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

Nimodipine is a calcium slow channel blocker with several pharmacologic properties suggesting the potential to favorably modify outcome in focal cerebral ischemia. Thirty adult cats underwent unilateral middle cerebral artery (MCA) occlusion for 4 hours. Seventeen cats were treated with an ipsilateral intracarotid infusion of nimodipine (1 microgram kg-1 min -1) beginning 15 minutes before MCA occlusion and continuing throughout the occlusion period. Eight nimodipine treated cats maintaining MAP greater than 90 mmHg were assigned to a Higher Pressure Nimodipine (HPN) group. The remaining nine treated cats with MAP less than 90 mmHg were assigned to the Lower Pressure Nimodipine (LPN) group. Thirteen cats were untreated, receiving an isovolumetric amount of vehicle through the ipsilateral carotid artery. Local cerebral blood flow (ICBF) was continuously monitored using thermal diffusion probes. The brains, assessed for colloidal carbon perfusion, fluorescein and Evans blue staining, electroencephalographic activity (EEG), and histological changes, revealed no significant differences by any of these methods between the HPN and control animals with the exceptions of: HPN treated cats exhibited a preservation of EEG activity at 15 minutes post-occlusion compared to the untreated cats, and Post-ischemic surface colloidal carbon perfusion was better preserved in the treated cats than in the untreated cats. Mild hypotension, as demonstrated by the LPN group, negated these two positive effects. Prior to MCA occlusion, ICBF was bilaterally significantly increased after nimodipine infusion in the HPN group as compared to vehicle infusion. Intra-arterially infused nimodipine did not reduce infarct size.
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PMID:Effects of nimodipine on acute focal cerebral ischemia. 376 59

Nitroglycerin improves perfusion to ischemic myocardial regions and therefore has theoretical advantages over sodium nitroprusside to treat hypertension (mean arterial pressure [MAP] greater than 95 mm Hg) following coronary bypass operation. Thirty-three hypertensive patients were randomized to an initial infusion of either nitroglycerin or nitroprusside in a crossover trial designed to reduce MAP to 85 mm Hg. Thermodilution cardiac output measurements permitted calculation of left ventricular stroke work index (LVSWI), and nuclear ventriculograms permitted estimation of left ventricular ejection fraction, left ventricular end-diastolic volume index (LVEDVI), and left ventricular end-systolic volume index (LVESVI). Coronary sinus blood flow was measured by the continuous thermodilution technique, and arterial and coronary sinus lactate measurements permitted calculation of myocardial lactate flux (MVL). Both nitroglycerin and nitroprusside reduced MAP (-25 +/- 12 mm Hg and -20 +/- 10 mm Hg, respectively; not significant [NS]). Nitroglycerin reduced LVSWI more than did nitroprusside (-15 +/- 13 gm-m/m2 and -7 +/- 9 gm-m/m2, respectively; p less than 0.01). Both agents increased left ventricular ejection fraction (nitroglycerin, +8 +/- 8%, and nitroprusside, +10 +/- 7%; NS), and decreased LVEDVI (-20 +/- 22 ml/m2 and -11 +/- 17 ml/m2, respectively; NS) and LVESVI (-13 +/- 14 ml/m2 and -10 +/- 12 ml/m2, respectively; NS). Coronary sinus blood flow decreased with both drugs (NS), but MVL increased with nitroglycerin (+0.02 +/- 0.14 mmol/min) and decreased with nitroprusside (-0.02 +/- 0.02 mmol/min) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of nitroglycerin and nitroprusside: I. Treatment of postoperative hypertension. 391 59

Molsidomine--a new vasodilator agent with predominant venous effect--is used for the treatment of coronary artery disease. Haemodynamic effects of i.v. molsidomine (300 micrograms X kg-1) during deliberate hypotension were investigated in 11 dogs and compared with nitroglycerin-induced-hypotension, at the same decrease in MAP (-25%). Hypotension was only obtained in 5 dogs with both drugs. Hypotension resulted from decrease in stroke volume due to a decrease in preload. Decrease in systemic vascular resistance and tachycardia were less important with molsidomine than with nitroglycerin. After molsidomine MAP decreased progressively over 30 minutes.
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PMID:[Hypotension induced by molsidomine or trinitroglycerin]. 393 64

The media cross-sectional area, the media thickness, the internal radius and the ratio between media thickness and internal radius were determined in consecutive sections of extraparenchymal cerebral arteries of 7- and 12-month-old normotensive and spontaneously hypertensive rats. The study included intracranial pial and basal arteries as well as extracranial cervical arteries. In the chronically hypertensive rats the media to radius ratio was consistently higher than in normotensive rats over the entire calibre spectrum investigated (radius 5-400 micron). The increase of the ratio in the extracranial arteries of the hypertensive rats was exclusively due to a thicker media. In the basal intracranial arteries the increase of ratio was due to a thicker media and/or a smaller internal radius in 7- and 12-month-old rats with moderate hypertension (mean arterial pressure, MAP 171 +/- 8 and 177 +/- 7 mm Hg respectively). In 7-month-old rats with severe hypertension (MAP 204 +/- 11 mm Hg) the increase of ratio was mainly due to a smaller internal radius. The observed structural alterations are likely to be of hemodynamic importance.
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PMID:The morphometry of consecutive segments in cerebral arteries of normotensive and spontaneously hypertensive rats. 397 70

The hemodynamic and cardiometabolic effects of dopamine were evaluated in propoxyphene-induced circulatory shock in eight pentobarbital anesthetized pigs. Circulatory shock was induced by an infusion of propoxyphene chloride 15 mg . min-1 i.v. At shock, i.e. CI less than or equal to 2.0 l . min-1 . m-2 and/or MAP less than or equal to 60 mmHg, dopamine was infused at 10, 20, 40, 80 and 160 micrograms . kg-1 . min-1 with an interval between increments of 8 min. After 30 min at 160 micrograms . kg-1 . min-1, the infusion rate was reversibly decreased. The propoxyphene infusion of 15 mg . min-1 was continued throughout the study. Dopamine improved the circulation in seven animals; one animal died in refractory shock during dopamine infusion. Dopamine infusion at shock level resulted in an increase of the following variables (% of baseline value): MAP (69%), HR (109%), CI (138%) and SVI (129%). Normalisation was seen in MRAP (120%) and in MPAOP (100%). A profound decrease in systemic vascular resistance was unchanged. Increases were seen in left and right ventricular stroke work index, to 88% and 176% of baseline, respectively. Left ventricular dP/dt increased (170%). In the coronary circulation myocardial blood flow increased (133%) as did myocardial oxygen consumption (65%) concomitant with a decrease in myocardial oxygen uptake (41%), but coronary vascular resistance progressively decreased (38%). The myocardial propoxyphene extraction changed from +54% to -86% during peak dopamine infusion. In conclusion, dopamine reversed cardiac failure in propoxyphene overdose by a marked positive inotropic stimulation restoring contractility. A marked positive chronotropic stimulation maintained a sufficient cardiac index and a normal blood pressure in spite of a profound vasodilatation which was unresponsive to dopamine.
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PMID:The effects of dopamine on central hemodynamics and myocardial metabolism in experimental propoxyphene-induced shock. 406 Oct 11

Twelve males with moderately severe essential hypertension (mean arterial pressure [MAP] ranging 113-162 mmHg) were studied at rest supine and sitting and during bicycle exercise (50, 100 and 150 W). Intraarterial blood pressure (BP), and heart rate (HR) were recorded continuously. Cardiac output (CO) was measured by dye dilution (Cardiogreen). After 6-8 months (enalapril dose 10-40 mg daily) patients were restudied. BP fell in all patients, at rest sitting from 184/107 mmHg to 150/87 (-19%) and during 100 W from 223/117 to 194/98 mmHg (p less than 0.001). Pretreatment total peripheral resistance index (TPRI) was greatly increased in all patients and fell from 4137 to 3651 dyn s cm-5 m2 (-16%) (p less than 0.05). No significant changes were seen in CO, HR or stroke volume. No side effects were seen. It is concluded that enalapril reduces BP in patients with moderately severe hypertension at rest and during exercise due to reduction in TPRI without significant changes in CO or HR.
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PMID:Long-term haemodynamic effects of enalapril at rest and during exercise in essential hypertension. 608 23

The haemodynamic effects of fazadinium were compared in two groups of elderly patients with class III functional heart failure about to undergo gastrointestinal surgery. Four patients were in sinus rhythm and four in atrial fibrillation. Following the assessment of baseline values fazadinium 1 mg kg-1 was injected i.v. and measurements obtained every 1 min for 15 min. In patients in sinus rhythm, fazadinium produced a decrease in total peripheral resistance, which was maximum at the 1st min (delta TPRI -738 +/- 88 dyn s cm-5 m2) and accompanied by a moderate decrease in arterial pressure (MAP -27 +/- 2.4 mm Hg) and cardiac index (delta CI -0.23 +/- 0.17 litre min-1 m-2) and a moderate increase in heart rate (delta HR +16 +/- 5.7 beat min-1). In patients in atrial fibrillation, a similar decrease in total peripheral resistance (delta TPRI -1160 +/- 174 dyn cm-5 m2) was accompanied by a significantly more pronounced tachycardia (delta HR +71 +/- 5.1 beat min-1) (P less than 0.001) and decreases in arterial pressure (delta MAP -51.7 +/- 5.9 mm Hg) (P less than 0.01) and stroke index (P less than 0.02).
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PMID:Influence of cardiac rhythm on the haemodynamic effects of fazadinium in patients with heart failure. 613 37

Cardiac function was studied in spontaneously breathing, adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). By rapid intravenous blood infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV) was determined while the cardiac nervous control was pharmacologically blocked. Since SV is greatly influenced by the level of afterload (mean arterial pressure, MAP), SV was also determined at increased MAP (constriction of abdominal aorta) and at decreased MAP (vasodilation by hydralazine). At low LVEDP levels, a rightward shift of the Frank-Starling relationship was observed in SHR. This rightward shift seems mainly to depend on the increased MAP present in SHR since it was less prominent if MAP was lowered to normotensive levels in SHR. Maximal SV during volume infusion was similar in SHR and WKY, despite a much higher MAP in SHR. When peak SV was instead compared at similar MAP levels for both (either at normotensive' or 'hypertensive' levels) it was always significantly greater in SHR, and was increased largely in proportion to their increased left ventricular weight. This indicates that the left ventricular hypertrophy present in SHR is, at least at this stage, a physiological adaptation of the heart to increase its performance, in order to maintain a normal SV and hence cardiac output, despite an increased arterial pressure.
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PMID:Left ventricular hypertrophy improves cardiac performance in spontaneously hypertensive rats. 621 29

Rats were subjected to a 30 minute period of combined hypoxia (F1o2 = .08) and hemorrhagic hypotension (MAP = 30 mm Hg), then resuscitated by restoration of F1o2 = .30 and reinfusion of shed blood and saline. Intracranial blood volume, hemoglobin saturation, and the cytochrome alpha, alpha 2 redox state were monitored through the intact skull during hypoxic hypotension and after resuscitation utilizing reflectance spectrophotometry. Although resuscitation returned arterial blood pressure, arterial pO2, and hemoglobin saturation toward normal, a sustained, significant (p less than .005) reduction in cytochrome alpha , alpha 2 remained. A parallel series of rats was subjected to identical hypoxic hypotension. At designated intervals the animals were sacrificed to determine brain ATP, ADP, and inorganic phosphate (P1). The data are discussed in terms of relationships between high energy phosphate metabolism and recorded changes in cerebral cytochrome alpha , alpha 2 redox state.
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PMID:Failure of brain cytochrome alpha , alpha 3 redox recovery after hypoxic hypotension as determined by in vivo reflectance spectrophotometry. 627 81

Ten patients were studied before, during and after enflurane anaesthesia for coronary vein grafting. All had good ventricular function and nine were receiving effective beta blockade. Cardiac output and vascular pressures were measured, plus coronary sinus blood flow (CBF), myocardial oxygen consumption (MVO2) and lactate extraction (MLE). Enflurane induction (10 minutes, mean 1.72 per cent end tidal) reduced blood pressure (MAP), due to decreased cardiac index (CI), with no change in heart rate or systemic resistance. Intubation returned MAP and CI to control level but the heart rate increased. Subsequently, enflurane kept MAP, CI and stroke work below the awake level. CBF decreased on induction, rose again on intubation and remained normal before bypass. MVO2 fell on induction from an increase in CS oxygen content, which remained elevated. Normal MLE continued in every patient. There was no evidence of myocardial ischaemia in patients on beta blockade, when haemodynamics were maintained at or below those of the sedated, awake state.
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PMID:Myocardial metabolism and haemodynamic responses with enflurane anaesthesia for coronary artery surgery. 633 14


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