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

We studied the direct vascular effects of dimethyl sulfoxide (DMSO) in isolated middle cerebral arteries and on pial arteriolar caliber after subarachnoid perivascular microinjection in chloralose-anesthetized cats, and on brain retraction in cats given DMSO intravenously. DMSO did not constrict isolated cerebral arteries at any of the concentrations studied (10(-10) to 4 X 10(-1) M). In middle cerebral arteries precontracted with potassium, 5-hydroxytryptamine, prostaglandin F2 alpha, or with mechanically raised tone, DMSO at concentrations of 10(-10) to 10(-2) M had no significant effects; at concentrations greater than 10(-2) M, DMSO consistently relaxed the arteries, probably because of the hyperosmolarity of the bathing solution. Microapplication of DMSO (10(-6) to 10(-2) M) around pial arterioles on the cortical surface did not change arteriolar caliber significantly. Higher concentrations of DMSO (1%) increased arteriolar caliber by 56 +/- 4% (p less than 0.001), probably as a consequence of solution hypertonicity. DMSO did not modify in vivo cerebrovascular responses to alterations in perivascular potassium ion concentrations. Intravenous administration of DMSO did cause obvious brain shrinkage. These data provide no support for the view that direct cerebral vascular effects play a major role in the clinical efficacy of DMSO, but are consistent with the hypothesis that DMSO's ability to lower intracranial pressure derives from its osmotic effect on cerebral issue.
Stroke
PMID:Vasomotor effects of dimethyl sulfoxide on cat cerebral arteries in vitro and in vivo. 371 47

We performed experiments in human cerebral arteries to determine the source of activator calcium during contractions induced by 5-hydroxytryptamine. Rings of human basilar artery obtained at autopsy were mounted for isometric tension recording in organ baths filled with a physiological salt solution. Contractile responses to 5-hydroxytryptamine were virtually abolished in Ca++-free solution, and inhibited significantly by nimodipine. In both cases, the depression of the response to 5-hydroxytryptamine was comparable to that seen when KCl was used to contract the vessels. These experiments demonstrate that 5-hydroxytryptamine mediates contraction of the smooth muscle in human basilar artery by increasing membrane permeability to extracellular calcium.
Stroke
PMID:5-hydroxytryptamine: source of activator calcium in human basilar arteries. 402 84

1. In artificially ventilated open-chest cats and dogs ventilation with 5-15% CO(2) reversed the bronchoconstriction caused by drugs or by pulmonary artery occlusion. Total lung resistance, ;static' lung compliance, and intratracheal or intrabronchial pressure at constant pump stroke were measured.2. CO(2) reduced resistance and increased compliance of the lung during infusions of 5-hydroxytryptamine (5-HT), histamine and acetylcholine in cats. In dogs CO(2) reduced resistance during 5-HT infusions; it caused small reductions in intratracheal pressure but no significant change in resistance during infusions of histamine and acetylcholine. Even in cats CO(2) had a larger effect during 5-HT than during histamine and acetylcholine infusions.3. Occlusion of a pulmonary artery caused increases in resistance and decreases in compliance in the affected lobes of both cats and dogs. These changes were partly reversed by ventilation with high CO(2) mixtures.4. The bronchodilator action of CO(2) took place over a wide range of P(a, CO2) values (20-100 torr).
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PMID:The action of carbon dioxide on constricted airways. 477 2

1 Spinal alpha-adrenoreceptors involved in cardiovascular control have been investigated using selective alpha-adrenoreceptor agonists and antagonists in urethane-anaesthetized rats. 2 Intrathecal injections of clonidine, alpha-methylnoradrenaline, guanfacine and M7 at the C7-T1 level reduced blood pressure and heart rate. In contrast, phenylephrine, 5-hydroxytryptamine and procaine had little or no effect. These results suggest the involvement of spinal alpha 2-adrenoreceptors. 3 The fall in blood pressure produced by clonidine appeared to be attributable to a reduction in heart rate and stroke volume. Lower body vascular resistance was unchanged. 4 The clonidine-induced bradycardia was antagonised by prazosin, WB4101, piperoxan or yohimbine. Their relative potencies suggest that alpha 1-rather then alpha 2-adrenoreceptors mediate this response. 5 piperoxan and yohimbine clearly prevented the clonidine-induced fall in blood pressure; prazosin and WB4101 also appeared to antagonise clonidine but these results were complicated by the fact that these antagonists themselves reduced blood pressure. 6 It was difficult to interpret these results simply in terms of alpha 1- or alpha 2-adrenoreceptors. Thus spinal alpha-adrenoreceptors may be different from peripheral alpha 1- or alpha 2-adrenoreceptors.
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PMID:Pharmacological characteristics of spinal alpha-adrenoreceptors in rats. 612 10

Fever frequently complicates stroke and subarachnoid haemorrhage. A transient rise in transmitter monoamine levels of plasma and cerebrospinal fluid occurs in these diseases. The present study demonstrates an enhanced vasoconstrictor response of cerebral vessels to noradrenaline-but not 5-hydroxytryptamine-following a rise in temperature. The augmented response is more likely due to an impaired inactivation (re-uptake) of the amine than to an altered sensitivity of the post-synaptic alpha-adrenergic receptor, since it could be reproduced by pretreatment with cocaine. The finding indicates that it may be important to combat fever in these patients.
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PMID:The effect of temperature elevation on the cerebrovascular response to noradrenaline and 5-hydroxytryptamine. 627 58

Subarachnoid hemorrhage (SAH) was induced in baboons by puncturing the middle cerebral artery. Four to seven days later cerebral blood flow (CBF) responses to changing PaCO2 and to intracarotid infusion of 1.0, 2.5 and 5.0 micrograms of 5-hydroxytryptamine (5-HT)/kg/min were studied using the intracarotid 133xenon clearance technique. Indices of cerebral metabolism were determined by measuring arterio-venous differences for oxygen, pyruvate, lactate and glucose. The results were compared with those from sham-operated baboons. In the sham-operated group normal CO2 reactivity was seen, and 5-HT infusion did not produce any significant change in CBF or cerebral metabolism. By contrast, the group in which SAH was induced showed a significant decrease in CBF and cerebral oxygen utilization, and attenuated CO2 reactivity.
Stroke
PMID:Cerebrovascular reactivity and metabolism after subarachnoid hemorrhage in baboons. 678 84

The contractile activity of various fresh, or incubated blood fractions was studied in vitro using the isolated canine basilar artery. Significantly greater contraction was induced by fresh platelet rich plasma (PRP) and serum compared to red blood cells (RBC). Following incubation, the contractile activity of RBC increased, reaching a plateau at day-3 and it was maintained for at least 14 days, while both PRP and serum lost most of their activity after 24 h of incubation. The contractions induced by fresh blood fractions were only partially blocked by desensitization of 5-hydroxytryptamine (5-HT) receptors or by the 5-HT antagonist methysergide. D-600 effectively antagonized the response to all blood fractions. Biochemical analysis of the incubated RBC by means of Sephacryl S-200 column chromatography and SDS-urea polyacrylamide gel electrophoresis revealed that the contractile substance possessed a molecular weight of about 60,000 daltons. Vasoactivity was only present in one peak of the chromatographically eluted fractions which was shown to possess a similar absorption spectrum to that of hemoglobin. Hemoglobin concentration was highest in day 3, 7, and 14 fractions and may be correlated with the contractile activity of incubated samples.
Stroke
PMID:Changes in vasoactive properties of blood products with time and attempted identification of the spasmogens. 730 68

Effects of Bromovincamine (BV) on cerebral noradrenaline (NA) and 5-hydroxytryptamine (5-HT) contents, and glucose metabolism in the brain were studied using stroke-prone spontaneously hypertensive (SHR-SP), stroke-resistant spontaneously hypertensive (SHR), age-matched normotensive Wistar Kyoto (WKR) and Wistar rats. In the SHR-SP which have a low level of NA in the hypothalamus, a continuous administration of BV for 1 week induced a normalization of the hypothalamic NA content. Under the same experimental conditions, a tendency toward normalization of hypothalamic NA was also observed in SHR. 5-HT contents in the cerebellum, striatum, hypothalamus, midbrain and hippocampus of SHR showed a significant increase following a single injection of BV. Similarly, 5-HT contents in the cerebellum and cerebral cortex of Wistar, WKR and SHR showed a significant increase following a continuous administration of BV for 1 week. Both in vitro and in vivo administration of BV significantly inhibited the high concentration of K+ evoked glucose consumption in cerebral cortical slices from SHR, WKR and Wistar rats, whereas glucose consumption in cerebral cortical slices from SHR determined in the absence of high concentration of K+ increased significantly following continuous in vivo administration of BV. The present results suggest that BV may be an useful drug for improving abnormal cerebral metabolisms of NA, 5-HT and glucose.
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PMID:[Effect of Bromovincamine on noradrenaline and 5-hydroxytryptamine contents, and glucose metabolism in rat brain: analysis using spontaneously hypertensive rats (SHR) (author's transl)]. 732 49

The Ca2+ responsiveness of vascular smooth muscle myofilaments is not unique: it is increased during neuro-humoral activation and decreased during beta-adrenergic stimulation. In this study we tested whether an augmented Ca2+ responsiveness of smooth muscle myofilaments may contribute to the increased coronary tone observed in hypertension using beta-escin-permeabilized coronary arteries from 3-mo-old stroke-prone spontaneously hypertensive rats (SHRSP) and their age matched normotensive reference strain (WKY rats). In intact coronary arteries, the response to 5-hydroxytryptamine (5-HT) but not to KCl was larger in SHRSP than in WKY rats. In beta-escin permeabilized coronary arteries in which the receptor effector coupling is still intact, 5-HT enhanced force at constant submaximal (Ca2+) (pCa 6.38) to a greater extent in SHRSP. The Ca2+ sensitizing effect of 5-HT was mimicked by GTP gamma S (0.01-10 microM); again this effect was larger in SHRSP. In the absence of 5-HT or GTP gamma S the Ca2+ force relation was similar in both groups. Forskolin induced relaxation at constant submaximal (Ca2+). This desensitizing effect was smaller in SHRSP than in WKY rats. In conclusion, this study shows that intracellular signalling pathways involved in modulating the Ca2+ responsiveness of coronary smooth muscle myofilaments are altered in the genetically hypertensive animals favoring a hypercontractile state in the coronary circulation.
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PMID:Augmented agonist-induced Ca(2+)-sensitization of coronary artery contraction in genetically hypertensive rats. Evidence for altered signal transduction in the coronary smooth muscle cells. 792 15

We examined 5-hydroxytryptamine-like immunoreactive cerebrovascular nerve fibers in rats after experimental thromboembolic stroke. Although there were no visible 5-hydroxytryptamine-like immunoreactive nerve fibers in normal animals, we found many of these fibers near the clot emboli 30 min after the stroke, and the number of fibers increased slightly with time. In immunohistochemical double staining, these fibers corresponded to neuropeptide Y-like immunoreactive nerve fibers. And they were not observed in animals after superior cervical ganglionectomy. These findings suggest that the sympathetic nerves take up serotonin released from intraluminal aggregating platelets.
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PMID:Enhancement of serotonergic immunoreactivity in sympathetic cerebrovascular nerve fibers after experimental embolic stroke. 819 Mar 64


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