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

Ten patients with ischaemic stroke were treated with prostacyclin (2.5-5.0 ng/kg/min i.v. in 6 h courses 4-10 times during 1-2.5 days). In all patients a dramatic regression of hemiplegia, or hemiparesis, or aphasia occurred in the first few hours of prostacyclin infusion. Four to eight weeks later 6 patients left the clinic without neurological deficit; 3 patients had minor residual hemiparesis in upper limbs. In one patient, the occlusion of the contralateral carotid artery led to his death. It is considered that an antagonism may exist between endogenous cerebral prostanoids and prostacyclin and may have been responsible for the beneficial effects of prostacyclin therapy.
Stroke
PMID:Treatment of ischaemic stroke with prostacyclin. 634 Feb 53

The object of this investigation was to study the effects of prostacyclin (PGI2) upon the evolution of acute focal cerebral ischemia in the cat. Twenty-five fasted adult cats, lightly anesthetized with nitrous oxide, underwent right middle cerebral artery (MCA) occlusion. Eleven cats received an intracarotid infusion of PGI2 in buffered saline pH 10.5 (100 ng/kg/min at 0.01 ml/kg/min), and 11 cats received intracarotid buffered saline pH 10.5 (0.01 ml/kg/min) without therapeutic agents. Treatment with PGI2 was started upon MCA occlusion and continued for 6 hours. Thirty minutes prior to perfusion, the animals were given fluorescein and Evans blue by intravenous injection. The cats were perfused-fixed in vivo with carbon and buffered formalin 6 hours after MCA occlusion. Another 3 cats received tritium labeled intracarotid PGI2, and peripheral venous samples were collected and assayed for PGI2 plasma levels. Mean arterial pressure was stable in PGI2 treated animals during 6 hours of MCA occlusion, while untreated cats had significant progressive hypertension during that period. The rCBF (measured by the intracarotid 133Xe method) decreased markedly in all animals immediately upon MCA occlusion. However, untreated animals had a significant progressive improvement in rCBF during the occlusion period, while PGI2 treated animals had no such improvement. Quantitative EEG changes, gross edema, areas of fluorescein extravasation, patterns of carbon perfusion, and infarct size were not significantly different in the two groups. While most untreated animals had marked Evans blue extravasation after 6 hours of MCA occlusion, most PGI2 treated animals had no such extravasation, indicating some protection of the blood-brain barrier in these animals.
Stroke
PMID:Treatment of acute focal cerebral ischemia with prostacyclin. 634 Feb 54

The purpose of this study was to assess the hemodynamic response after prostacyclin infusion into the venous system and into the carotid artery in the pig. During the study the following circulatory variables were studied: mean systemic arterial pressure, mean pulmonary arterial pressure, wedge pressure, heart rate, cardiac output, systolic and diastolic left ventricular pressure, stroke volume, total systemic resistance, total pulmonary resistance, left ventricular stroke work. Our results confirm that prostacyclin is a powerful hypotensive agent. The hypotensive effect seems to be due to a peripheral vasodilatation of arterial and venous vessels. Venous infusion caused only 19% tachycardia, as opposed to 36% caused by arterial infusion for the same percentage of blood pressure reduction. This suggests that prostacyclin probably stimulates cardiopulmonary vagal receptors. The effect of prostacyclin on heart rate, therefore, may be twofold and in opposite directions: one action causing tachycardia secondary to hypotension, and the other inviting bradycardia through direct vagal stimulation.
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PMID:Prostacyclin effect on heart rate in the pig. 634 2

In normothermic cats under light barbiturate anesthesia, cerebral blood flow was arrested for one hour by intrathoracal occlusion of the innominate, the left subclavian, and both mammary arteries. Recirculation of the brain after ischemia resulted in reactive hyperemia, followed by a decrease of blood flow to about 70% of control (post-ischemic hypoperfusion). During postischemic hypoperfusion, CO2-reactivity was completely abolished. Intravenous infusion of prostacyclin 2 hours after ischemia (1.8 micrograms/kg/min) decreased systemic arterial blood pressure and reduced platelet aggregability but did not improve cerebral blood flow, did not restore CO2-reactivity, and did not influence postischemic changes of blood coagulation. It is concluded that prostacyclin deficiency is not or not the only reason for the development of post-ischemic hypoperfusion and the associated disturbance of flow regulation.
Stroke
PMID:No effect of prostacyclin on blood flow, regulation of blood flow and blood coagulation following global cerebral ischemia. 636 92

Hemodynamic effects of prostacyclin (PGI2) given as an intravenous infusion at a rate of 8 ng/kg/min were assessed in 50 patients with coronary artery disease at the time of aortocoronary bypass surgery. 1. During steady-state neuroleptic anesthesia, after sternotomy and pericardiotomy, before cannulation of the aorta and vena cava PGI2 led to the following changes: decreases in mean arterial pressure (-24%), total peripheral resistance (-46%), left ventricular pressure (-12%) and left ventricular end-diastolic pressure (-48%), increases in heart rate (+9%), cardiac output (+41%), stroke volume (+30%) and dp/dtmax (+26%) as well as nonsignificant decreases in right ventricular filling pressure (-13%) and mean pulmonary arterial pressure (-9%) together with an unaltered rate-pressure product. 2. In a randomized double-blind study PGI2 was infused throughout the period from two minutes prior to, until termination of extracorporeal circulation. The effects on compliance of the extrathoracic venous system were analyzed on the basis of changes in venous pressure and oxygenator volume. As compared with controls, patients receiving PGI2 were found to have a significant increase in compliance (.157 ml/mm Hg X kg). Thus, in this setting, PGI2 can affect marked vasodilatation with reductions in peripheral resistance and mean arterial pressure together with increases in cardiac output and heart rate.
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PMID:[Hemodynamics and changes in compliance of the extra-thoracic capacity system following administration of prostacyclin (PGI2)]. 637 Aug 14

Therapy to decrease the load in congestive heart failure is now classified as acute and chronic vasodilator therapy. In this symposium, we presented prostacyclin (PG I2) as an acute and prazosin as a chronic vasodilator. Their hemodynamic and clinical effectiveness were evaluated and their effect on the sympathetic nervous system was also studied. We studied the effect of intravenous prostacyclin infusion in doses of 22 +/- 11 ng/kg/min in nine patients with severe congestive heart failure refractory to digitalis and diuretic drugs. After prostacyclin infusion, mean pulmonary capillary wedge pressure decreased from 21.0 +/- 7.9 to 15.0 +/- 6.6 mmHg (p less than 0.001), mean arterial pressure from 98.9 +/- 12.8 to 76.2 +/- 7.0 mmHg (p less than 0.001), systemic vascular resistance from 2,574 +/- 384 to 1,368 +/- 283 dynes X sec X cm-5 (p less than 0.001), pulmonary vascular resistance from 1,008 +/- 451 to 443 +/- 135 dynes X sec X cm-5 (p less than 0.001) and pulmonary arteriolar resistance from 330 +/- 111 to 189 +/- 73 dynes X sec X cm-5 (p less than 0.001). The cardiac index increased from 2.0 +/- 0.37 to 3.2 +/- 0.59 l/min/m2 (p less than 0.001), and the stroke index from 27.6 +/- 8.69 to 42.0 +/- 0.62 ml/m2 (p less than 0.001). Moreover, prostacyclin therapy counteracted the sensation of coldness of the limbs and face, and patients felt warmth and mild flushing of the face. The effect of prazosin on the exercise duration time until dyspnea was evaluated by the treadmill test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostacyclin and prazosin in the treatment of congestive heart failure; with special reference to the sympathetic nervous system. 637 Dec 82

"Antiplatelet" drugs and certain life styles seem to have an "antithrombotic" effect that may help protect against stroke and heart attack. This review of the experience with aspirin, dipyridamole, and sulfinpyrazone offers new interpretations of some of the major clinical trials, suggests guidelines for use of antiplatelet drugs, and integrates novel observations on diet and exercise into the "thromboxane-prostacyclin balance" hypothesis. It is argued that the Canadian stroke study showed that aspirin protects men with transient ischemic attacks from coronary death as well as from stroke, that type II errors may have been made in some clinical trials, that aspirin protects women as well as men, that aspirin benefits patients who have had a heart attack, that the effect of aspirin in angina varies with the type of angina, that the dose of aspirin used may not be critical, that guidelines for use of dipyridamole and sulfinpyrazone are still inconclusive, and that exercise and fish oil supplements may be "antithrombotic."
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PMID:Platelets, carotids, and coronaries. Critique on antithrombotic role of antiplatelet agents, exercise, and certain diets. 638 36

After a brief survey of the already well known functions of tromboxane and prostacyclin both in physiological and pathological conditions, the data found in the literature on the therapeutical use of prostacyclin are discussed. The positive results obtained in the treatment of arteriosclerosis obliterans of the lower limbs, of Raynaud's syndrome, of ischaemic stroke and of ischaemic heart diseases, together with the very modest side effects of prostacyclin, suggest to continue with prostacyclin therapy even if its mechanism of action is not yet clear.
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PMID:[Therapeutic use of prostacyclin in cardiovascular pathology]. 641 78

Hypercoagulability may contribute to stroke in young adults. Lupus anticoagulants (LA) were identified in six patients (4%) of 145 young adults with cerebral infarction. The clinical features of the 6 patients in this survey plus an additional patient from another institution with LA-associated stroke are presented. Four had systemic lupus erythematosus and 3 had idiopathic LA; all had mild thrombocytopenia. In 2 patients, no other conditions associated with stroke were discovered after thorough evaluation. Recurrent arterial thrombosis occurred in 4 of 7 patients during an average of two years of follow-up. Evidence suggests that inhibition of prostacyclin formation may occur with LA, promoting a prothrombotic state.
Stroke
PMID:Cerebral infarction associated with lupus anticoagulants--preliminary report. 642 Sep 43

It has been postulated that metabolites of the arachidonic acid pathway exert an important influence on hemostasis and thrombosis. This notion is based on in vitro experiments. We have utilized two experimental models to elucidate the physiologic roles of thromboxane A2 (TxA2) and prostacyclin (PGI2) in the modulation of thrombus formation. The role of TxA2 in promoting thrombus formation was evaluated in a rabbit model where the aorta was deendothelialized by a balloon catheter technique and indium-111-labeled platelets were used as a marker for quantifying platelet deposition. Both 1-benzylimidazole, a thromboxane synthase inhibitor, and 13-azaprostanoic acid, an antagonist of thromboxane/endoperoxide receptors significantly reduced the platelet deposition onto the damaged vessel wall. The data indicate the TxA2 plays an important role in thrombosis and hemostasis. The influence of PGI2 insufficiency due to accelerated PGI2 degradation on microvascular thrombosis was evaluated in a unique clinical disease, i.e. thrombotic thrombocytopenic purpura (TTP). Accelerated PGI2 degradation was observed in several patients with chronic TTP. The degradation abnormalities were corrected by plasma infusion in vivo or serum supplement in vitro. To test the hypothesis that PGI2 must be bound to serum macromolecules to prevent rapid hydrolysis, serum binding capacity for PGI2 was measured by Sephadex G-25 gel filtration. The binding capacity was significantly reduced in the patients and was corrected by serum supplement. Abnormalities of PGI2 binding were also noted in a group of patients with ischemic stroke. Our findings suggest that there exist in the serum certain constituents which bind and stabilize PGI2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of vascular thrombosis by products of arachidonic acid metabolism. 643 30


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