UMLS:C0022116 - FACTA Search

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

Following middle cerebral artery occlusion in Wistar rats, the immunoreactivity of neuropeptide Y increased ipsilaterally in the insular cortex and basolateral nucleus of the amygdala. In addition, the immunoreactivity of leucine-enkephalin, dynorphin, and neurotensin increased in the ipsilateral central nucleus of the amygdala. The amygdalar neurochemical changes are likely the result of damage to the insular cortex, although other cortical areas were also affected by the ischemia. To investigate whether damage to the insular cortex is essential in eliciting these changes, a localized lesion of the right or left insular cortex was produced by microinjection of D,L-homocysteic acid. Control animals received injections of vehicle into the right or left insular cortex or D,L-homocysteic acid into the right primary somatosensory cortex. Neurochemical changes were examined immunohistochemically with the peroxidase-antiperoxidase reaction 5 days after the injection. The immunoreactivity of neuropeptide Y increased locally after excitotoxic damage to the insular cortex or primary somatosensory cortex. The amygdalar neurochemical changes, including neuropeptide Y increase in the basolateral nucleus and leucine-enkephalin, dynorphin, and neurotensin increase in the central nucleus, were seen only when the ipsilateral insular cortex was lesioned. These neurochemical changes were similar to those seen 5 days after middle cerebral artery occlusion. Our findings indicate that damage to the insular cortex is essential in eliciting the neurochemical changes in the ipsilateral amygdala. In addition, the change in neuropeptide Y in the cortex appears to be a local reaction occurring irrespective of location of the lesion and glutamate receptor activation may be involved.
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PMID:Neuropeptide changes following excitotoxic lesion of the insular cortex in rats. 863 66

To investigate whether differences in vulnerability to free radicals might underlie differences among striatal neurons in their vulnerability to neurodegenerative processes such as occur in ischemia and Huntington's disease, we have analyzed the localization of superoxide free radical scavengers in different striatal neuron types in normal rhesus monkey. Single- and double-label immunohistochemical experiments were carried out using antibodies against the enzymes copper, zinc superoxide dismutase (SOD1), or manganese superoxide dismutase (SOD2), and against markers of various striatal cell types. Our results indicate that the striatal cholinergic and parvalbumin interneurons are enriched in SOD1 and/or SOD2, whereas striatal projection neurons and neuropeptide Y/somatostatin (NPY+/SS+) interneurons express only low levels of both SOD1 and SOD2. We also found that projection neurons of the matrix compartment express significantly higher levels of SOD than those in the striosome compartment. Since projection neurons have been reported to be more vulnerable than interneurons and striosome neurons more vulnerable than matrix neurons to neurodegenerative processes, our results are consistent with the notion that superoxide free radicals are at least partly involved in producing the differential neuron loss observed in the striatum following global brain ischemia or in Huntington's disease.
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PMID:Differential abundance of superoxide dismutase in interneurons versus projection neurons and in matrix versus striosome neurons in monkey striatum. 872 Aug 60

Infrarenal aortic cross-clamping is associated with remote vascular events, including myocardial infarction and renal insufficiency. The purpose of this study was to determine whether hindlimb ischaemia and reperfusion associated with infrarenal aortic cross-clamping results in the production of vasoactive regulatory neuropeptides. A canine model of infrarenal aortic cross-clamping was used for the study. Serial blood samples were drawn, prior to, at the time of, and serially following placement of the clamp and subsequent release of the clamp and reperfusion. Ischaemia resulted in increased mean(s.e.m.) plasma levels of neuropeptide Y (NPY) (initial 10.0(1.8) pmol/l versus ischaemia 24.7(2.3) pmol/l, P < 0.001) and vasoactive intestinal polypeptide (VIP) (initial 2.53(0.5) pmol/l versus ischaemia, 7.3(1.3) pmol/l, P < 0.05). Reperfusion produced three-fold elevation of VIP (initial 2.5(0.5) pmol/l versus reperfusion 9.6(1.5) pmol/l, P < 0.001), two-fold elevation in the plasma levels of endothelin-1 (initial 1.3(0.1) pmol/l versus reperfusion maximum 2.5(0.3) pmol/l, P < 0.01) and NPY (initial 10.0(0.8) pmol/l versus reperfusion maximum 23.9(2.3) pmol/l, P < 0.001). Ischaemia and reperfusion did not alter calcitonin gene-related peptide (CGRP) (a potent vasodilator) levels. Endothelin-1 (ET-1) plasma levels were also increased following haemorrhagic shock (initial 1.3(0.1) pmol/l versus exsanguination 3.4(0.4) pmol/l, P < 0.001), but not during ischaemia (initial 1.3(0.1) pmol/l versus ischaemia maximum 1.7(0.2) pmol/l, P = 0.7). It was concluded that vasoactive regulatory peptides are released following ischaemia, reperfusion and shock in the canine infrarenal aortic revascularization model and, therefore could contribute to remote vascular events observed with infrarenal aortic cross-clamping.
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PMID:Effects of ischaemia and reperfusion on vasoactive neuropeptide levels in the canine infrarenal aortic revascularization model. 886 83

An attempt to determine the consequences of prolonged ischemia on simultaneous regional changes in norepinephrine (NE) and neuropeptide Y (NPY) interstitial myocardial concentrations in a pig model in vivo was made. The aim of the authors was to investigate further the mechanism of the major NE release previously observed in perfused hearts preserved using a Langendorff technique. Regional myocardial ischemia was induced by ligation of the left anterior descending coronary artery (LAD) in ten anesthetized pigs. NE and NPY release was studied using interstitial microdialysis, a technique initially used to monitor neurotransmitter kinetics in brain dialysate samples. Four dialysis probes were implanted into the left ventricular wall of the beating heart. Two were implanted into the ischemic region (LAD) (for NE and NPY determinations, respectively) and the remaining two into the non-ischemic left circumflex coronary artery region (LCX). Dialysate NE and NPY concentrations, as indices of interstitial myocardial NE and NPY concentrations, were measured by HPLC and RLA, respectively. A slight but significant increase in NPY levels was observed in both territories (LAD: from 190 +/- 27 to 349 +/- 62 pmol/l, LCX: 146 +/- 30 to 257 +/- 52 pmol/l) suggesting moderate stimulation of cardiac sympathetic nerve activity following LAD occlusion. On the contrary, a marked but progressive increase in NE release was observed in the ischemic region (from 8.8 +/- 1.0 to 251.4 +/- 44.8 nmol/l), when NE levels in the non-ischemic region remained stable (from 10.3 +/- 2.1 to 11.0 +/- 1.9 nmol/l). These results demonstrate the utility of regional in-vivo myocardial NE and NPY monitoring using microdialysis. The strong and sustained NE accumulation occurring in the ischemic region is consistent with the hypothesis of a local non-exocytotic metabolic NE release in case of prolonged myocardial ischemia, when exocytotic release remain only minimal as attested by the slight increase in NPY observed.
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PMID:Consequences of coronary occlusion on changes in regional interstitial myocardial neuropeptide Y and norepinephrine concentrations. 889 58

Transient cerebral ischemia causes extensive cell death in hippocampal CA1 pyramidal cells and selective loss of interneurons in the dentate hilus. Many hippocampal interneurons can be classified by their contents of somatostatin (SS) and/or neuropeptide Y (NPY). Following ischemia in the rat, most of the NPY immunoreactivity is permanently lost in hippocampus. Furthermore, SS interneurons in the dentate hilus die, whereas CA1 interneurons survive and their expression of SS mRNA and peptide returns to preischemic levels within 16 days after ischemia. We have addressed the following questions: (1) Does the loss of NPY involve a specific downregulation in surviving CA1 interneurons that pre-ischemically expressed both SS and NPY? (2) Can the subpopulation of dying interneurons in hilus be identified from their preischemic coexpression of SS and NPY? We investigated the coexpression of SS mRNA and NPY peptide using combined in situ hybridization and immunocytochemistry. Cells containing one or both markers were counted in control sections and sections taken 2-16 days after ischemia from the hippocampal formation. In CA1, a decrease in the number of neurons containing NPY alone as well as a decrease in the number of neurons coexpressing NPY and SS was observed, whereas the number of neurons containing SS alone increased 16 days after ischemia. We conclude that neurons coexpressing SS and NPY before ischemia added to the number of neurons containing SS alone after ischemia, because NPY expression was selectively down regulated in the coexpressing population. In hilus, we demonstrated both survival and ischemic cell death of neurons expressing either SS, NPY or both, indicating that hilar interneurons dying from ischemia cannot unequivocally be identified from their preischemic colocalization of SS and NPY.
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PMID:Ischemia changes the coexpression of somatostatin and neuropeptide Y in hippocampal interneurons. 926 97

Electrical stimulation of the left stellate ganglion in guinea pig heart evoked a calcium-dependent, exocytotic release of neuropeptide Y (NPY). Stimulation after 10 min of global ischemia (S2), compared with control period stimulation (S1), had no significant effect on the NPY release. The release of NPY produced by the same stimulation after 20 min of ischemia was inhibited to certain extent (S2/S1: 0.72, P < 0.05), whereas the inhibition of NPY release disappeared after 5 min of reperfusion (with a S2/S1 of 1.01). Ischemia alone, without electric stimulation, did not apparently induce NPY release, suggesting that electrical stimulation may induce a calcium-dependent, exocytotic release of NPY. It is further suggested that the inhibition of NPY release may be produced by some metabolites and the abolishment of the inhibition after reperfusion may be due to washout of the metabolites.
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PMID:[A study on the change of myocardial neuropeptide Y release induced by electric stimulation and myocardial ischemia in guinea pig heart]. 938 74

To evaluate the relative ability of those striatal neuron types containing calbindin or parvalbumin to withstand a Ca(2+)-mediated excitotoxic insult, we injected the NMDA receptor-specific excitotoxin quinolinic acid (QA) into the striatum in mature adult rats and 2 months later examined the relative survival of striatal interneurons rich in parvalbumin and striatal projection neurons rich in calbindin. To provide standardization to the survival of striatal neuron types thought to be poor in Ca2+ buffering proteins, the survival was compared to that of somatostatin-neuropeptide Y (SS/NPY)-containing interneurons and enkephalinergic projection neurons, which are devoid of or relatively poorer in such proteins. The various neuron types were identified by immunohistochemical labeling for these type-specific markers and their relative survival was compared at each of a series of increasing distances from the injection center. In brief, we found that parvalbuminergic, calbindinergic, and enkephalinergic neurons all showed a generally comparable gradient of neuronal loss, except just outside the lesion center, where calbindin-rich neurons showed significantly enhanced survival. In contrast, striatal SS/NPY interneurons were more vulnerable to QA than any of these three other types. These observed patterns of survival following intrastriatal QA injection suggest that calbindin and parvalbumin content does not by itself determine the vulnerability of striatal neurons to QA-mediated excitotoxicity in mature adult rats. For example, parvalbuminergic striatal interneurons were not impervious to QA, while cholinergic striatal interneurons are highly resistant and SS/NPY+ striatal interneurons are highly vulnerable. Both cholinergic and SS/NPY+ interneurons are devoid of any known calcium buffering protein. Similarly, calbindin does not prevent striatal projection neuron vulnerability to QA excitotoxicity. Nonetheless, our data do suggest that calbindin may offer striatal neurons some protection against moderate excitotoxic insults, and this may explain the reportedly slightly greater vulnerability of striatal neurons that are poor in calbindin to ischemia and Huntington's disease.
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PMID:Relative resistance of striatal neurons containing calbindin or parvalbumin to quinolinic acid-mediated excitotoxicity compared to other striatal neuron types. 950 Sep 58

The levels of brain-derived neurotrophic factor (BDNF) vary between different forebrain areas and show region-specific changes after cerebral ischemia. The present study explores the possibility that the levels of endogenous BDNF determine the susceptibility to ischemic neuronal death. To block BDNF activity the authors used the TrkB-Fc fusion protein, which was infused intraventricularly in rats during 1 week before and 1 week after 5 or 30 minutes of global forebrain ischemia. Ischemic damage was quantified in the striatum and hippocampal formation after 1 week of reperfusion using immunocytochemistry and stereological procedures. After the 30-minute insult, there was a significantly lower number of surviving CA4 pyramidal neurons, neuropeptide Y-immunoreactive dentate hilar neurons, and choline acetyltransferase- and TrkA-positive, cholinergic striatal interneurons in the TrkB-Fc-infused rats as compared to controls. In contrast, the TrkB-Fc treatment did not influence survival of CA1 or CA3 pyramidal neurons or striatal projection neurons. Also, after the mild ischemic insult (5 minutes), neuronal death in the CA1 region was similar in the TrkB-Fc-treated and control groups. These results indicate that endogenous BDNF can protect certain neuronal populations against ischemic damage. It is conceivable, though, that efficient neuroprotection after brain insults is dependent not only on this factor but on the concerted action of a large number of neurotrophic molecules.
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PMID:Evidence for neuroprotective effects of endogenous brain-derived neurotrophic factor after global forebrain ischemia in rats. 1056 68

Severe perinatal asphyxia can lead to injury and dysfunction of the basal ganglia. Post insult administration of insulin-like growth factor-1 is neuroprotective, particularly in the striatum. Insulin-like growth factor-1 is also known to be a neuromodulator of several types of striatal neurons. The striatum comprises various phenotypic neurons with a complex neurochemical anatomy and physiology. In the present study, we examined the specificity of neuronal rescue with insulin-like growth factor-1 on different striatal neurons. Bilateral brain injury was induced in near term fetal sheep by 30 min of reversible carotid artery occlusion. A single dose of 3 microg of insulin-like growth factor-1 was infused over 1 h into the lateral ventricle 90 min following ischemia. The histological and immunohistochemical outcome were examined after 4 days recovery using paraffin tissue preparations. Insulin-like growth factor-1 treatment (n = 11) significantly reduced the percentage of neuronal loss in the striatum compared with the vehicle treated group (n = 10, 28.3+/-5.1% vs 55.5+/-17.3%, P < 0.005). Immunohistochemical studies showed that ischemia resulted in a significant loss of calbindin-28kd, choline acetyltransferase, parvalbumin, glutamate acid decarboxylase, neuronal nitric oxide synthase and neuropeptide Y immunopositive neurons, compared with sham controls. Insulin-like growth factor-1 markedly prevented the loss of calbindin-28kd (n = 7, P < 0.05), choline acetyltransferase (n = 7, P < 0.05), neuropeptide Y (n = 7, P < 0.05), neuronal nitric oxide synthase (n = 8, P < 0.05) and glutamate acid decarboxylase (n = 9, P < 0.05) immunopositive neurons, but failed to protect parvalbumin (n = 6) immunopositive neurons. The present study indicates that the therapeutic effect of insulin-like growth factor-1 in the basal ganglia is selectively associated with cholinergic and some phenotypic GABAergic neurons. These data suggest a potential role for insulin-like growth factor-1 in preventing cerebral palsy due to perinatal asphyxia.
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PMID:Selective neuroprotective effects with insulin-like growth factor-1 in phenotypic striatal neurons following ischemic brain injury in fetal sheep. 1067 Apr 51

An antisense oligodeoxynucleotide selective for the rat neuropeptide Y1 receptor gene was given into the left lateral ventricle in the experimental group of rats, whereas a missense oligodeoxynucleotide or saline was given in the control groups. Some rats were decapitated at 1-2h after the last injection of the oligodeoxynucleotides to examine their effects on the Y1 receptor density in the insular cortex. When compared to the Y1 and Y2 binding density of the untreated rats, the antisense-treated rats had reduced Y1 binding in the insular cortex but the Y2 binding was unaffected; treatment with missense oligodeoxynucleotide had no effect. Other rats underwent a right-sided middle cerebral artery occlusion at 1-2h after the last injection of the oligodeoxynucleotides or saline to examine the effect on the infarction volume at three days following stroke. The antisense treatment resulted in a doubling of the mean infarction volume when compared to the missense or saline treatment.Thus, reducing the Y1 receptor density prior to middle cerebral artery occlusion is harmful. Neuropeptide Y may mediate neuroprotection against focal ischemia via the cortical Y1 receptor, since the immunoreactivity for neuropeptide Y has been shown to increase within the peri-infarct cortex after middle cerebral artery occlusion.
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PMID:Neuropeptide Y-Y1 receptor antisense oligodeoxynucleotide increases the infarct volume after middle cerebral artery occlusion in rats. 1089 20

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