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

The case of a neonate who presented with symptoms of upper limb ischemia related to spontaneous multiple arterial and venous thromboses that were demonstrated by colour Doppler sonography and digital subtracted angiography is reported. The presentation of limb ischaemia at birth may be the warning sign of simultaneous cerebral infarction.
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PMID:Imaging of neonatal arterial thrombosis. 175 Jul 68

This experiment evaluated the potential for ketamine HCl, a non-competitive glutamate antagonist, to minimize injury resulting from temporary focal cerebral ischemia. Male spontaneously hypertensive rats were randomly assigned to receive either ketamine (n = 13) or halothane anesthesia (n = 12) during 2 h of reversible middle cerebral artery occlusion (MCAO). Ketamine was administered as a 50 mg/kg i.v. loading dose followed by a continuous 1.25 mg/kg/min i.v. infusion beginning 25 min prior to ischemia and continued until 30 min after reperfusion. An additional group of rats (ketamine-shams, n = 8) underwent craniectomy and ketamine administration (as above) but the middle cerebral artery was not ligated. Physiologic values were similar between groups with the exception of plasma glucose which was elevated in the halothane-MCAO group. After 4 days recovery, rats in all groups were neurologically evaluated. There were no differences between the two groups undergoing MCAO for neurologic grading or open field behavior, although both groups performed worse than did ketamine-shams (P less than 0.05). In contrast, motor performance revealed more severe deficits in the ketamine-MCAO rats vs either the halothane-MCAO or ketamine-sham groups (P less than 0.05). Cerebral infarct volume was then planimetrically measured after triphenyl tetrazolium chloride (TTC) staining of fresh brain sections. Mean +/- S.D. infarct volume was not different between the halothane-MCAO (134 +/- 51 mm3) and ketamine-MCAO (131 +/- 64 mm3) groups. Seven of 8 sham rats were free of TTC demarcated injury and in the remaining rat injury was minimal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of ketamine on outcome from temporary middle cerebral artery occlusion in the spontaneously hypertensive rat. 177 49

Effects of calcium antagonists, Nicardipine and Nilvadipine, on neurologic deficits and size of infarct were studied in the rat middle cerebral artery (MCA) occlusion model. Each drug was administered immediately after induction of ischemia, and neurologic grade was evaluated 1 to 24 hours after MCA occlusion. At 24 hours post-occlusion, size of the infarct was compared with that of the control group. In addition, evolution of cerebral infarction was studied at 6 hours and 12 hours post-occlusion by magnetic resonance imaging (MRI). In the Nilvadipine-treated group, neurologic deficits improved more rapidly and the size of infarct was significantly smaller than in the Nicardipine-treated group. MRI showed a progressive extension of cortical infarct in the untreated rat, whereas the infarct size remained unchanged in the Nilvadipine-treated rat. These results suggest the potential therapeutic usefulness of calcium antagonist for acute cerebral ischemia.
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PMID:[Ca++ antagonist and acute brain ischemia: effects of nilvadipine and nicardipine on middle cerebral artery occlusion in rats]. 181 38

Glucocorticoid therapy is frequently used in perinatology and neonatology for its beneficial pulmonary effects. We investigated the influence of neonatal glucocorticoid administration on brain damage caused by a concurrent episode of cerebral hypoxia-ischemia. Various doses of dexamethasone in several treatment schedules were administered to 7-d-old rats that were also subjected to unilateral cerebral hypoxia-ischemia. In 79% of control rats, a large unilateral cerebral infarction occurred, whereas all rats pretreated with dexamethasone in doses of 0.01 to 0.5 mg/kg/d for 3 d had no infarction (p less than 0.001). The neuroprotective effect of dexamethasone pretreatment was dose- and time-dependent. Treatment with dexamethasone after the insult or with lower doses before the insult did not prevent infarction. The neuroprotective effect was not immediate: single doses 0 to 3 h prehypoxia were not effective but a single dose 24 h before hypoxia-ischemia prevented cerebral infarction. The results demonstrate that glucocorticoid administration in the neonatal period, even in low doses, protects the brain during subsequent periods of hypoxia-ischemia.
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PMID:Dexamethasone prevents hypoxic-ischemic brain damage in the neonatal rat. 186 11

We investigated the temporal threshold for focal cerebral infarction in the spontaneously hypertensive rat. The right middle cerebral artery and common carotid artery were occluded for 0, 1, 2, 3, 4, or 24 hours, and all the animals were sacrificed 24 hours after the onset of ischemia. Cortical infarct volumes and edema volumes were quantified in serial frozen sections of hematoxylin and eosin-stained tissue using image analysis. Upon occlusion, blood flow in the core of the ischemic zone, measured with laser-Doppler flowmetry, fell to a mean +/- standard deviation of 21 +/- 7% of the preocclusion baseline value (n = 26). During the first hour of ischemia, blood flow in the densely ischemic zone rose to 27 +/- 8% of baseline (n = 25). Release of the middle cerebral artery and common carotid artery occlusions rapidly restored cortical blood flow to 213 +/- 83% of baseline (n = 21). Focal ischemia of 1 hour's duration caused little or no infarction, while ischemic intervals of 2 and 3 hours produced successively larger volumes of infarcted cortex. Ischemic intervals of 3-4 hours' duration followed by approximately 20 hours of recirculation yielded infarct volumes that were not significantly different from those after 24 hours of permanent focal ischemia. The results indicate that 3-4 hours of focal cerebral ischemia in this rat model is sufficient to attain maximal infarction and suggest that recirculation or pharmacological interventions after this time will provide little benefit.
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PMID:Temporal thresholds for neocortical infarction in rats subjected to reversible focal cerebral ischemia. 186 50

Lateral medullary syndrome is known to cause hemiparesis ipsilateral to the medullary lesion. However, it's clinical significance has not been fully evaluated. In this study, we made clinical and angiographic studies in patients with syndrome to elucidate the pathogenesis of ipsilateral hemiparesis. Thirty-four patients with cerebral infarction presenting with this syndrome were studied. Their mean age was 51 years and all the patients were examined within 6 months of their first attack. Diagnosis of ipsilateral hemiparesis was made if subjective feeling of weakness in the upper and lower extremities was associated with increased deep tendon reflexes. Ipsilateral hemiparesis was observed in 38% of all the patients. Cerebral angiography was performed in 26 patients and divided into two groups; group A with ipsilateral hemiparesis (n = 9) and group B without ipsilateral hemiparesis (n = 7). In 56% of patients in group A, angiography showed non-visualization of ipsilateral vertebral artery (VA) and posterior inferior cerebellar artery (PICA). Non-visualization of these two arteries never occurred in the patients of group B. On the other hand, non-visualization of VA alone was observed in 35% of the patients in group B, but it was none in the patients of group A. However, there were no differences in concerning the frequency of non-visualization of PICA alone or non-occlusion at all between both groups. Therefore, the focal ischemia in the region below the pyramidal decussation due to the occlusion of both VA and PICA, regardless of thrombotic or embolic episode, was considered to be responsible for ipsilateral hemiparesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pathogenesis of ipsilateral hemiparesis in patients with lateral medullary syndrome]. 191 24

We examined the relationships between intracellular pH (pHi) and interstitial pH (pHe) in a rat model of focal ischemia. Interstitial pH was measured with pH-sensitive microelectrodes, and the average tissue pH was measured with the [14C]dimethadione method in rats subjected to occlusion of the right middle cerebral and common carotid arteries (MCA-CCAO). In normal cortex, pHe and pHi were 7.24 +/- 0.97 and 7.01 +/- 0.13 (means +/- SD, n = 6), respectively. In the ischemic cortex, pHe fell to 6.43 +/- 0.13, whereas pHi decreased only to 6.86 +/- 0.11 (n = 5) 1 h after MCA-CCAO. After 4 h of ischemia, the pHe was 6.61 +/- 0.09 and pHi was 6.62 +/- 0.20 (n = 4). Treatment with glucose before ischemia markedly lowered the pHe (5.88 +/- 0.17) but not pHi (6.83 +/- 0.03, n = 4) measured 1 h after ischemia. In the ischemic cortex of animals made hypoglycemic by pretreatment with insulin, neither pHe (7.25 +/- 0.06) nor pHi (6.99 +/- 0.13, n = 4) decreased. The demonstrated difference in pHi and pHe indicates that some cells remained sufficiently functional to maintain a plasma membrane gradient of protons within the evolving infarct. If the calculated pHi values accurately reflect the true pHi of cells within zones of severe focal ischemia, then cerebral infarction can proceed at pHi levels not greatly altered from normal.
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PMID:Dynamics of interstitial and intracellular pH in evolving brain infarct. 200 Oct 8

Ischemic cerebral infarction is caused primarily by occlusion of a large arterial vessel. Local circulatory disturbances in the center of ischemic tissue and in ischemic penumbra and the degree of sensitivity to ischemia in different brain regions influence subsequent ischemic progression. Postischemic recirculation is impaired by hemodynamic disturbances and formation of microthrombi, hemorrheologic changes and degeneratively altered vessels of microcirculation. Increased postischemic coagulation can be demonstrated in laboratory tests of few minutes extending up to two weeks after the onset of ischemia. Morphological observations on microthrombi after experimental focal ischemia as well as in patients with cerebral infarction show that formation of microthrombi is dependent on the duration of ischemia and the extent of infarcted tissue. Microthrombi are most prevalent in early stages of tissue damage. This suggests that microthrombi have an effect on the progression of ischemic necrosis. On the basis of our results, we can state that 1) microcirculatory disturbances are triggered by focal cerebral ischemia, 2) formation of microthrombi is a contributing factor to the evolution of postischemic microcirculatory disturbances, and 3) microthrombi promote the progression of ischemic necrosis.
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PMID:The role of microthrombi and microcirculatory factors in localization and evolution of focal cerebral ischemia. 203 Aug 32

In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain, which, depending on a multitude of factors, can result in cerebral infarction. It is highly likely that the erythrocyte is the most important blood element in the pathophysiology of this process. The exact mechanism by which the blood vessel is forced into this destructive spasm remains to be elucidated. Significant steps have been taken to avoid the consequences of vasospasm by using hypertension and hypervolemia (or at the very least avoiding iatrogenic hypotension and hypovolemia). These measures have resulted in a reduced incidence of delayed ischemia. Because clot has been shown to cause vasospasm, it has seemed only logical that the early removal of clot would be efficacious in its prophylaxis. Experimental and clinical evidence to support this view has been gathered. Therapeutic measures based on it have been shown to be effective in the experimental situation but await controlled clinical evaluation. In the past decade, thanks to such trials, one of the calcium antagonist drugs has been shown to be effective in improving the outcome following subarachnoid hemorrhage, probably on the basis of reducing the frequency and extent of infarction by small vessel dilatation or neuronal protection. Although patients still die from this lethal complication of subarachnoid hemorrhage, it is difficult not to have some measure of optimism, based on the history just reviewed, that cerebral vasospasm will be a treatable disease within a few decades.
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PMID:The history of cerebral vasospasm. 213 40

This experiment was designed to determine if nitrous oxide alters neurologic and pathologic outcome from temporary focal cerebral ischemia in spontaneously hypertensive rats deeply anesthetized with a barbiturate. Two groups of rats were given intravenous methohexital such that a stable EEG pattern of burst suppression was achieved. In one group of rats (n = 11), the lungs were mechanically ventilated with 70% N2O/30% O2, and in the other group (n = 10), ventilation was done with 70% nitrogen/30% O2. The middle cerebral artery was then occluded for 2 h, during which time mean arterial pressure, blood gases, hematocrit, plasma glucose, and head temperature were held constant between groups. The total doses of methohexital administered were similar in both groups as were the plasma methohexital concentrations immediately prior to onset of ischemia. After reperfusion of the middle cerebral artery, the animals were allowed to awaken. Neurologic evaluations were performed prior to ischemia and at 24 and 96 h postischemia. Cerebral infarct volume was measured at 96 h postischemia using triphenyl tetrazolium chloride staining and computer imaging techniques. There were no neurologic differences between the N2O and nitrogen groups at any experimental interval although both groups exhibited deficits at both 24 and 96 h postischemia relative to preischemic values. The two groups also had nearly identical cerebral infarct volumes (N2O = 231 +/- 97 mm3; nitrogen = 226 +/- 75 mm3; mean +/- SD).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitrous oxide does not alter infarct volume in rats undergoing reversible middle cerebral artery occlusion. 222 37


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