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

Six male non-endurance trained subjects (S) and six marathon runners (M) underwent graded treadmill exercise (T) and isoproterenol stimulation (I; 2 and 4 microgram X min-1). beta-adrenergic receptor density was additionally determined as the amount of 3H-Dihydroalprenolol (DHA) specifically bound on intact polymorphonuclear leucocytes. Heart rate, VO2 uptake, lactate, plasma noradrenaline, and adrenaline were estimated during T. Heart rate, stroke volume, cardiac output, as well as lactate, glucose, free fatty acids (FFA), and glycerol levels in the blood were determined during I. M showed the known training-dependent responses during T, such as lower heart rates, lactate levels, and plasma catecholamines at identical work loads, as well as higher VO2 max than S. I-induced cardiac output increase was quite similar in both groups. Stroke volume, however, increased significantly in M and stayed constant in S. Lactate decreased (S), glucose increased significantly (M), glycerol increased similarly in both groups, FFA rise was less marked in S. I-induced stroke volume response (I) may be indicative of a more economic regulation of heart work in M than S. Lactate decrease and less marked FFA increase, as observed in S, may be the result of a somewhat higher cardiac energy demand, dependent on less economic heart work. Higher DHA-binding as observed in M, as well as stroke volume response and glucose increase, may be indicators of a training-dependent rise in sensitivity to catecholamines. The unsolved question is, however, to what extent beta-receptor responses in intact blood cells are significant for receptor behavior in other organs.
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PMID:Plasma catecholamines, beta-adrenergic receptors, and isoproterenol sensitivity in endurance trained and non-endurance trained volunteers. 608 22

Cerebral microembolism was performed in rats by injecting radioactive calibrated 50 mu microspheres into the left internal carotid artery. The use of radioactive microspheres as embolic agents enabled the number of microspheres to be determined in each cerebral hemisphere. Edema was assessed 24 h after embolization by measuring brain water, sodium, and potassium content. Equiosmolal doses (40 mmol/kg) of glycerol or urea were injected i.p. at various times before sacrifice. Both treatments caused similar changes in water and electrolyte content, brain dehydration being maximal 30 min after urea and 2 h after glycerol injection. Cerebral energy metabolism and regional blood flow were evaluated at the times of maximal brain dehydration. Urea treatment resulted in an improvement of the cerebral circulation whereas glycerol treatment led to a deterioration of cerebral blood flow which cannot be explained by failure to reduce edema and the consequent microcirculatory impairment. Urea treatment had no marked effect on cerebral energy metabolism whereas glycerol injection resulted in an important increase in brain lactate level which may be relevant to the impairment of cerebral reperfusion. These results point out that administration of a metabolized solute like glycerol may exert deleterious effects on the ischemic brain.
Stroke
PMID:Comparison of the effects of hypertonic glycerol and urea on brain edema, energy metabolism and blood flow following cerebral microembolism in the rat. Deleterious effect of glycerol treatment. 665 38

A heat-balance study was carried out on conscious rabbits exposed to ambient temperatures (Ta) from 8 degrees to 40 degrees C. At Ta = 40 degrees C, heat gain exceeded heat loss and led to hyperthermia and heat stroke, and the latency for the onset of heat stroke was found to be around 87 minutes. At the onset of heat stroke, the comatose animals showed higher levels of rectal temperature, ear skin blood flow, respiratory evaporative heat loss, metabolic rate, intracranial pressure (ICP), and cerebral water content as compared to those of control animals (kept at an ambient temperature of 24 degrees C). Before the start of heat stress, the animals had an average mean arterial blood pressure (MABP) of 94 mm Hg and cerebral perfusion pressure (CPP) of 80 mm Hg. However, at the onset of heat stroke, the average MABP and CPP decreased to 67 and 19 mm Hg, respectively. The reduction in CPP at the onset of heat stroke was due to both a decrease in MABP and an increase in ICP. In addition, the comatose animals which received an intravenous infusion of 10% glycerol (3 ml/min) had a survival time (interval between onset of heat stroke and death) longer than that of the comatose animals which received the control-vehicle solution. The prolongation of survival time in the glycerol-treated animals may be due to lower rectal temperature, lower cerebral water content, or lower ICP during the development of heat stroke. The present data indicate that not only hyperthermia but also cerebral edema, intracranial hypertension, decreased MABP, and decreased CPP are the main causes of heat stroke. The therapeutic values of glycerol on heat stroke may be related to the depressant action on cerebral edema, intracranial hypertension, and body temperature.
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PMID:Experimental study on the pathogenesis of heat stroke. 672 68

On giving a dose of glycerol (orally), mannitol or lasix (intravenously) to patients with a cerebral stroke in the acute period the cerebrospinal fluid (CSF) pressure in them dropped, on the average, by 70-80%, 65-70%, and 25-30%, respectively. However in 6.5 to 7.5 hours it rose again and the after-effect phenomenon appeared. The effects of the drugs having been over, the CSF pressure was found to exceed the initial level by 50-60% after the glycerol intake; by 75 to 80% after the mannitol, an by 4 to 6% after the lasix injections. When glycerol, mannitol, and lasix were given rectally the CSF pressure dropped, respectively, by 35-45%, 35-40%, and 20-25% below the initial level, and did not rise throughout the whole period of the observation.
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PMID:[Effect of glycerol, mannitol, and lasix on cerebrospinal fluid pressure in the acute period of a stroke]. 679 62

Glycerol is a potent osmotic dehydrating agent with additional effects on brain metabolism. In doses of 0.25-2.0 g/kg glycerol decreases intracranial pressure in numerous disease states, including Reye's syndrome, stroke, encephalitis, meningitis, pseudotumor cerebri, central nervous system tumor, and space occupying lesions. It is also effective in lowering intraocular pressure in glaucoma and shrinking the brain during neurosurgical procedures. Hyperosmolality with rebound cerebral overhydration is of concern, especially in patients with altered blood brain barriers. They may be avoided if glycerol is administered on an intermittent rather than a continuous basis. Intravascular hemolysis does not occur with oral use. When administered intravenously, hemolysis can be minimized by using glycerol 10% in dextrose 5% with normal saline at rates of 6 mg/kg/min or less. However, intravenous doses of 1-2 g/kg every 2 hr can be administered safely in severe cases of elevated ICP. In such patients, glycerol serum concentration, serum osmolality and ICP monitoring are required to optimize glycerol therapy.
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PMID:Glycerol: a review of its pharmacology, pharmacokinetics, adverse reactions, and clinical use. 692 4

Purified human and bovine thrombin produced comparable tonic contractions in isolated canine basilar arteries. The magnitude of the contractions was closely related to the number of thrombin Units studied rather than to the amount of protein added to the isolation bath. Thrombin had a much slower onset of action, but was more potent in generating sustained contractions than either serotonin or prostaglandin F2 alpha. Moreover, in contrast to serotonin and prostaglandin F2 alpha, the contractions caused by thrombin were not terminated by equivalent washing. The thrombin-induced contractions were significantly inhibited by prostacyclin, meclofenamic acid, phenoxybenzamine and glycerol. Prostacyclin was the most potent of these inhibitors. The results suggest that thrombin in a "free" form may cause vasoconstriction, in addition to platelet aggregation, in hemostasis and could contribute to the genesis of cerebral vasospasm associated with subarachnoid hemorrhage.
Stroke
PMID:Cerebral arterial contractions induced by human and bovine thrombin. 699 61

The hydroxyl radical scavengers dimethyl sulfoxide (DMSO) and glycerol were effective inhibitors of platelet aggregation in an in vivo mouse model of pial arteriolar injury. Aggregability was expressed in terms of the time required for a noxious stimulus (light + dye) to initiate aggregation. These drugs, given 1 hour before the injury, also eliminated the dilation which accompanied the damage. The same drugs failed to influence the constriction which accompanied an identical injury to mouse mesenteric arterioles, but again impaired platelet aggregation in the damaged mesenteric vessel. The data support the concept recently introduced by others, that, in the brain, hydroxyl radicals may mediate vascular damage and/or dilation accompanying the damage. The data also support the concept platelet aggregation may be stimulated, directly or indirectly, by hydroxyl radical. The effects of DMSO and glycerol in this study, irrespective of the molecular basis for the effects, may be relevant to the reported therapeutic benefit of these agents in cerebrovascular disease.
Stroke
PMID:Dimethyl sulfoxide (DMSO) and glycerol, hydroxyl radical scavengers, impair platelet aggregation within and eliminate the accompanying vasodilation of, injured mouse pial arterioles. 706 77

Critical evaluation of the literature was use to identify remediable flaws in the design of clinical trials of stroke treatment. Trials of dexamethasone, dextran, and glycerol were reviewed. Available studies have in common major weaknesses in case selection (failure to exclude arteriolar strokes due to hemorrhage or lacunar infarction), and failure to estimate required sample size. Problems of case selection can be avoided with computerized tomography; the sample size required to show superiority of active treatment over placebo can be estimated using standard formulas. Prognostic stratification is suggested as a method of overcoming problems of unbalanced allocation. Further studies with improved design are required to evaluate the prospects for medical limitation of cerebral infarct size.
Stroke
PMID:Problems in design of stroke treatment trials. 706 85

Ischemic brain edema promotes focal cerebral ischemia by increasing intracranial pressure and thereby reducing perfusion pressure, obstructing capillaries and prolonging transport routes within ischemic tissue. There is clinical and experimental evidence that osmotic agents counteract these mechanisms. Moreover, glycerol may act as a free radical scavenger, antioxidant, and activator of plasma prostaglandin (PGI2), resulting in vasodilation. Improvements in ischemic brain energy metabolism after glycerol administration has also been postulated. Results of clinical trials on glycerol treatment of acute ischemic stroke were not conclusive: some demonstrated improved survival in the acute stage, in others survivors benefited in terms of neurological status and/or daily living activities. Other trials did not reveal any superiority of glycerol treatment over placebo. Glycerol is given intravenously as a 10% solution or orally. By the oral route higher intravascular glycerol concentration can be achieved with smaller quantities of fluid. Possible side effects include elevation of blood glucose level with subsequent lactate acidosis in the ischemic brain, serum hyperosmolarity after long-term glycerol administration and--when given intravenously--volume overload in patients with congestive heart failure and hemolysis that may cause renal failure.
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PMID:[Treatment of ischemic cerebral infarct with glycerine]. 756 70

In ten patients we treated with distal arch aneurysms exposed through left posterolateral incisions, we induced profound hypothermia and circulatory arrest. Before circulatory arrest, thiopental, nicardipine and glycerol were used to protect the brain. The brain function was objectively evaluated through continuous recording of EEG and PO2 tension of the internal jugular vein. A cardiopulmonary bypass was introduced via the left atrium, pulmonary artery and left femoral artery cannulation. After proximal anastomosis between the graft and transverse aorta, graft cannulation was added. The distal aortic arch was replaced in all patients, with the entire descending thoracic aorta additionally replaced in two. No patients died in hospital. Two suffered neurological deficit, i.e., one having slight memory impairment and the other having a left-sided stroke due to right cerebral infarction, but recovering completely within a week. Our results indicate that profound hypothermia and circulatory arrest can be implemented safely when treating patients with distal arch aneurysm.
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PMID:[The treatment of patients with distal arch aneurysms--hypothermic circulatory arrest and left posterolateral exposure]. 759 44


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