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

The effects of Ca++ and Mg++ infusion on the cardiovascular system were studied in 96 normotensive subjects and 85 hypertensive patients. The results obtained were as follows: (1) The effects of Ca++ infusion on the systolic time intervals were characterized by the shortening of QS2I, PEPI, and ICT, and increase in ET/PEP. The responses of the systemic hemodynamics were elevation of mean blood pressure and increase in cardiac index and stroke index. The heart rate was not altered. (2) These results support that Ca++ has a positive inotropic action and increases the left ventricular performance. (3) The effects of Mg++ infusion on the systolic time intervals were characterized by the prolongation of QS2I, PEPI, and ECT. The responses of systemic hemodynamics were elevation of mean blood pressure and increase in heart rate. The ET/PEP and cardiac index tended to decrease, but these changes were not significant. (4) From these results it is suggested that Mg++ depress myocardial contractility and has a positive chronotropic action. (5) There were no significant differences in the systolic time intervals and hemodynamic responses to the infusion of Ca++ and Mg++ between normotensives and hypertensives.
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PMID:The effects of infusion of calcium and magnesium ions on the cardiovascular system in man. 65 Sep 6

Coronary and systemic circulations, and contractility and oxygen consumption of the left ventricular myocardium were depressed as arterial enflurane concentration increased in acute experiments with 22 adult mongrel dogs. Uneven transmural blood flow in the left ventricular free wall did not appear and the inner/outer ratio remained near 1.0 until a very deep stage of the anesthesia was attained and as far as diastolic aortic pressure was maintained above 40 mmHg, according to the microsphere injection study. Once diastolic pressure fell below 35--40 mmHg, the ratios started to be reduced significantly. When arterial enflurane content reached 53.0 +/- 2.1 mg/100 ml (mean +/- s.e.), the ratio became 0.84 +/- 0.08 (p less than 0.001), and simultaneously calculated DPTI/TTI ratio also showed a significant redution from the control (0.79 +/- 0.03, p less than 0.001). The I/O and DPTI/TTI ratios, however, did not correlate significantly with each other until very deep enflurane anesthesia was attained. The lower limit of autoregulation of coronary vascular bed was suggested to be near 35--40 mmHg of diastolic aortic pressure during deep enflurane anesthesia in the dog. Among systolic time intervals measured directly during the study, PEP and ICT showed significant negative correlations with Vmax and LV dp/dt max, while LVET neither changed nor correlated significantly with stroke volume or other parameters representing myocardial contractility during the course of enflurane anesthesia.
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PMID:Enflurane-induced hypotension modifies transmural blood flow distribution in the canine left ventricle. 73 52

Systolic time intervals and the a/H ratio were recorded in 20 patients with uncomplicated acute myocardial infarction over a period of five days. The initial high heart rate and systolic blood pressure and the short PEP and ICT indicating a sympathetic overactivity were spontaneously normalized during the first week of infarction. LVET was reduced indicating a fall in stroke volume and the a/H ratio was unchanged at the high levels suggestive of elevated preload or LVEDP. In 10 patients with acute myocardial infarction and recurrent chest pain recordings on noninvasive parameters were made before and 30 min after intravenous injection of practolol. In addition, 7 patients with chest pain, classified as acute myocardial infarction, were given practolol. The average dose of practolol was 17.9 mg ranging from 5 to 30 mg. An almost immediate and pronounced relief of pain was observed in all patients and no signs of impaired left ventricular function appeared. The product of systolic blood pressure and heart rate was decreased by practolol and the PEP and the ICT were prolonged to normal values while no changes were seen in LVET and a/H ratio. On 126 occasions practolol was given in dosages ranging from 5 to 30 mg (mean 8 mg) to 75 patients with acute myocardial infarction and recurrent chest pain. A satisfactory pain relief was seen on 108 occasions. It is suggested that an inappropriate sympathetic overactivity is an important factor in provoking recurrent chest pain in acute myocardial infarction. Administration of the beta-adrenergic blocking agent practolol resulted in pain relief due to reduction of heart work and in severity of myocardial ischemia. The beta-blocking agent was well tolerated in the present study. Continuous beta-blockade during the whole hospital stay to patients with acute myocardial infarction seems to be a very attractive therapy in order to preserve the ischemic myocardium and limit the size of infarction.
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PMID:Effect of cardioselective beta-blockade on heart function and chest pain in acute myocardial infarction. 106 28

The acute effects of ethanol (ETOH) on cardiac function in 32 normal subjects has been studied utilizing systolic time intervals. Seven (group I) 13 (group II), and 12 subjects (group III), reported an average daily consumption of less than 1 oz, 1-2 oz, and more than 2 oz of ETOH, respectively. Progressively higher control values from group I to group III in PEP, PEPI, ICT and PET/LVET were observed (PEP-I vs PEPI-III: P smaller than 0.05; PEP/LVET-I vs PEP/LVET-II and PEP/LVET-III: P smaller than 0.05). There was progressively less change in these variables following acute ETOH (P smaller than 0.02-0.05 in group I; P equals NS in group III, group II intermediate). This indicates some degree of chronic myocardial impairment in group II and especially in group III, which tends to be proportionate to the degree of chronic ETOH exposure. These data are not necessarily disparate with previous reports of little or even a salutary hemodynamic effect of ETOH in normal subjects. Thus, the relative stability of LVET post ETOH, coupled with the observed increase in heart rate, is consistent with previous reports of ETOH-induced rate-dependent increments in cardiac output with unchanging stroke volumes, in spite of the presence of acute myocardial depression. The observations reported herein demonstrate the probable incremental influence of ETOH consumption in a chain of events which may culminate in alcoholic cardiomyopathy.
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PMID:The basis for differences in ethanol-induced myocardial depression in normal subjects. 113 3

In animals without myocardial infarction the new beta-sympathicolytic agent atenolol (4-[2'-hydroxy-3'-iso-propylaminopropoxy]-phenyl acetamide, ICI 66 082) dose-dependently decreased heart rate, systolic aortic pressure and cardiac output. Coronary mean flow, coronary resistance, stroke volume, left ventricular enddiastolic pressure and total peripheral vascular resistance did not change significantly. Atenolol significantly reduced myocardial contractility, expressed by (dp/dtmax), Vpm, t-(dp/dtmax) and pre-ejection period. Furthermore, the comparative studies in animals with myocardial infarction and concomitant reduced cardial efficiency revealed, that atenolol has neither a positive intrinsic activity as has practolol nor a negative intrinsic activity as has propranolol. The dose-contractility relation of atenolol resembles that of practolol: in low dosages a strong decrease is achieved, in higher dosages no further reduction of the contractility parameters is observed. Because of the strong negative inotropic and blood pressure lowering effect it is suggested to use atenolol only with great caution in patients with reduced cardiac efficiency.
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PMID:[The effect of atenolol on contractility and hemodynamics of the infarcted heart in comparison to propranolol and practolol (author's transl)]. 124 85

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

Pharmacological and radio-ligand binding studies have recently indicated the existence of beta 2-adrenoceptors in the human heart. Their physiological role, however, remains to be elucidated. The present study investigated in 17 normal, young volunteers the effect on resting left ventricular (LV) function of two types of beta-blockers; a predominant beta 1-adrenoceptor antagonist (atenolol, 50 mg once daily) and ICI 118,551 (20 mg t.i.d.), a new, predominant beta 2-antagonist. LV function was assessed using M-mode echocardiograms and systolic time intervals. Atenolol, ICI 118,551, and placebo were given according to a randomized, double-blind, cross-over protocol. As compared with placebo, both drugs caused a decrease in resting heart rate, but the reduction by ICI 118,551 was less pronounced. Systolic blood pressure was only reduced by atenolol 8 mm Hg on average. Cardiac output was decreased to the same extent following treatment with atenolol (-20%) as after ICI 118,551 (-17%). These decreases in cardiac output were related to the beta-blocker-induced bradycardia, since stroke volumes were not affected during either selective beta 1- or beta 2-blockade. In addition, all other echocardiographic variables reflecting LV pump function, such as fractional shortening, velocity of diameter change and of displacements, pre-ejection period, and the ratio of PEP/LVET, were not different from placebo. We conclude that in normal young subjects, global LV pump function is not affected by beta 1- or by beta 2-blockade, despite the negative chronotropic effect of both drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of beta 1- versus beta 2-adrenoceptor blockade on left ventricular function in humans. 242 84

1. A bicycle exercise test was used to investigate functional capability and haemodynamics in 30 patients with heart failure (13 NYHA Class II, 17 Class III), before and after i.v. xamoterol (Corwin, Carwin, Corwil, Xamtol, ICI 118,587) 0.2 mg kg-1. 2. Resting heart rate fell from 78 to 74 beats min-1 (P less than 0.05) and cardiac index rose from 2.5 to 2.8 l min-1 m-2 (P less than 0.001) after xamoterol. Blood pressure fell slightly, and systemic vascular resistance was reduced. Stroke work index improved and double product decreased. There were no changes in pulmonary artery wedge pressure ejection fraction or plasma noradrenaline concentrations. 3. On exercise, xamoterol produced a considerable reduction in heart rate increase, improved stroke volume and left ventricular stroke index and lowered double product. Exercise duration increased by 10%, but this did not quite achieve statistical significance. 4. These results are consistent with the concept that a beta 1-partial adrenoceptor agonist with the level of intrinsic sympathomimetic activity (43%) of xamoterol provides moderate inotropic support at rest, and protects the heart against overstimulation on exercise, when sympathetic drive is high. 5. Reduction of double product on exercise implies a lowered oxygen demand, which could be of considerable importance in patients with ischaemic heart disease.
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PMID:Effects of xamoterol on resting and exercise haemodynamics in patients with chronic heart failure. 257 50

The effects of acute intravenous administration of ICI 118,587 (Corwin), a partial beta 1 agonist, were studied in nine patients with dilated cardiomyopathy and symptomatic congestive heart failure. Hemodynamic and metabolic parameters were measured using Swan-Ganz, arterial, and coronary sinus catheters. Repeated doses of Corwin produced no significant change in left ventricular performance, while a trend towards decreased blood pressure and stroke work was seen. No change occurred in coronary sinus blood flow, transmyocardial lactate extraction, or catecholamine release. One patient had significant depression of left ventricular function with hypotension. Thus, acute infusion of Corwin produced no beneficial inotropic responses, but rather produced features suggestive of further myocardial depression.
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PMID:Acute hemodynamic and metabolic effects of ICI 118,587 (Corwin), a selective partial beta 1 agonist, in patients with dilated cardiomyopathy. 286 73

ICI 141,292 is a new beta 1-adrenoceptor blocking drug. The beta 1-adrenoceptor antagonistic effect of ICI 141,292 was examined in a double-blind, randomised crossover study in eight healthy young volunteers and compared with atenolol. Three doses of ICI 141,292 (1, 2 and 4 mg) and atenolol 5 mg were administered intravenously. The attenuation in exercise induced tachycardia varied between 16.0 and 21.2% (P less than 0.01). A significant reduction in blood pressure could be demonstrated following all three doses of ICI 141,292 and atenolol during exercise. At rest in the sitting position HR decreased approximately 8% following all three doses of ICI 141,292 and 14.9% after atenolol 5 mg. No changes in blood pressure were observed under resting conditions after any of the drugs. In six patients with ischaemic heart disease the intrinsic sympathomimetic activity following intravenous administration of four sequential doses (0.5, 0.5, 1.0 and 2.0 mg) of ICI 141,292 was examined. HR decreased 7% (P less than 0.05) following ICI 141,292 1 mg with no further decrease following the succeeding doses. Cardiac output decreased 5.2% (P less than 0.05) following a cumulative dose of 4 mg. No significant changes were observed in mean arterial blood pressure, stroke volume or total peripheral resistance whereas an increase in supine resting mean pulmonary arterial pressure of 3.4 mm Hg (P less than 0.05) could be demonstrated. ICI 141,292 seems to be a potent (at least five times as potent as atenolol) beta 1-adrenoceptor blocking agent possessing moderate intrinsic sympathomimetic activity.
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PMID:Immediate haemodynamic effects of a novel partial agonist, beta 1-adrenoceptor blocking drug ICI 141,292 after intravenous administration to healthy young volunteers and patients with ischaemic heart disease. 288 Jun 3


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