Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The effect of CL 115,347, a topically active antihypertensive PGE2 analog, and PGE2 on changes in blood pressure (BP), heart rate (HR) response and plasma epinephrine (E) and norepinephrine (NE) levels induced by stimulation of the sympathetic spinal cord outflow were studied in pithed stroke-prone spontaneously hypertensive rats (SHRSP). Surgical pithing significantly reduced plasma E but not NE levels suggesting that the sympathoadrenal medullary system differentially affects E and NE release. Sympathetic stimulation of the spinal cord of pithed SHRSP increased HR, BP, plasma E and NE levels. Topically applied CL 115,347 (0.001-0.2 mg/kg) dose-dependently decreased BP, while intravenously infused PGE2 (30 micrograms/kg/min) did not alter BP except for a brief initial drop. Topical application of CL 115,347 (0.1 mg/kg) also inhibited BP responses to sympathetic stimulation without effects on HR or plasma E or NE levels. Intravenous infusion of PGE2 (30 micrograms/kg/min) inhibited both BP and HR responses to spinal cord stimulation but did not alter plasma catecholamine levels. These studies in SHRSP suggest that CL 115,347 and PGE2 modulate cardiovascular responses mainly via postjunctional effects, but act differently on the cardiovascular elements, viz. CL 115,347 acts primarily on blood vessels while PGE2 acts on blood vessels and heart.
 ...
PMID:Effects of CL 115,347, (+/-)-15-deoxy-16-hydroxy-16-vinyl-PGE2 methyl ester, on cardiovascular responses and plasma catecholamines in pithed stroke-prone spontaneously hypertensive rats during sympathetic stimulation. 658 70

Prostaglandins are involved in the modulation of various central functions (neurotransmitters and hypothalamic hormone release, thermoregulation, cerebrovascular tone) and their levels increase in pathological situations [subarachnoid hemorrhage (SAH), stroke, convulsive disorders, etc.]. This study, using sensitive and specific antibodies, examined levels of four eicosanoids, prostaglandins E2 and F2 alpha (PGE2, PGF2 alpha); and the metabolites of PGI2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and of thromboxane A2, thromboxane B2 (TxB2), in the cerebrospinal fluid (CSF) obtained atraumatically from three species (human, canine, and feline). An assessment of the methodologic procedures (extraction and radioimmunoassay) was carried out. Human lumbar cerebrospinal fluid was shown to contain PGF2 alpha (15-44 pg/ml), 6-keto-PGF1 alpha (undetectable to 39 pg/ml), and TxB2 (undetectable to 28 pg/ml), whereas PGE2 was undetectable (less than 18 pg) in all cases. In both animals species the eicosanoid concentrations were 3- to 30-fold higher than humans for every prostaglandin examined. Although the prostaglandin profile for a given species remained constant (cat, PGE2:6-keto-PGF1 alpha:TxB2:PGF2 alpha; dog, TxB2:PGE2:6-keto-PGF1 alpha:PGF2 alpha), the absolute levels were found to be lower in the pentobarbital-anesthetized animals than in conscious cats. The correspondence of the prostaglandin profiles found in cerebrospinal fluid with the profiles reported in the literature in brain homogenates for the same species supports the hypothesis that cerebrospinal fluid levels of prostaglandins reflect the relative rates of synthesis in neural tissue.
 ...
PMID:Measurement of prostaglandins in the cerebrospinal fluid in cat, dog, and man. 659 32

The hemolysate (10(-5)-10(-2) times dilution; original hemoglobin concentration was 0.83 +/- 0.10 X 10(-3)M) evoked the contraction in a dose dependent manner, and this contraction was composed of low and high sensitive responses as estimated from the Eadie-Hofstee's plot. Indomethacin (10(-7)-10(-5)M) inhibited the latter component in the hemolysate-induced contraction. The membrane potential of smooth muscle cells was -50 mV and the cell was electrically quiescent. The hemolysate (greater than 10(-2) times dilution) depolarized the membrane and increased the ionic conductance of membrane. In rare occasions, the spike potential was triggered on the hemolysate-induced depolarization. The hemolysate (10(-5)-3 X 10(-3) times dilution) produced the contraction with no change in the membrane property. Carbocyclic thromboxane A2 ( cTXA2 ; 2.8 X 10(-10)M) produced the contraction without depolarization of the membrane, yet the TXA2 synthesis inhibitor, OKY-1581 (10(-5)M), had no effect on the hemolysate-induced contraction. PGE1, PGE2 and PGF2 alpha (2.8 X 10(-6)M) produced the contraction with no change in the membrane property. The contraction evoked by 2.8 X 10(-6)M PGF2 alpha corresponded well with that evoked by 3 X 10(-3) times dilution of the hemolysate. Removal of the endothelium by mechanical rubbing modified the hemolysate-induced contraction. Under the assumption that OKY-1581 is a selective inhibitor for TXA2 synthesis, the major part of the contraction (the indomethacin sensitive component) of the basilar artery is postulated to be due to synthesis of the primary PG rather than TXA2 by the hemolysate, yet the hemolysate itself, has to some extent a direct action in evoking the small contraction.
Stroke
PMID:Hemolysate-induced contraction in smooth muscle cells of the guinea pig basilar artery. 672 80

Rats were subjected to severe incomplete cerebral ischemia followed by recirculation. The levels of several of the cyclooxygenase products of arachidonic acid were measured at 5 and 15 minutes of ischemia and at 30 minutes of recirculation following 15 minutes of ischemia, PGE2 accumulated during the first 5 min. of ischemia and its level declined at 15 min. and returned to control level at 30 min. of recirculation. TXB2, on the other hand, increased during the whole time course of the experiment and at the end of the post ischemic period its level was 5 times higher than control. Treatment of the animals with indomethacin (4 mg/Kg, i.v.) prior to ischemia reduced the levels of these products without altering the pattern of their changes. During the ischemic period the EEG was isoelectric and the mean recovery time of electrical cortical activity after 15 min. of ischemia was 10.4 +/- 3.5 min. in the control rats. The rats which received indomethacin recovered faster (43. +/- 0.9 min) and were more resistant to the induction of ischemia. We suggest that the reversibility of cortical activity may be correlated to the accumulation of TXB2 during ischemia and recirculation, and inhibition of its synthesis might improve the post-ischemic reflow.
Stroke
PMID:The effect of incomplete cerebral ischemia on prostaglandin levels in rat brain. 689 89

1. In basal conditions, plasma arterial prostaglandin (PG) E2 was significantly increased in borderline hypertensive patients (BH) (28.5 +/- 6.7 pg/ml) in comparison with sustained essential hypertensive patients (EH) (11.6 +/- 3.2 pg/ml) and in comparison with control normotensive subjects (NTS) (5.8 +/- 1.4 pg/ml). 2. Plasma arterial PGE2 was positively significantly correlated with cardiac index and negatively significantly correlated with total peripheral resistance in basal conditions. 3. Indomethacin induced more pronounced haemodynamic changes in borderline than in sustained hypertensive patients, with a significant increase in arterial blood pressure and total peripheral resistance and a significant decrease in stroke volume and cardiac index. 4. Indomethacin significantly decreased arterial PGE2 in borderline hypertensive patients. The decrease was less important in sustained hypertensive patients. 5. In the overall population, a significant positive correlation between arterial PGE2 concentration and cardiac index was observed before and after indomethacin treatment. 6. The study suggests an important role of PGE2 in the regulation of cardiac output (positive inotropic effect) and blood pressure of essential hypertensive patients.
 ...
PMID:Central haemodynamics and plasma prostaglandin E2 in borderline and sustained essential hypertensive patients before and after indomethacin. 694 67

To provide more effective vasodilator agents for the therapy of severe left ventricular (LV) failure the cardiocirculatory actions of prostaglandin E1 (PGE1) were evaluated in nine coronary patients. PGE1 infusion modestly decreased mean systemic blood pressure (85 to 76 mm Hg, p less than 0.025) and LV filling pressure (19 to 15 mm Hg, p less than 0.01) while heart rate was unchanged (p less than 0.05). Simultaneously, PGE1 augmented cardiac index from 1.9 to 2.5 1/min/m2 (p less than 0.005), raised stroke index from 28 to 35 ml/beat m2 (p less than 0.01) and increased stroke work index from 26 to 30 g-m/m2 (p less than 0.02). Additionally, total systemic vascular resistance decreased from 1862 to 1282 dynes-sec-cm-5 (p less than 0.02) and double product of heart rate and systolic blood pressure diminished from 9492 to 8278 mm Hg (p less than 0.02) while the effective endocardial perfusion pressure was maintained (p less than 0.05). Concomitantly, forearm vascular resistance fell, forearm blood flow was raised, and forearm venous tone remained unchanged. Thus, our results demonstrate that PGE2 is a potent arteriolar vasodilator with markedly beneficial effects of myocardial energetics and on cardiac function in patients with severe ischemic congestive cardiac failure.
 ...
PMID:Beneficial effects of prostaglandin E1 on myocardial energetics and pump performance in severe CHF. 694 63

A total of 27 patients were examined: 12 of them had non-coronarogenic cardialgias and 15 had ischemic heart disease. Prostaglandin E2 intravenous infusion followed the coronary angiography and ventriculography against the background of stabilized pressure in the left ventricle. The infusion lasted 10 minutes, then ventriculography was repeated. The total dose of prostaglandin E2 was 0.5-1.5 mg. Prostaglandin E2 had positive chronotropic and inotropic effects, as well as hypotensive and venodilatative ones. Stroke volume was decreased in most observations. Prostaglandin E2 eliminated the attacks of cardiac asthma and angina pectoris, caused by the increase of the left ventricle cavity.
 ...
PMID:[Effect of intravenous prostaglandin E2 administration on central hemodynamics in ischemic heart disease patients]. 695 70

The roles of PGI2 and TXA2 in recurring reduction of carotid artery and cerebral blood flow induced by partial constriction of the common carotid artery and cerebral blood flow induced by partial constriction of the common carotid artery were examined in anesthetized dogs. The recurring reduction was eliminated by OKY 046 and 1580 which inhibit TX synthetase, acetylsalicylic acid which inhibits cyclo-oxygenase and lipoxygenase, PGI2 and by papaverine which enhances PGI synthesis. But the recurring reduction was not eliminated by phentolamine. The recurring reduction was induced by epinephrine which activates phospholipase A2 and cyclo-oxygenase and causes platelet aggregation. It was also induced by tranylcypromine which inhibits PGE2 synthetase and, although infrequently, by TXA2. The recurring reduction was also induced by indomethacin that inhibits cyclo-oxygenase. The indomethacin-induced recurring reduction, however, was eliminated not by OKY 046 and 1580 but by PGI2. It is suggested that TXA2 acted as an inducer and PGI2 as an inhibitor in the recurring reduction of carotid artery and cerebral blood flow.
Stroke
PMID:Role of prostaglandin I2 and thromboxane A2 in recurring reduction of carotid and cerebral blood flow in dogs. 702 92

Endogenous biosynthetic capacities for prostaglandin (PG)E2, thromboxane (TX)B2 (a stable degradation product of TXA2) and 6 keto-PGF1 alpha (a stable degradation product of PGI2) in the brain-stem fractions of stroke-resistant spontaneously hypertensive rats (SHRSR) and control Wistar-Kyoto rats (WKR) were determined with novel methods and presented in an original report. In comparison with WKR, it is characteristically found that TXB2 synthesis is increased in excess of threefold in the pons-medulla oblongata of SHRSR, while being decreased by 75% in the hypothalamic region of SHRSR (0.01 less than p less than 0.05). On the other hand, the biosynthesis of PGE2 is adaptively elevated in both hypothalamus and pons-medulla oblongata regions of each animal, although the PGI2/PGE2 ratio was lowered in both these regions of SHRSR.
 ...
PMID:Metabolic alterations in the endogenous formation of 6 keto-prostaglandin F1 alpha, thromboxane B2 and prostaglandin E2 in the brain-stem of stroke-resistant spontaneously hypertensive rats. 722 40


<< Previous 1 2 3 4 5 6 7 Next >>