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

In two identical experiments, A and B, we studied the effect of the simultaneous l.v. injection of propranolol (Inderal, 0.5 mg/kg) on the circulatory effects of triiodothyronine (T3 500 microgram/kg i.v. 3 hours before measuring). The two substances act at different rates and so the blocking effect of propranolol preceded the development of the circulatory effects of T3. Cardiac output was measured by the Evans blue dilution method, the heart rate was calculated from the ECG recording and blood pressure was measured with a mercury manometer; stroke volume and total peripheral vascular resistance were also calculated. The isolated injection of T3 was followed by a significant increase in cardiac output (experiment A: 129%, B: 118%) and stroke volume (A: 125%, B: 118%) and by a drop in total peripheral vascular resistance (A: 82%, B: 85%). There was no change, in this early phase, in the heart rate or blood pressure. No changes were found 3 hours after the isolated administration of Inderal (the maximum effect of propranolol is attained in 30-60 min). During the same period, the above initial effects of T3 were completely suppressed by the simultaneous injection of Inderal. These results were probably related to the experimental conditions (early and not very marked changes after T3), but they demonstrate that the initial effects of T3 on cardiac performance and on the peripheral blood vessels can be completely suppressed by a block of beta receptors. From this it can be concluded that beta-adrenergic regulation is an important part of the mechanism of the early haemodynamic action of T3.
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PMID:Inhibition of the early circulatory effects of triiodothyronine in rats by propranolol. 645 55

Regional brain tissue prostaglandin (PG) levels have been measured during ischaemia produced by bilateral carotid occlusion for 1 hour and following restoration of flow. In the normal gerbil, the frontal cortical levels of PGF2 alpha were: 6.7 +/- 1.3 pg/mg and for PGE2: 6.4 +/- 1.1 pg/mg of brain tissue protein. Following 1 hour of ischaemia PGF2 alpha rose to 50.4 +/- 8.3 pg/mg whilst there was only a slight rise in PGE2 (10.7 +/- 1.6 pg/mg). Post ischaemic values for parietal and occipital areas were somewhat higher, but showed the same trend. Within 15 minutes of the restoration of flow there was a massive increase in PGF2 alpha levels which reached a peak at 2 hours (300 pg/mg) and then subsided to control values. PGE2 levels did not change for the first 30 minutes of recirculation, but then rose for the rest of the period of observation. The pattern of cytotoxic oedema resembled PGF2 alpha closely while the Evans blue staining (vasogenic oedema) was similar in time to the PGE2 pattern.
Stroke
PMID:Prostaglandin synthesis and oedema formation during reperfusion following experimental brain ischaemia in the gerbil. 647 41

Evidence was found for different outcomes to middle cerebral artery occlusion in the young genetically hypertensive stroke-prone rat (SHRSP) compared to sham operated controls and the Wistar Kyoto rat (WKY). Qualitatively and quantitatively different gross lesions marked by Evans blue-albumin, cortical atrophy, large areas of strikingly altered cortical histology, postoperative survival and motor behavioral deficits differentiate young SHRSP from sham operated controls and the normotensive WKY. We conclude that the limited focal lesion observed in normotensive and sham operated rats is primarily due to surgical trauma of exposing the vessel and passing the ligature deep to it. The grossly larger and qualitatively different lesion in the SHRSP is the result of an inadequate circulation provided by the dorsal cerebral arterial collaterals. Since the 5-6 week old SHRSP were only mildly hypertensive (systolic blood pressure 140 mm Hg), the inadequate collateral circulation appears to be related to either a genetic or acquired problem rather than being secondary to a vascular lesion of chronic hypertension.
Stroke
PMID:Differential outcome to middle cerebral artery occlusion in spontaneously hypertensive stroke-prone rats (SHRSP) and Wistar Kyoto (WKY) rats. 665 39

The present study was designed to clarify the relationship of cerebral blood flow (CBF) to blood-brain barrier (BBB) in the ischemic brains with or without recirculation, which were produced by clipping of both common carotid arteries in spontaneously hypertensive rats. CBF was measured by the hydrogen clearance method and BBB function was evaluated by the permeability of 131I-albumin and Evans blue dye. Cortical CBF was reduced from 48.8 +/- 9.5 to 4.0 +/- 1.2 ml/100 gm/min during 1 hr ischemia and further to 2.6 +/- 0.3 ml/100 gm/min during 3 hrs ischemia, while thalamic CBF was reduced much less from 50.0 +/- 3.6 to 17.9 +/- 6.5 ml/100 gm/min and to 17.5 +/- 11.0 ml/100 gm/min, respectively. There was no increase in permeability to protein tracers observed in such 1 hr or 3 hrs ischemic brain. Both cortical and thalamic CBF were markedly increased 2.5 to 6 fold of resting values at 5 min after recirculation in the 1 hr ischemic brain. In the 3 hrs ischemic brain, however, both CBF were only slightly increased but never restored to the resting level even at 30 min after recirculation. In such reperfused brains, exudation to Evans blue dye was observed in none of 16 animals with 1 hr ischemia, but in 18 of 23 with 3 hrs ischemia. Disruption of BBB was twice more frequent in the cortex (77.8%) than in either thalamus (33.3%) or hippocampus (33.3%). Permeability index of 131I-albumin (brain albumin/blood albumin) was significantly higher in the ischemic areas stained with blue dye (2.07 +/- 0.45%) than in non-ischemic control brain (0.10 +/- 0.01%).(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke
PMID:Disruption of blood-brain barrier following bilateral carotid artery occlusion in spontaneously hypertensive rats. A quantitative study. 665 89

Alternative hypotheses concerning the pathogenesis of hypertensive encephalopathy are that vasospasm produces cerebral ischemia and cerebral edema, or that passive dilation of cerebral vessels during severe hypertension produces disruption of the blood-brain barrier and cerebral edema. Stroke-prone spontaneously hypertensive rats (SHRSP) were studied when they developed signs of neurological dysfunction. We measured regional cerebral blood flow (rCBF) with 14C-iodoantipyrine, and permeability of the blood-brain barrier with Evans blue dye. Twelve rats had focal disruption of the barrier without histological evidence of ischemic infarction or cerebral hemorrhage: areas with disruption of the barrier had severe focal edema in seven rats and minimal edema in five rats. In areas with disruption of the barrier and marked focal edema, rCBF was decreased to 38 +/- 8 (mean +/- SE) ml/min/100 g vs 102 +/- 13 (p less than 0.05) in other areas of the ipsilateral hemisphere, and 86 +/- 16 in the homologous area of the contralateral hemisphere (p less than 0.05). In contrast, in areas with disruption of the blood-brain barrier with only minimal edema, rCBF was normal or increased: rCBF was 100 +/- 11 ml/min/100 g vs 85 +/- 12 in other areas of the ipsilateral hemisphere (p greater than 0.05) and 64 +/- 8 in the homologous area contralaterally (p less than 0.05). The findings indicate that edema precedes reduction in rCBF in SHRSP and suggest that the initiating event in hypertensive encephalopathy is disruption of the blood-brain barrier, and not vasospasm.
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PMID:Evidence that disruption of the blood-brain barrier precedes reduction in cerebral blood flow in hypertensive encephalopathy. 672 73

Propranolol's potential as a protective agent against tissue injury has been noted in experimental myocardial, renal and early acute focal cerebral ischemia. The purpose of the present investigation was to study further the effects of racemic (d,l) propranolol on blood-brain barrier permeability, morphological changes, cortical electrical activity, and regional cerebral blood flow (rCBF) in experimental focal cerebral ischemia. Thirty adult cats, anesthetized with nitrous oxide, underwent 6 hours of right middle cerebral artery (MCA) occlusion. Fifteen cats were untreated. Fifteen cats were given a continuous infusion of racemic propranolol (1 mg/kg/hr) for 7 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion, both directly into the right carotid artery. Right Sylvian rCBF did not significantly differ in the treated and untreated groups. Carbon filling defects and vital dye (i.e., Evans blue and fluorescein) extravasation were less severe in the propranolol treated animals. Light microscopic findings demonstrated no difference in infarct size between the two groups. The findings suggest that at doses given, racemic propranolol does not exert a protective effect upon cerebral tissue subjected to 6 hours of incomplete ischemia.
Stroke
PMID:Treatment of acute focal cerebral ischemia with propranolol. 672 77

Noninbred Long-Evans rats fed Sudan III at 24 hours before they were given an injection of 7,12-dimethylbenz[a]anthracene (DMBA) displayed prominently suppressed DMBA-induced chromosome aberrations (CA) in their bone marrow cells. Rats fed Sudan III simultaneously with the DMBA injection showed no suppressed CA effect. The suppressive effect of Sudan III on DMBA-induced CA paralleled the dose rate of Sudan III when given in the range between 1 and 10 mg Sudan III/kg body weight; higher doses produced no additional suppression. The capacity of various Sudan III-related chemicals to prevent DMBA-induced CA paralleled their capacity to prevent DMBA-induced adrenal apoplexy and mammary cancer. Among the azo dyes investigated, Sudan III was most efficient in protecting against DMBA-induced CA. Polychlorinated biphenyl and phenobarbital, inducers of drug-metabolizing enzymes, also suppressed DMBA-induced CA.
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PMID:Suppression of 7,12-dimethylbenz[a]anthracene-induced chromosome aberrations in rat bone marrow cells after treatment with Sudan III and related azo dyes. 681 64

Echocardiography and the method of dye dilution (Evans blue) were used to study parameters of the central and intracardiac haemodynamics in 28 men with uncomplicated essential hypertension during treatment with diuretics. Tests were undertaken thrice: after a 5-6 day control period, after a 3-day furosemide load (120 mg per 24 hrs), after 2-3 weeks course of treatment with hypothiazide (50-100 mg per 24 hrs). As a result there was a decrease of end-systolic, end-diastolic and stroke volumes of the left ventricle. In patients with hypotensive effect minute volume did not diminish. In the group without effect there was no significant decrease of arterial pressure, minute volume and general peripheral resistance but an increase in the heart rate. The initial volumes of the circulating blood and plasma in both groups were indistinguishable and decreased significantly as a result of treatment.
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PMID:[Effect of diuretic agents on central and intracardiac hemodynamics in hypertension]. 707 2

Disruption of the blood-brain barrier may play a major role in the pathogenesis of hypertensive encephalopathy. In this study we determined whether sympathetic nerves to cerebral vessels protect the blood-brain barrier during chronic hypertension. We removed the cervical sympathetic ganglion on one side in 24 stroke-prone hypertensive rats when they were 1 month old. After signs of cerebral dysfunction developed at the mean age of 160 +/- 5 days (SE), we injected 125I-albumin and Evans blue dye intravenously to evaluate the permeability of the 125I-albumin was 3.53 +/- 0.83 (brain albumin x 100/blood albumin) in areas of the cerebrum stained with blue dye and 0.24 +/- 0.02 in unstained areas (p less than 0.05). We conclude that sympathetic nerves protect the blood-brain barrier against disruption during chronic hypertension and thereby may protect against hypertensive encephalopathy.
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PMID:Sympathetic nerves protect the blood-brain barrier in stroke-prone spontaneously hypertensive rats. 714 13

This investigation describes a surgical approach for ligation of the middle cerebral artery (MCA) in the young rat and evaluates consequences of the occlusion with a neurologic exam for motor deficits, Evans blue test for blood-brain barrier leaks, and light microscopy for histologic changes after 3 days. Evans blue extravasation and the lesion were limited to cortex at the burr hole site in occluded and sham operated rats. MCA occlusion beyond the point of origin of the striate branches in the young rat results in neither neurological deficits, dye markings, nor histologic changes in the distal vascular field to indicate an infarct. Apparently, the young rodent collateral supply maintains the tissue in a viable state.
Stroke
PMID:Middle cerebral artery occlusion in the young rat. 714 5


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