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

While long term beta-adrenergic blockade, introduced in the convalescent stage of myocardial infarction, may reduce subsequent mortality, the value of early beta-blockade in the acute phase is less certain. Therefore, the influence of beta-blockade on left ventricular performance and eventual infarct size was assessed in 61 consecutive patients with acute myocardial infarction. Metoprolol (15 mg i.v. followed by 200 mg day-1 orally) or placebo was administered in a double-blind, randomised fashion with a median delay of 5.9 hours from onset of symptoms. After 15 days of double blind therapy all patients were started on open treatment with metoprolol. All patients underwent haemodynamic monitoring for 24 hours and serial radionuclide ventriculography and thallium 201 scintigraphy. In the first hour metoprolol produced a decrease in cardiac output (1.3 l min-1; P less than 0.001) due to a reduction in heart rate (15 min-1; P less than 0.001) and a decrease in left ventricular stroke work index (10.7 g m m-2; P less than 0.001) due to a reduction in mean arterial pressure (10 mmHg; P less than 0.001). There was then a gradual attenuation in these changes. While metoprolol produced an increase in pulmonary capillary wedge pressure and in both end-diastolic and end-systolic volumes (P less than 0.05), these changes were confined to patients with a baseline pulmonary capillary wedge pressure below the median of 13 mmHg mercury. There was no significant change in stroke volume or in ejection fraction in response to metoprolol. There was no significant difference between the groups in left ventricular performance, as assessed by radionuclide ventriculography, or in scintigraphic infarct size, either at the end of the 15 days double-blind treatment or after 3 months open treatment with metoprolol. Thus, early intervention with metoprolol in acute myocardial infarction appeared to reduce myocardial oxygen consumption with no adverse haemodynamic effect. However, metoprolol failed to preserve left ventricular function, or to reduce apparent infarct size. These data suggest that the modest reduction in mortality reported in the acute phase studies of beta-blockade in myocardial infarction, is unlikely to be due to infarct reduction. It is more likely to be due to a secondary prevention or to an antiarrhythmic effect.
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PMID:Beta-adrenergic blockade in acute myocardial infarction: a haemodynamic and radionuclide study. 331 55

Abnormalities of renin release and of venous distensibility have been described in essential hypertension. We have postulated that decreased venous distensibility could contribute to the blunted renin response to upright posture in hypertension. Stiffer veins might prevent venous pooling in the lower extremities, which in turn might affect the stretch on cardiopulmonary mechanoreceptors, thereby influencing the reflex release of renin. We investigated this hypothesis in the present study of 47 patients with mild hypertension and 26 (male) healthy volunteers of similar age and race. To induce isolated changes in the stretch of cardiopulmonary mechanoreceptors, systemic hemodynamics were measured before and after thigh cuff inflation at 60 mm Hg for 30 minutes. Cardiac output was determined by dye dilution. Before the intervention, variable thigh cuff pressures were used to measure venous pressure volume with mercury-in-Silastic strain gauge plethysmography. Venous distensibility was diminished in hypertension, as evidenced by a shift in the calf venous volume/pressure curve toward the pressure axis. During the 30-minute experiment, the hypertensive subjects had less blood pooling in their legs in response to thigh cuff inflation, as compared with the control subjects. The hemodynamic and renin responses reflected this diminished effect of thigh cuff inflation on venous return. The smaller increase of renin in the hypertensive group was associated with a smaller fall in the stroke index and right atrial pressure; the reflex rise in the heart rate was also decreased. By pooling blood in the lower extremities, thigh cuff inflation simulates upright posture. It is customary to classify the renin status of hypertensive patients according to the renin response to upright posture.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased venous distensibility and reduced renin responsiveness in hypertension. 352 19

The changes in pial arterioles of 7 cats were examined by electron microscopy after injury that eliminates endothelium-dependent relaxation to acetylcholine or bradykinin. The injury was produced by exposing the vessels to mercury light in situ in the presence of intravascular sodium fluorescein dye. Previous studies showed that, at the time of initial injury and loss of endothelium-dependent responses, the endothelial cells displayed minimal ultrastructural evidence of injury. Because these changes might indicate the beginning of a sequence of irreversible alterations representing or leading to cell death, the present study was carried out 31/2-4 hours later, when ultrastructural evidence of progressive cell degeneration should readily be recognized. No such changes were observed. Instead, most vessels showed only the minimal alterations observed initially (endothelial vacuolation, blebs, and lucencies). Four of 19 vessels were completely normal. The findings fail to support the hypothesis that irreversible cell damage or death caused by the light + dye injury has caused the associated loss of endothelium-dependent relaxation. Rather, the findings support the concept that much lesser degrees of trauma are sufficient to impair the dilating responses of cerebral microvessels. This greatly expands the potential spectrum of pathologic states that might result in loss of endothelium-dependent relaxation.
Stroke
PMID:Ultrastructural studies of pial vascular endothelium following damage resulting in loss of endothelium-dependent relaxation. 362 54

In two identical experiments, A and B, we studied the effect of the simultaneous l.v. injection of propranolol (Inderal, 0.5 mg/kg) on the circulatory effects of triiodothyronine (T3 500 microgram/kg i.v. 3 hours before measuring). The two substances act at different rates and so the blocking effect of propranolol preceded the development of the circulatory effects of T3. Cardiac output was measured by the Evans blue dilution method, the heart rate was calculated from the ECG recording and blood pressure was measured with a mercury manometer; stroke volume and total peripheral vascular resistance were also calculated. The isolated injection of T3 was followed by a significant increase in cardiac output (experiment A: 129%, B: 118%) and stroke volume (A: 125%, B: 118%) and by a drop in total peripheral vascular resistance (A: 82%, B: 85%). There was no change, in this early phase, in the heart rate or blood pressure. No changes were found 3 hours after the isolated administration of Inderal (the maximum effect of propranolol is attained in 30-60 min). During the same period, the above initial effects of T3 were completely suppressed by the simultaneous injection of Inderal. These results were probably related to the experimental conditions (early and not very marked changes after T3), but they demonstrate that the initial effects of T3 on cardiac performance and on the peripheral blood vessels can be completely suppressed by a block of beta receptors. From this it can be concluded that beta-adrenergic regulation is an important part of the mechanism of the early haemodynamic action of T3.
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PMID:Inhibition of the early circulatory effects of triiodothyronine in rats by propranolol. 645 55

Regional function parameters under myocardial ischemia are frequently clearly changed when the parameters as the stroke volume, cardiac output, ejection fraction and the like are still unchanged by a compensation mechanism. Length changes can be measured regionally and phasically by means of a mercury wire strain gauge. The active shortening during the ejection time in relation to the total length change in this region is a possibility for the registration of the relative systolic shortening (delta LS%). Changes will be quantified still clearer and earlier if in the x-y display a vector representation of the regional displacements with the pressure in the left ventricle takes place. The plane of this vector decreased already a few seconds after the coronary occlusion. This is therefore a special early change in ischemia. The important for the estimation of therapeutic measures and other indirect measuring methods is accentuated.
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PMID:[Evaluation of regional heart function by means of local changes in pressure and direction in the vector cardiogram]. 721 Jul 62

Aortic distensibility has been determined by non-invasive techniques: radioisotope measurement, quantitative radiocardiography and indirect arterial pressure measurement with calculation of the aortic rigidity index by the formula D = PP pulse (mm or mercury) / stroke volume (ml). The index value, equalling in normotensive subjects D = 0.55 was quite close to the value obtained in haemodynamic laboratories by invasive techniques (intracardiac stroke volume and arterial pressure measurements). Using the hereby determined aortic is rigidity index by non-invasive techniques, it was established that aortic distensibility is reduced since the early phases of arterial hypertension and in early age. Lowering of aortic distensibility correlates very well with diastolic pressure rise and with advancing age of patients with arterial hypertension. The aortic rigidity index, determined by non-invasive techniques, in suggested as an additional diagnostic and prognostic criterion in arterial hypertension.
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PMID:Determination of aortic distensibility and its variations in arterial hypertension. 724 60

A comparison of parallel measurements of body temperature with infrared tympanic thermometry (First Temp 2000A) in both ears and with rectal mercury thermometer were performed in 100 patients with stroke (n = 60) or spinal cord injury (n = 40). Agreement between the two methods of temperature determination was assessed by calculating limits of agreement within which 95% (+/- 2 SD) of the individual differences would fall. Ear temperature was on average 0.3 +/- 1.0 (2 SD) degrees C above rectal temperature (p < 0.01). The upper and lower limits of agreement between the two methods were -0.7 degrees C and +1.3 degrees C, respectively. Mean difference between ear temperature in right and left ear was 0.0 +/- 0.7 (2 SD) degrees C. According to these results tympanic membrane temperature measured with First Temp 2000A appears to give clinical significant erroneous readings, and should be used with caution.
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PMID:[Infrared tympanic thermometry--worse than reported?]. 827 48

Mental stress induces changes in hemodynamic variables and in the plasma level of many hormones and plasma peptides. These changes can be modulated by various drugs, eg, beta-blockers. In a double-blind, placebo-controlled crossover study, the authors evaluated the hormonal and hemodynamic changes during psychological stress and the effect of felodipine 10 mg (plain tablet). Eight male volunteers participated. Heart rate, blood pressures, and stroke volume were measured by ECG, mercury sphygmomanometer, and impedance cardiography. Catecholamines and atrial natriuretic factor in plasma were measured by electrochemical and radioimmunoassay techniques. A single dose of felodipine, 10 mg, exaggerates the heart rate decreases the left ventricular ejection time and augments the plasma level increment of noradrenaline. The stress-induced changes in other variables were not influenced by felodipine treatment. In conclusion, acute felodipine treatment influences the reflex activation of the sympathetic nervous system during psychological stress. In the treatment of patients, especially patients with heart disease, these findings could be important but further investigations in patients need to be done.
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PMID:Hormonal and hemodynamic changes following single-dose felodipine treatment during mental stress. 828 74

Clinical practice often conflicts with epidemiologic evidence in the management of blood pressure. Antihypertensive therapy is generally prescribed if blood pressure exceeds some arbitrary level, thus committing many persons with minimal cardiovascular risk to long-term drug therapy. By contrast, below that level, regardless of cardiovascular risk, blood pressure reduction is rarely sought. Epidemiologic data, however, consistently show a continuous, positive, linear relationship of the height of both systolic and diastolic blood pressure with the incidence of stroke and heart attack. No threshold level distinguishes those who will have a cardiovascular event from those who will not. In fact, most heart attacks and many strokes occur among persons with "normal" blood pressures. Observational experience suggests that benefit could be obtained from universal blood pressure reduction of even a few millimeters of mercury. This public health strategy can be augmented by identifying those individuals, at every level of blood pressure, whose risk for cardiovascular disease justifies the cost of pharmacologic intervention. Antihypertensive drug therapy will be most efficient and effective if directed at those who, by virtue of their constellation of risk factors or evidence of preclinical vascular disease, are likely to have a heart attack or stroke. The resulting redirection of clinical resources will spare many hypertensive persons whose absolute risk for a cardiovascular event is small, from life-long treatment. At the same time, other persons, currently classified as normotensive, will become candidates for blood pressure reduction because their cardiovascular risk is high.
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PMID:Blood pressure management: individualized treatment based on absolute risk and the potential for benefit. 825 86

The study group consisted of 8 men with congestive heart failure. They ranged in age from 33 do 63 years (mean 48). Three patients were in class III NYHA, five in class IV. Idiopathic cardiomyopathy was diagnosed in 6 patients, one individual displayed ischemic heart disease and one patient was after mitral and aortic-valve replacement despite a normally functioning prosthetic valve. L-dopa was given orally beginning with 250 mg every six hours until a total daily dose of 4.0 g was achieved with no side effects (patients additionally received 50 mg of pyridoxine hydrochloride). Afterwards L-dopa was withheld for 24-36 hours. Having completed this washout period, patients underwent right heart catheterization, with placement of a balloon-tipped thermodilution catheter in a pulmonary artery, so that balloon inflation allowed recording of the pulmonary capillary wedge pressure. Right atrial and pulmonary arterial pressures were monitored continuously. Systemic arterial pressure was measured by mercury manometer. Cardiac output was determined by the thermodilution technique. Rest and effort hemodynamic measurements were repeated before and one, three hours after administration of 1-dopa. The base-line hemodynamic values were consistent with the clinical presentation of severe congestive heart failure. The average cardiac index (CI-1/min/m2--rest--1.93; 25 Watt-3.1) and stroke volume index (SVI-m1/m2--rest--22.2; 25 Watt-32.0) were markedly lowered. Left ventricular filling pressure and pulmonary artery pressure were elevated. The systemic vascular resistance was significantly increased (SVR -j.W.--rest--22.7; 25 Watt-14.2). Administration of 1-dopa resulted in the increase in cardiac index and stroke volume index accompanied by a substantial reduction in systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamic effects of one administration of l-dopa in patients with left ventricular heart failure (introductory remarks)]. 836 41


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