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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
Stroke
PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

The high incidence of stroke has been considered and the importance of measuring cerebral blood flow (CBF) in patients with transient ischemic attacks has been emphasized. A brief description has been given of the non-invasive method of measuring CBF using a brief bolus injection of 133xenon into any convenient arm vein. The values of CBFg = 75 +/- 8 and CBFw = 24 +/- 2 in ml per 100 g per M compared closely to those obtained by the internal carotid method of measurement. Cerebral blood flow in the gray matter, CBFg is the more sensitive measurement and is used almost exclusively to evaluate patients undergoing microneurosurgical anastomosis for cerebral ischemia in an attempt to prevent or modify stroke. The post operative studies in patients who had a pre operative depression of CBFg greater than 2 S.D. showed improvement in both the frontal and parietal regions. The latter was more significant with p less than 0.04 using paired t-tests.
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PMID:Cerebral blood flow in patients undergoing microanastomosis for modification for prevention of stroke. 116 89

Unilateral ligation of a common carotid artery in gerbils causes a major depletion of brain dopamine, which is most marked in brain regions known to receive dopaminergic projections. To determine whether this depletion reflects release of stored dopamine, a radioactive label (H-3-dopamine) was introduced into brain dopamine pools 4 hours prior to ligation. Twenty-four hours later, brain H-3-catecholamines were profoundly depressed ipsilateral to the lesion among animals exhibiting clinical signs of stroke. Within brain regions known to receive dopaminergic projections, common carotid ligation also was associated with a selective decrease in the concentration of H-3-deaminated metabolites. These data suggest that cerebral ischemia is associated with release of catecholamines, as well as with impaired oxidative metabolism of catecholamines.
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PMID:Brain H-3-catecholamine metabolism in experimental cerebral ischemia. 116 7

Male and female, arteriosclerotic (breeder) and nonarteriosclerotic (virgin), Sprague-Dawley rats were made severely diabetic with alloxan. Two weeks later experimental animals had both carotid arteries ligated to induce a state of acute cerebral ischemia. After six weeks of cerebral ischemia either with or without severe diabetes the animals were killed. Animals which survived either the acute induction of diabetes or cerebral ischemia did not manifest any new episodes of cerebral ischemia. Subjects with combined diabetes and cerebral ischemia manifested the greatest loss in body weight, adrenal hypertrophy and thymus gland involution, increased levels of serum CPK and SGOT, but decreased SGPT and LDH, hyperglycemia and hypertriglyceridemia, and the most extensive cerebral edema. It is suggested that diabetic rats may have a greater predilection toward cerebrovascular accidents because the diabetic state contributes not only to an exacerbation of atherosclerosis, but also complicates any condition of cerebrovascular ischemia by creating extracerebral edema.
Stroke
PMID:Chronic diabetes followed by chronic cerebral ischemia induced by bilateral carotid artery ligation in arteriosclerotic versus nonarteriosclerotic rats. 117 43

Amaurosis fugax (transient monocular blindness) is a symptom of retinal ischemia just as contralateral hemiparesis and sensory loss are symptoms of cerebral ischemia. These symptoms are produced by atherosclerotic stenosis of the carotid vessels at the ipsilateral carotid bifurcation and emboli from these areas causing focal, repetitive, retinal ischemia. A study of 31 endarterectomy patients was undertaken to see if eight patients with amaurosis fugax (25%) could be differentiated from 22 patients with transient cerebral ischemia. The patients with amaurosis fugax were found to be younger. They all had 75% or greater stenosis of the internal carotid artery at the bifurcation on the symptomatic side. They all had unilateral visual symptoms and these symptoms were relieved by surgery. The patients with amaurosis fugax were devoid of cardiac disease, while 45% of the cerebral ischemic patients had documented myocardial disease. Amaurosis fugax (transient monocular blindness) in the setting of clinically significant atheroslerosis of the carotid vessels is an indication for carotid endarterectomy.
Stroke
PMID:Amaurosis fugax: a clinical comparison. 117 55

Adenosine diphosphate (8 mg per minute for five minutes) was infused into the carotid artery of 63 rabbits. The effects were twofold: systemic hypotension and platelet aggregation in the cerebral circulation. As a consequence of the last effect, platelet emboli were produced which occluded cerebral arteries in a number and size sufficient to cause cerebral ischemia. Areas of focal ischemia were observed through a cranial window, and documented with antipyrine autoradiography. Platelet thrombi were almost entirely transient, being fragmented and removed within a very short time of cessation of ADP infusion. Consequently, no permanent tissue damage ensued. This experimental model approaches the spontaneous transient ischemia attacks (TIAs) in man, demonstrating that these can be caused by pure platelet emboli. A high cholesterol diet administered for two months prior to ADP infusion did not enhance the effect of the procedure or make the platelet aggregation and the following ischemia longer in duration or more severe.
Stroke
PMID:Animal model of TIA: an experimental study with intracarotid ADP infusion in rabbits. 119 26

The permissible duration of brain ischemia without sustaining damage is short. Less clear are the mechanisms accounting for the vulnerability of brain to ischemic insults. Neurochemical factors implicated include impairment of energy synthesis by mitochondria and of energy-dependent processes such as synaptic transmission, ATPase activity, membrane conductance and altered protein and lipid synthesis. To clarify the vulnerability of energy metabolism, we investigated energy availability and synthesis in our model of global cerebral ischemia. Our studies evaluated in vitro mitochondrial ATP synthesis and the in vivo quantitation of the cortical adenylate pool. Results of our investigations support a growing body of evidence showing the energy state to be relatively stable to ischemia. We conclude that an energy-dependent process of brain is primarily vulnerable to ischemia.
Stroke
PMID:Energy metabolism during brain ischemia. Stability during reversible and irreversible damage. 119 33

A rapid embolic method for consistent induction of stroke in the rat is described. Brain scans were performed using a micro-pinhole collimator system, and the value of the model for studies in localization of radiopharmaceuticals in cerebral ischemia is demonstrated.
Stroke
PMID:Brain scan in cerebral ischemia. An experimental model in the rat. 119 36

Seventy-seven carotid endarterectomies performed on fifty-nine patients, using induced systemic hypertension during carotid artery clamping, were reviewed. The risk of cerebral ischemia is reduced to a minimum by this technic. The measurement of the internal carotid artery stump pressure is an excellent guideline for the need of additional brain protection. An internal shunt is rarely necessary. Thromboembolic phenomena contributed to the major neurologic complications encountered (two deaths and one stroke). Extreme gentleness and careful surgical technic cannot be overemphasized.
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PMID:Carotid endarterectomy: Is a shunt necessary? 120 Feb 96

Endothelium exerts an important influence on cerebral vascular tone through the production and release of a diverse group of vasoactive factors. Relaxing factors produced by endothelium include nitric oxide (or a nitric oxide-containing compound), a hyperpolarizing factor, and prostacyclin. Endothelium-derived contracting factors include cyclooxygenase products of arachidonic acid and endothelins. Several pathophysiological conditions are associated with increased formation of endothelium-derived contracting factors. Such endothelial dysfunction in the cerebral circulation may shift the balance of vascular tone toward constriction and may potentially contribute to the onset or maintainance of cerebral ischemia and stroke.
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PMID:Regulation of the cerebral circulation by endothelium. 129 44


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