by the procedure. We suppose that the method of therapy proposed by us restores promptly the motility of patients with compression neuropathy by inducing a long-lasting activation of some central neural mechanisms.
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PMID:Transient peripheral ischemia may restore quickly the motility in patients with compression neuropathy. 801 78

The effect of dynorphin A-(1-13), an endogenous kappa-opioid receptor agonist, on memory dysfunctions induced by transient cerebral ischemia in mice was investigated by using three different tasks, namely, spontaneous alternation, elevated plus-maze performance, and passive avoidance behavior. Transient ischemia produced a marked memory dysfunction in mice, as assessed in the three tasks, which were carried out consecutively 1 to 3 days after the ischemic insult. The i.c.v. injection of dynorphin A-(1-13) before the ischemic insult potently prevented the impairment of spontaneous alternations, the prolongation of transfer latency in the elevated plus-maze and the shortening of step-through latency in the passive avoidance task induced by transient ischemia. Dynorphin A-(1-13) (10 micrograms), however, did not affect the body temperature of the sham-operated or the ischemic mice. The protective effect of dynorphin A-(1-13) (10 micrograms) on ischemia-induced memory dysfunctions observed in the three tasks was almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms, i.c.v.), a kappa-selective opioid receptor antagonist. These results suggest that dynorphin A-(1-13) prevents memory dysfunctions in ischemic mice through the activation of kappa-opioid receptors.
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PMID:Dynorphin A-(1-13) potently prevents memory dysfunctions induced by transient cerebral ischemia in mice. 809 64

We studied the postischemic alteration of muscarinic acetylcholine binding sites in the rat brain using in vitro [3H]quinuclidinyl benzilate (QNB) autoradiography. Transient ischemia was induced by the occlusion of the middle cerebral artery (MCA) for 90 min and such occlusion followed by various recirculation periods of up to 4 weeks. After 90 min of ischemia followed by 3 days of recirculation, [3H]QNB binding sites were found to be significantly decreased in the cerebral cortex (P < 0.01) and lateral segment of the caudate putamen (P < 0.05), both supplied by the occluded MCA; thereafter, the binding sites decreased progressively in those ischemic foci. Moreover, 3 days after the ischemia, significant decreases of [3H]QNB binding sites were observed in the ipsilateral thalamus and the amygdala, and also in the substantia nigra 1 week after the ischemia, areas which had not been directly affected by the original ischemic insult. This postischemic phenomenon observed in the thalamus and the substantia nigra developed concurrently with 45Ca accumulation, which was detected there in our previous study. These results indicate that alteration of muscarinic acetylcholine binding sites may be involved not only in the ischemic foci, but also in the exo-focal remote areas, in which delayed neuronal degeneration due to neuronal network disturbances after the ischemia was observed. We suggest that multifocal postischemic alterations of muscarinic acetylcholine binding sites may exacerbate the clinical symptoms of patients during the chronic stage of stroke.
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PMID:Alteration of muscarinic acetylcholine binding sites in the postischemic brain areas of the rat using in vitro autoradiography. 813 8

Transient ischemia-induced perturbations in calcium homeostasis have been proposed to lead to pathological activation of the cysteine protease calpain I and subsequent delayed neuronal death in the CA1 region of hippocampus. We report here on the design and characterization of antibodies selective for calpain-generated fragments of brain spectrin, and their use for immunoblot and immunohistochemical analyses of calpain activation following cerebral ischemia in the gerbil. Although spectrin was susceptible to degradation in vitro by many mammalian proteases, only calpain degraded spectrin to generate fragments immunoreactive with the antibodies. Following 5 min of global ischemia, immunoreactivity for calpain-degraded spectrin was rapidly (within 30 min) and markedly elevated in the perikarya and dendrites of several populations of forebrain neurons. The rapid calpain activation was completely prevented by the NMDA receptor antagonist MK-801. At later times postischemia, but prior to frank neuronal necrosis, calpain-degraded spectrin was restricted to hippocampal area CA1 pyramidal neurons. Silver impregnation histochemistry confirmed that neuronal damage was confined to area CA1. The results indicate that while nonpathological NMDA receptor stimulation can activate calpain, only those neurons showing sustained calpain activation are destined to die.
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PMID:Immunolocalization of calpain I-mediated spectrin degradation to vulnerable neurons in the ischemic gerbil brain. 820 97

To assess whether myocardial stunning occurs following brief episodes of effort ischemia, ventricular function was assessed by radionuclide angiography in 29 patients with coronary artery disease. No patient had evidence of previous myocardial infarction. Patients were divided into two groups according to presence of single (14 patients, Group 1) or multi-vessel (15 patients, Group 2) coronary artery disease. Equilibrium radionuclide angiocardiography was performed in the left anterior oblique projection by a small field-of-view gamma-camera. Acquisition were performed at baseline, at peak exercise, then again at 1 and 5 minutes of the recovery phase. For each acquisition, ejection fraction, peak filling rate and wall motion index were measured and compared. No difference in baseline and stress measurements was found between Group 1 and Group 2, except for the wall motion index that was more impaired during ischemia in patients of Group 2. Global and regional indexes of ventricular function did not show significant differences also in the two recovery periods when compared to the relative baseline values. Transient ischemia caused by an increase of oxygen demand did not reproduce the phenomenon of systolic and diastolic stunning observed in animal experiments, although in all patients the ischemia was of sufficient duration and severity to induce transient ventricular dysfunction.
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PMID:Ischemia on effort is not a determinant of stunned myocardium in man: a radioisotopic study based on quantitative evaluation of ventricular dynamics. 821 58

Receptor autoradiographic and histological techniques were used to investigate sequential alteration of naloxone receptors in the gerbil brain 1 h-7 days after transient cerebral ischemia. Transient ischemia was induced for 10 min. [3H]Naloxone binding showed a transient elevation in the striatum 1 h after ischemia, whereas the hippocampus revealed no significant alteration in the binding. Thereafter, no conspicuous alteration in [3H]naloxone binding was seen in the striatum and hippocampus up to 24 h after ischemia. However, a significant elevation in [3H]naloxone binding was found in the hippocampal region 48 h after ischemia. In contrast, the striatum showed no significant alteration in [3H]naloxone binding. Seven days after ischemia, a severe reduction in [3H]naloxone binding was seen not only in the dorsolateral striatum and hippocampal CA3 pyramidal cell layer, where irreversible neuronal damage was found, but also in the histopathological intact dentate gyrus. However, the hippocampal CA1 sector which was most vulnerable to ischemia, revealed no conspicuous alteration in [3H]naloxone binding. These results demonstrate that alteration of naloxone receptors precedes ischemic neuronal damage to the striatum and hippocampus. They also suggest that the damage between striatum and hippocampus may be produced with different processes.
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PMID:Naloxone receptor binding in gerbil striatum and hippocampus following transient cerebral ischemia. 822 Jan 73

We investigated the long-term changes that occur in the gerbil brain following transient cerebral ischemia using histology and receptor autoradiography. Transient ischemia was induced for 3 and 10 min, and animals were allowed to survive for 8 months. A histological study showed that 3-min ischemia caused neuronal damage and mild atrophy only in the hippocampal CA1 sector, and that 10-min ischemia produced severe neuronal damage and marked shrinkage in the hippocampal CA1 and CA3 sectors. Furthermore, severe neuronal damage was seen in the striatum after 10-min ischemia. Autoradiography study revealed that 3-min ischemia caused a significant reduction in [3H] naloxone binding in the frontal cortex, striatum, dentate gyrus, and thalamus, whereas [3H]SCH 23390 and [3H] forskolin binding was not significantly altered in all regions. In contrast, 10-min ischemia produced marked alteration in these binding sites in the striatum, hippocampus, thalamus, and substantia nigra. The alteration was especially notable in the hippocampal region and substantia nigra. These results indicate that hippocampal damage after transient ischemia, compared with that in other regions, is not static, but particularly progressive. Furthermore, they demonstrate a reduction in adenylate cyclase system in the striatum and substantia nigra after transient ischemia. Moreover, our results suggest that long-term survival after ischemia may induce synaptic modification of neurotransmitter and adenylate cyclase system in the hippocampus.
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PMID:Long-term observations in gerbil brain following transient cerebral ischemia: autoradiographic and histological study. 827 28

Chronological changes of protein kinase C (PKC) activity were measured using in vitro [3H]phorbol 12,13-dibutyrate (PDBu) autoradiography to investigate the postischemic alteration of this second messenger system in the rat brain. Transient ischemia was induced by the occlusion of the middle cerebral artery (MCA) for 90 min and such occlusion followed by various recirculation periods of up to 4 weeks. After 90 min of ischemia followed by 3 hours of recirculation, [3H]PDBu binding sites were found to be significantly decreased in the cerebral cortex and lateral segment of the caudate putamen, both supplied by the occluded MCA; thereafter, the binding sites decreased progressively in those ischemic foci. On the contrary, there was no alteration on day 1, but 3 days after ischemic insult, a significant decrease of [3H]PDBu binding sites was first detected in the ipsilateral thalamus and the substantia nigra, which both areas had not been directly affected by the original ischemic insult. This postischemic delayed phenomenon observed in the thalamus and the substantia nigra developed concurrently with 45Ca accumulation, which was detected there in our previous study. These results suggest that alteration of second messenger (PKC) pathways may be involved not only in the ischemic foci, but also in neuronal degeneration of the exo-focal remote areas in relation to the disruption of intracellular calcium homeostasis which plays a key role in the pathogenesis of postischemic neuronal damage and that marked alteration of intracellular signal transduction may precede the neuronal damage in the exo-focal postischemic brain areas.
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PMID:Alteration of protein kinase C activity in the postischemic rat brain areas using in vitro [3H]phorbol 12,13-dibutyrate autoradiography. 836 4

Receptor autoradiographic and histological techniques were used to investigate the long-term changes that occur in the gerbil brain following the induction of transient cerebral ischemia. Transient ischemia was induced for 3 and 10 min, and animals were allowed to survive for eight months. Autoradiographic analysis of second messenger systems showed that 3-min ischemia caused a significant reduction in [3H]inositol-1,4,5-trisphosphate binding in the hippocampal CA1 sector, whereas the alteration in [3H]phorbol 12,13-dibutyrate, [3H]forskolin and [3H] cyclic-AMP bindings was not found in this region. In the striatum, 3-min ischemia caused no significant alteration in [3H]phorbol 12,13-dibutyrate, [3H]inositol-1,4,5-trisphosphate and [3H]forskolin binding sites, whereas the [3H]cyclic-AMP binding showed a significant elevation. The thalamus exhibited a significant elevation only in the [3H]inositol-1,4,5-trisphosphate binding sites. Following 10-min ischemia, [3H]phorbol 12,13-dibutyrate, [3H]inositol-1,4,5-trisphosphate and [3H]cyclic-AMP binding sites revealed a significant reduction in the hippocampus, whereas the [3H]forskolin binding showed a significant elevation in this area. In the striatum, 10-min ischemia caused no significant alteration in [3H]phorbol 12,13-dibutyrate, [3H]inositol-1,4,5-trisphosphate and [3H]cyclic-AMP binding sites. However, marked reduction in the [3H]forskolin binding was seen in the striatum. Furthermore, the substantia nigra also exhibited a significant reduction in [3H]forskolin binding. Histological studies suggested that 3-min ischemia can produce severe neuronal damage and mild shrinkage to the hippocampal CA1 sector. They also showed that 10-min ischemia can cause severe tissue shrinkage and severe neuronal damage in the hippocampal CA1 sector and hippocampal CA3 sector. Thus, the hippocampal damage following ischemia was not static but progressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postischemic changes of intracellular second messengers in the gerbil brain after long-term survival: an autoradiographic study. 838 52

Transient ischemia produced marked memory dysfunctions in mice on three different tasks, spontaneous alternation, elevated plus-maze and passive avoidance, as tested 1, 1-2, and 2-3 days after ischemic insult, respectively. U-50,488H, a kappa-opioid receptor agonist, administered 20 min before ischemic insult markedly prevented the impairment of spontaneous alternation, the prolongation of transfer latency in elevated-plus maze and the shortening of step-through latency in passive avoidance induced by transient ischemia. The protective effect of U-50,488H (30 mg/kg) on ischemia-induced memory dysfunctions observed in the three tasks was almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms, i.c.v.), a kappa-selective opioid antagonist. Although U-50,488H (30 mg/kg) did not affect body temperature in sham mice, it blocked hypothermia induced by ischemic insult. These results suggest that the protective effect of U-50,488H on memory dysfunctions in ischemic mice is associated with the activation of kappa-opioid receptors and is not based upon hypothermia.
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PMID:U-50,488H, a kappa-opioid receptor agonist, markedly prevents memory dysfunctions induced by transient cerebral ischemia in mice. 839 52


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