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

1. In previous experiments in conscious, water-replete Long Evans and Brattleboro rats the non-peptide angiotensin II-receptor antagonist, DuP 753, caused only slight hypotension and peripheral (particularly renal) vasodilatations. However in water-deprived (i.e. renin-dependent) Brattleboro rats, DuP 753 caused marked hypotension and regional vasodilatations. The major objective of the present study was to determine if the hypotensive effects of DuP 753 under any of the experimental conditions studied previously were contributed to by negative effects on cardiac haemodynamics. 2. Male, Long Evans and Brattleboro rats were chronically instrumented with electromagnetic flow probes on the ascending aorta and with intravascular catheters. Data were collected by use of a microcomputer-based system that provided digitised print-out of instantaneous heart rate, mean arterial blood pressure, cardiac output, stroke volume, peak aortic flow, maximum positive slope of the aortic flow signal (+ dF/dtmax), total peripheral conductance and central venous pressure. 3. Incremental i.v. bolus doses (0.1-10 mg kg-1, at 15 min intervals) of DuP 753 were administered to water-replete Long Evans (n = 8) and Brattleboro (n = 8) rats, and to water-deprived (14 h) Brattleboro rats (n = 9) (the latter animals show marked activation of the renin-angiotensin system). In all groups, 15 min after the highest dose of DuP 753 had been given, a supramaximal dose of captopril (2 mg kg-1) was injected to determine if it had any additional effects. 4. In water-replete, Long Evans and Brattleboro rats, DuP 753 (0.1-1 mg kg-1) caused slight, transient hypotension, with rises in total peripheral conductance; increases in cardiac output, peak aortic flow, + dF/dtmax and stroke volume were inconsistent and central venous pressure did not change. Higher doses of DuP 753 (3 and 10mgkg-') caused modest, sustained hypotension that was due entirely to an increase in total peripheral conductance, since cardiac output, peak aortic flow and + dF/dtmax showed transient elevations; captopril had no additional hypotensive or vasodilator effects. 5. Under resting conditions, water-deprived Brattleboro rats showed an increase in mean arterial blood pressure, but there were reductions in total peripheral conductance, cardiac output and + dF/dtmax. DuP 753 (0.1-10 mg kg- 1, i.v., boluses at 15 min intervals) caused incremental hypotension and tachycardia and dose-dependent rises in total peripheral conductance that were accompanied by transient increases in cardiac output, peak aortic flow and + dF/dtmax; captopril had no additional hypotensive or vasodilator effects. 6. Under no conditions were there any negative effects of DuP 753 on myocardial function; moreover, it is likely the transient increases in cardiac function following DuP 753 were indirect and due to the reduction in afterload. Thus, it appears the haemodynamic effects of DuP 753 can be explained by its vasodilator action.
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PMID:Cardiac haemodynamic effects of the non-peptide, angiotensin II-receptor antagonist, DuP 753, in conscious Long Evans and Brattleboro rats. 188 12

We used television microscopy and an image-splitting technique to monitor the changes in diameter produced by histamine applied locally to mouse pial arterioles in vivo. A high dose (50 micrograms/ml, 3 X 10(-4) M) of histamine constricted the arterioles, whereas lower doses (20 and 10 micrograms/ml) relaxed them. Constriction was blocked and dilation occurred when selective injury of the endothelium was produced by light from a helium-neon laser in the presence of intravascular Evans blue. From this we conclude that the constriction was endothelium-dependent and was caused by the release of an endothelium-derived constricting factor. Constriction was also blocked by each of two antagonists of the H1 histamine receptor and by pretreatment of the arterioles with indomethacin. H1 blockade unmasked a dilating action of 1 micrograms/ml histamine, a dose too low to affect the diameter of arterioles not treated with the H1 blocker. An H2 blocker interfered with the relaxation by low-dose (10 micrograms/ml, 6 X 10(-5) M) histamine. These data indicate that for mouse pial arterioles, histamine can interact with H1 receptors on the endothelium to release an endothelium-derived constricting factor that causes constriction of the underlying muscle while simultaneously interacting with H2 receptors in the muscle that mediate relaxation of the vessel.
Stroke 1990 Feb
PMID:Histamine elicits competing endothelium-dependent constriction and endothelium-independent dilation in vivo in mouse cerebral arterioles. 196 94

Positron emission tomography (PET) and MR have been compared with histochemical pathology to show affected tissue areas in rat brain after right middle cerebral artery (MCA) occlusion combined with temporary bilateral common carotid artery occlusion in Long Evans rats. The glucose metabolic rate was 65 +/- 8 mumol/100 ml/min in the right cortical gray matter corresponding to the occluded middle cerebral artery territory and 93 +/- 8 mumol/100 ml/min in the corresponding (left) normal side. Infarcted tissue showed decreased PET activity and increased signal in MR T2-weighted scans ipsilateral to the MCA occlusion. These regions correspond to a zone of focal infarction identified in coronal tissue sections stained with 3-4-5 triphenyl tetrazolium chloride. This study demonstrates that PET can be used to study glucose utilization in rat stroke model in vivo and noninvasively.
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PMID:PET and MR studies of experimental focal stroke. 202 95

1. Measurements of changes in renal, mesenteric and hindquarters haemodynamics or cardiac haemodynamics in response to i.v. bolus doses of arginine vasopressin (AVP) or lysine vasopressin (LVP, 0.7 and 7.0 pmol) were made in conscious, chronically-instrumented Long Evans rats. 2. In some experiments AVP and LVP were administered during an infusion of NG-nitro-L-arginine methyl ester (L-NAME; 1.0 or 0.3 mg kg-1 h-1) to determine whether or not inhibition of nitric oxide production influenced the cardiovascular effects of the peptides. In other experiments, indomethacin (bolus dose of 5 mg kg-1 followed by infusion at 5 mg kg-1 h-1) was given to determine the possible involvement of cyclo-oxygenase products in the responses to AVP and LVP. 3. Under control conditions, the lower dose of LVP had significantly greater effects than AVP on heart rate, mean arterial blood pressure, renal, mesenteric and hindquarters conductances, total peripheral conductance, cardiac index, peak aortic flow and +dF/dtmax. The higher dose of LVP had significantly greater effects than AVP on all variables (i.e. including stroke index and central venous pressure). 4. In the presence of L-NAME (1 mg kg-1 h-1) there was a sustained increase in mean arterial blood pressure (+23 +/- 3 mmHg) and reductions in mesenteric (-38 +/- 4%) and hindquarters (-30 +/- 6%) vascular conductances. Under these conditions the difference in the pressor effects of AVP and LVP was abolished, but their differential effects on regional and cardiac haemodynamics persisted. This dose of L-NAME did not change cardiac baroreflex sensitivity. 5. During infusion of L-NAME at a lower rate (0.3mgkg-th-1), baseline cardiovascular status was unchanged and regional haemodynamic effects of AVP and LVP were enhanced, but the differences in the regional vasoconstrictor responses to the two peptides persisted. 6. Indomethacin (5 mg kg-1 bolus, then 5 mg kg- 'h-1 infusion) augmented the renal vasoconstrictor responses to AVP and LVP, but abolished the difference in the hindquarters vasoconstrictor responses to the two peptides. However, the differences in the pressor and the renal and mesenteric vasoconstrictor effects of AVP and LVP still occurred in the presence of indomethacin. 7. The results indicate that AVP normally has lesser cardiovascular effects than LVP but this difference does not seem to be due to more effective stimulation of nitric oxide-mediated or cyclo-oxygenase-dependent vasodilator mechanisms by AVP than LVP.
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PMID:Effects of NG-nitro-L-arginine methyl ester or indomethacin on differential regional and cardiac haemodynamic actions of arginine vasopressin and lysine vasopressin in conscious rats. 204 32

1. Regional haemodynamic responses to i.v. bolus doses (0.1-10.0 mg kg-1) of NG-nitro-L-arginine methyl ester (L-NAME) were measured in conscious, Long Evans rats (n = 8) chronically instrumented with renal, mesenteric and hindquarters pulsed Doppler flow probes and intravascular catheters. 2. L-NAME caused dose-dependent pressor effects associated with renal, mesenteric and hindquarters vasoconstrictions. The mesenteric vascular bed showed earlier onset with more rapid, and greater, maximum vasoconstrictions than the renal or hindquarters vascular beds; however, the hindquarters vasoconstriction was more persistent. D-NAME was without significant effects (n = 2). 3. Primed infusion of L-arginine (100 mg kg-1 bolus followed by 100 mg kg-1 h-1 infusion), starting 10 min after an i.v. bolus injection of L-NAME (10 mg kg-1), caused significant reversal of the pressor responses, and renal and mesenteric vasoconstrictions, but not of the hindquarters vasoconstriction. Primed infusions of L-arginine (100 mg kg-1, 100 mg kg-1 h-1) starting 5 min after L-NAME (1 mg kg-1) additionally caused some reversal of the hindquarters vasoconstriction, but this effect was transient. 4. Primed infusion of L-arginine (100 mg kg-1, 100 mg kg-1 h-1) starting 30 min before i.v. bolus injection of L-NAME (10 mg kg-1) caused significant attenuation of the pressor effects and the renal and mesenteric vasoconstrictions but not of the hindquarters vasoconstriction. 5. In a separate group of rats (n = 8) chronically instrumented with thoracic aortic electromagnetic flow probes for the measurement of cardiac haemodynamics, i.v. bolus injection of L-NAME (10mgkg-1) produced significant reductions in total peripheral conductance, cardiac output, stroke volume, peak thoracic aortic flow and the maximum rate of rise of aortic flow; these were coincident with the maximum pressor and vasoconstrictor effects. 6. These results, collectively, are consistent with L-NAME interfering with L-arginine-nitric oxide pathways that have important influences on regional vascular conductances in vivo. The pressor effect resulting from L-NAME-induced vasoconstrictions is offset by a substantial reduction in cardiac function that may depend on direct and/or indirect effects of L-NAME on the heart.
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PMID:Regional and cardiac haemodynamic effects of NG-nitro-L-arginine methyl ester in conscious, Long Evans rats. 207 81

The diameters of pial arterioles of mice were monitored in vivo with an image-splitting technique and television microscopy. Concentrations of leukotriene C4 as low as 10(-7) M constricted the arterioles. The leukotriene C4-D4 receptor blocker ICI 198615 (10(-8) M) inhibited the response. Endothelial injury by helium-neon laser/Evans blue technique eliminated the constriction and unmasked a slight but consistent relaxation that was not inhibited by 10(-8) M ICI 198615. Since leukotrienes are produced by the brain and enter the cerebrospinal fluid in ischemia, head trauma, and subarachnoid hemorrhage, the possibility that leukotrienes C4 and D4 contribute to decreases in cerebral blood flow during these conditions should be considered. However, the present data makes such a possibility far less likely because the endothelium is frequently injured in these conditions, and therefore the ability of leukotrienes to constrict vessels would be severely curtailed.
Stroke 1990 Nov
PMID:Leukotriene constriction of mouse pial arterioles in vivo is endothelium-dependent and receptor-mediated. 217 72

Conscious, Long-Evans rats, chronically-instrumented for the direct measurement of intra-arterial and central venous pressures and ascending aortic blood flow (i.e. cardiac output), were given bolus, intravenous doses (4 and 40 pmol) of endothelin-1, -2, or -3 or sarafotoxin S6b in random order. The lower dose of endothelin-1 and -3 and sarafotoxin S6b caused a significant increase in cardiac output. The higher bolus dose of the same three peptides caused initial hypotension and increases in cardiac output, stroke volume and total peripheral conductance. Endothelin-2 did not have these initial effects in all animals. Subsequently, all peptides increased mean arterial blood pressure and decreased cardiac output and total peripheral conductance. Overall the effects of endothelin-1 and sarafotoxin S6b were very similar, consistent with them acting at the same site.
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PMID:Cardiac output effects of endothelin-1, -2 and -3 and sarafotoxin S6b in conscious rats. 219 9

Cerebral edema, resolution of edema, and subsequent development of cerebral atrophy were studied prospectively in 83 patients with ischemic stroke with CT 3 days, 2 weeks, and 6 months post-stroke. Nineteen patients had large (diameter greater than 3 cm), 25 medium sized (diameter greater than or equal to 1.5 less than or equal to 3 cm), and 15 lacunar infarcts (diameter less than 1.5 cm). In 24 patients no infarcts were seen. Changes of Evans' ratio (ER), septum-caudate distance (S/C), and width of widest cortical sulci (SuW) were taken as markers of mass effect/atrophy. These parameters were within normal limits in most cases. However, when all CT scans performed in each patient were compared, changes of ER, S/C, and SuW became apparent as evidence of mass effect and subsequent atrophy development. Mass effect occurred in 81 percent and atrophy in 58 percent of patients with large infarcts. In patients with medium sized infarcts, mass effect occurred in 38 percent and atrophy in 45 percent.
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PMID:Mass effect and atrophy after stroke. 226 Dec 85

Unilateral reversible osmotic opening of the blood-brain barrier can be produced in mice. Infusion of 1.8 molal arabinose in water at a rate of 0.64 ml/min for 30 seconds into the internal carotid artery consistently results in ipsilateral brain staining by intravascular Evans blue dye. Osmotic opening is concentration-dependent (threshold, 1.6 molal arabinose) and reversible within 4 hours. No long-term neurologic deficit occurs. These results suggest that reversible osmotic blood-brain barrier opening can be applied to disease models in mice.
Stroke 1988 Feb
PMID:Reversible osmotic opening of the blood-brain barrier in mice. 244 47

Our study describes the anatomy of the middle cerebral artery (MCA) in 65 Sprague-Dawley rats and the spatial distribution of ischemic cortical lesions caused by occluding major MCA branches. The rats characteristically had at least two major MCA branches, frontal and parietal. Many rats had additional branches supplying the pyriform and temporal cortexes. Permanent occlusion of the frontal or parietal branches combined with 30 minutes of bilateral carotid artery occlusion produced visible Evans blue dye uptake by ischemic cortical areas after 24 hours. No lesions distal to the occlusion were apparent in 38% and 43% of rats with frontal and parietal branch occlusions, respectively; small lesions contiguous with the occlusion site were observed in 38% and 32% of the rats. Only 6% of the frontal and 7% of the parietal branch occlusions produced isolated distal infarcts as expected if these branches were end-arteries. Blood flow was reversed in arteries distal to the occlusion. We conclude that extensive collateral connections of the frontal and parietal MCA branches with other arterial systems protect the anterior and posterior cortical regions. In contrast, occlusions of the pyriform branch of the MCA invariably caused infarcts in the frontopyriform region. In about one third of the rats, frontal or parietal branch occlusions produced lesions involving much of the proximal MCA territory; the frontopyriform region was most consistently affected. Combined, these data suggest that the pyriform MCA branch is an end-artery and that the cortical region it supplies is prone to ischemic damage resulting from any reduction of blood flow through the main MCA trunk.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1988 Jul
PMID:Ischemic cortical lesions after permanent occlusion of individual middle cerebral artery branches in rats. 245 67


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