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

Ischemia-induced skeletal muscle injury was studied in rats subjected to tourniquet hindlimb ischemia for 3, 4, or 5 hr. The extent of injury was evaluated morphologically after 5 or 20 hr of reperfusion by a dye exclusion test using Evans blue/albumin (EBA) and a histochemical stain for calcium, Alizarin red S (ARS). In addition, the distribution of Evans blue in the postischemic muscle served as a means for detecting areas of defect reperfusion--no reflow. The combination of EBA and ARS allowed easy and reproducible quantification of induced injury in adequately reperfused areas. In areas of no reflow none of the markers used were useful. Muscle cells in these areas appeared structurally well preserved even 20 hr after release of the tourniquet and no cytoplasmic calcium accumulation could be demonstrated in muscle cells by staining with ARS. In many of these areas, however, ARS-positive structures were found between muscle cells, distributed in a pattern corresponding to the capillary network. The nature of these structures, constituting a morphological correlate to the no-reflow phenomenon, is unclear. It is concluded that for the proper evaluation of postischemic skeletal muscle injury, a suitable marker allowing estimation of the adequacy of the reperfusion must be used.
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PMID:Postischemic skeletal muscle injury: patterns of injury in relation to adequacy of reperfusion. 372 Sep 16

The development of ischemic edema and blood-brain barrier (BBB) disruption during the 1st day of experimental cerebral infarction induced by transorbital occlusion of the middle cerebral artery (MCA) in cats was evaluated by computerized tomography (CT) scanning and compared to gravimetric and pathological studies. Regional cerebral blood flow was measured using the hydrogen clearance technique or stable xenon-enhanced CT scanning. Edema was observed gravimetrically and microscopically as early as 1 hour after the onset of ischemia in the cortex and at 3 hours or later in both the cortex and white matter. However, a significant decrease of Hounsfield numbers on the CT scans was not detectable at 1 or 3 hours and was scarcely visible at 9 hours after occlusion. Disruption of the BBB was detected by leakage of Evans blue dye at 3 hours after the occlusion in two of six animals and at 9 hours in five of five animals. However, CT scanning after infusion of contrast material showed no significant increase in Hounsfield number even 24 hours after MCA occlusion. These discrepancies should be emphasized when the dynamics of ischemic edema and BBB disruption are evaluated for clinical therapy by CT scanning.
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PMID:Discrepancies among CT, histological, and blood-brain barrier findings in early cerebral ischemia. 376 Sep 62

The effect of ischemia on arterial endothelial permeability was assessed by surgically interrupting arterial blood flow for 45 min in the left carotid artery of 12 foxhounds. The right carotid artery served as control. Twenty-four hours before sacrificing the animals at 1 day, 1 week, 1 month, and 3 months postoperatively. Evans blue dye (1.5 ml/kg) was administered intravenously. Carotid arteries were harvested, opened, and scanned with a reflectometer to measure Evans blue dye uptake, and scanning electron microscopy was performed on a section of tissue from each harvested vessel. A statistically significant increase in permeability of the ischemic vessel occurred at 1 day (79 +/- 42% (SD], 1 week (186 +/- 75%), and 1 month (229 +/- 125%), but was not present at 3 months (7 +/- 8%) postinjury. Scanning electron microscopic examination of all specimens was essentially normal. This study demonstrates that arterial endothelium has increased permeability at 1 month following a brief ischemic period. What effect this ischemia-induced endothelial dysfunction will have on lipid uptake by the arterial wall will be the subject of future study.
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PMID:The effect of ischemia on canine carotid endothelial permeability. 377 1

The potential interactive effects between subarachnoid hemorrhage (SAH) and blood brain barrier (BBB) disruption were studied in a rat model. Experimental subarachnoid hemorrhage was produced in twenty rats (experimental group) by the intracisternal injection of blood. In ten additional rats (control group), saline was administered in place of blood. Analysis of mean blood pressure (MBP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP) demonstrated an increase in ICP and MBP and a drop in CPP in all animals following intracisternal injection. Subsequent infusion of the left internal carotid artery with sodium dehydrocholate resulted in blood-brain barrier (BBB) disruption in both groups as evidenced by Evans blue staining of the infused cortex. The extent of BBB disruption was significantly greater in the control group than the experimental group. Analysis of the experimental group demonstrated that animals with the lowest pre-SAH MBP and the lowest CPP during the maximum blood pressure response to SAH demonstrated the greatest resistance to experimental BBB disruption. The possibility of ischemia as a contributing factor in BBB protection subsequent to SAH is discussed.
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PMID:The protective effect of experimental subarachnoid haemorrhage on sodium dehydrocholate-induced blood-brain barrier disruption. 381 38

Arterial vasodilatation was obtained by a slow injection of nicardipine (0.1 microgram/20 min) to normotensive Long Evans rats. Reflex tachycardia was a consequence of a sympathetic activation as labetalol injected prior to nicardipine prevented the calcium antagonist-induced heart rate changes. The slope of the mean blood pressure (mmHg) - heart period (msec) curve was reproducible after a 75 min interval. This index of baroreflex sensitivity was calculated before and after a transient cerebral ischemia. Hemispheric ischemia was induced by electrocauterization of the vertebral arteries and a transient occlusion of the common carotid arteries for 10 min. Brainstem perfusion was maintained with this protocol. The second dose of nicardipine was injected 15 min after recirculation. The tachycardic response to the vasodilatation was markedly reduced after ischemia (1st slope: 0.48 +/- 0.05 msec/mmHg, 2nd slope: 0.12 +/- 0.05 msec/mmHg, n = 12, p less than 0.001, paired t test). We conclude that nicardipine injection is applicable to the study of baroreflex sensitivity in rats. The impairment of baroreflex sensitivity after a transient hemispheric ischemia could reflect a hemispheric interference with brainstem cardiovascular centres involved in the baroreceptor-heart rate reflex.
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PMID:[Adaptation to hypotension may involve the cerebral hemispheres]. 393 37

In gerbils the hemispheric blood flow was interrupted for 5 min by bilateral carotid artery occlusion to produce delayed selective destruction of the CA 1 sector of hippocampus. The influence of hemodynamic factors was studied by evaluating the microcirculation before and at two times after ischemia (3 min and 7 days), using Evans blue as an intravital vascular tracer. The density of perfused capillaries and the fractional volume of circulating blood were determined by quantitative morphometry and the values for the vulnerable CA 1 sector compared with those for the resistant CA 3 sector and cerebral cortex. In control animals the number of perfused capillaries in the CA 1 sector was about 20% lower, and the volume of circulating blood about 30% lower, than in the CA 3 sector or cerebral cortex. This difference was markedly enhanced after 5-min ischemia. During the early recirculation phase, capillary perfusion improved in the cortex, whereas in the CA 1 sector (and to a lesser degree also in the CA 3 sector) it declined. After 7 days, the density of perfused capillaries and the volume of circulating blood had returned to control levels in the cerebral cortex and CA 3 sector of hippocampus. In the CA 1 sector, in contrast, the microcirculation had further deteriorated. The density of perfused capillaries was less than 30%, and the circulating blood volume even less than 50%, of that in the cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphometric evaluation of post-ischemic capillary perfusion in selectively vulnerable areas of gerbil brain. 396 5

Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.
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PMID:Actinomycin D suppresses the protective effect of dexamethasone in rats affected by global cerebral ischemia. 400 66

Five hours of elevated intraocular pressure produced evidence of an altered blood-brain barrier at the optic nerve head in 27 of 29 monkey eyes. The change in vascular permeability was documented by fluorescein angiography (18 of 21 eyes), by Evans blue fluorescence microscopy (21 of 23 eyes), or by both methods. Leakage occurred from major blood vessels as well as from microvasculature of the nerve head. In 22 eyes, rapid axonal transport was studied after intravitreal injection of tritiated leucine. In 18 of these 22 eyes, autoradiography demonstrated a local interruption of axonal transport. In 15 eyes examined by all three methods, leakage from microvasculature (as opposed to leakage from the major vessels) was loosely associated with severe and widespread blockade of axonal transport at the lamina cribrosa. Although cause-and-effect relationships are not proved, ischemia may be responsible both for the focal endothelial damage with breakdown of the normal blood-brain barrier and for the local abnormalities of axonal transport.
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PMID:Breakdown of the normal optic nerve head blood-brain barrier following acute elevation of intraocular pressure in experimental animals. 615 39

Unilateral cerebral microembolism was performed in the rat by injecting calibrated, 50 micrometers in diameter, carbonized microspheres into the internal carotid artery. The events that follow brain ischemia due to cerebral embolization were studied by the analysis of the blood-brain barrier (BBB) function, the degree of regional cerebral blood flow (CBF) and the development of brain edema. Two hours after embolization there was no change in the brain water content. The local CBF (14C-ethanol technique) was only reduced in the ipsilateral hemisphere. Twenty-four hours after embolization the brain water content was increased significantly in the ipsilateral, but not in the contralateral hemisphere. Local CBF further decreased in the ipsilateral hemisphere and a reduction in flow was also observed in the contralateral hemisphere. Embolization led to an increase in the BBB permeability, analysed as regional penetrability of 3H-dextran and of Evans blue-albumin complexes, which was restricted to the side of the injection of the microspheres.
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PMID:Cerebral microembolization in the rat: changes in blood-brain barrier permeability and cerebral blood flow as related to the degree of ischemia. 617 52

Cerebral blood volume, hemoglobin saturation and the cytochrome a, a3 redox state were monitored simultaneously by using three wavelengths of light in the near infrared portion of the spectrum for transillumination of the intact skull of rats. The changes in these parameters following incomplete cerebral ischemia were assessed in Wistar and Long-Evans rats submitted to carotid ligation. Another group of Wistar rats was submitted to vertebral + carotid occlusion. The experiments, performed under N2O/O2 anesthesia, showed that in all three groups carotid occlusion induced a decrease in blood volume, Hb saturation and a reduction of cyt. a, a3. However, the cytochrome redox state tended to normalize during ischemia as a consequence of higher O2 extraction from blood. The primary finding of this study was the marked hyperoxidation of cyt. a, a3 which occurred after reestablishing of the carotid blood supply, in spite of a secondary post-ischemic hypoperfusion of the brain. Although uncoupling of oxidative phosphorylation cannot be excluded the dissociation between blood supply and metabolism could well be due to ischemia-induced hypermetabolism of the central nervous tissue. In view of the marked oxidation of cyt. a, a3 during the reperfusion period as compared with the small extent of its reduction during the ischemic episode, the data also support the hypothesis that under steady state conditions in vivo, cytochrome oxidase is mainly reduced.
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PMID:Incomplete cerebral ischemia in the rat: vascular and metabolic changes as measured by infrared transillumination in vivo. 631 78


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