scholarly journals THE COMPARATIVE EFFECTS OF SMALL INTRAVENOUS DOSES OF L-NOR-EPINEPHRINE UPON ARTERIAL PRESSURE AND PULSE RATE IN NOR-MOTENSIVE SUBJECTS AND IN HYPERTENSIVE PATIENTS BEFORE AND AFTER THORACOLUMBAR SYMPATHECTOMY

1950 ◽  
Vol 29 (10) ◽  
pp. 1414-1420 ◽  
Author(s):  
Walter E. Judson ◽  
Franklin H. Epstein ◽  
Robert W. Wilkins
1964 ◽  
Vol 206 (2) ◽  
pp. 289-293 ◽  
Author(s):  
H. L. Stone ◽  
V. S. Bishop ◽  
A. C. Guyton

Chronic heart failure was produced by giving 20,000 r Co60 irradiation to either the right or left ventricle in nine closed-chest animals. Measurements of right and left atrial pressures, arterial pressure, pulse rate, body weight, and blood volume were made before and after irradiation. The right and left atrial pressures rose progressively until death in three animals irradiated on the right side. In six animals irradiated on the left side, the left atrial pressure rose progressively, but the right atrial pressure either did not rise or rose only during the latter stages of failure. Declining arterial pressure and increasing pulse rate were common to both groups. Increases in blood volume were observed in all animals, but this increase was only significant in the group irradiated on the left side. At autopsy, 70–100% of the right ventricular muscle was damaged in dogs irradiated on the right side, and 40–70% of the left ventricle in dogs irradiated on the left side. Hydrothorax and liver congestion were found in the right-sided group and pulmonary congestion in the left-sided group.


1978 ◽  
Vol 55 (s4) ◽  
pp. 329s-332s ◽  
Author(s):  
A. J. Man in 't Veld ◽  
G. J. Wenting ◽  
R. P. Verhoeven ◽  
M. A. D. H. Schalekamp

1. Haemodynamic responses to diazoxide (300 mg intravenously) were studied in 15 hypertensive patients before and after chronic β-adrenoreceptor blockade by 320 mg of propranolol daily. After diazoxide alone, mean arterial pressure and total peripheral resistance were lowered by 24 ± 3 and 35 ± 5% (mean ± sem) respectively. Cardiac output and heart rate rose by 25 ± 9 and 21 ± 3%. During β-adrenoreceptor blockade, the percentage changes of mean arterial pressure, heart rate, cardiac output and total peripheral resistance after vasodilatation were not significantly different from those after diazoxide alone. 2. Atropine, 0·04 mg/kg body weight, was given to 12 hypertensive patients chronically treated with β-adrenoreceptor blockade, before acute vasodilatation by diazoxide. Diazoxide caused no increase in heart rate after combined β-adrenoreceptor and parasympathetic blockade. However, cardiac output rose by 14 ± 5%. 3. We conclude that withdrawal of parasympathetic tone is an important determinant of circulatory homeostasis after acute vasodilatation during β-adrenoreceptor blockade.


2011 ◽  
Vol 8 (2) ◽  
pp. 26-31
Author(s):  
S D Oshorova ◽  
Tatyana Ivanovna Romantsova ◽  
T E Morozova

The aim of the study was to investigate the pharmacodynamic characteristics of the modern antihypertensive therapy in obese hypertensive patients. Materials and methods. The activity of leptin, adiponectin and endothelin-1 and cardiohemodynamics were studied in 61 patients with essential hypertension and obesity (body mass index 34,3±4,8 kg/m2) before and after the 12-weeks treatment with zofenopril (n=31) and nebivolol (n=29). Results. It was revealed that obese hypertensive patients had abnormal circadian profile of blood pressure (63.9%), hyperleptinemia together with the decrease of the adiponectin activity (67%), as well as the increased activity of endothelin-1 (54%). The 12-weeks therapy with zofenopril and nebivolol has resulted in the improvement of the daily profile of the arterial pressure with the achievement of the target level of the arterial pressure in 72% and 79% of patients correspondingly. The following was recorded: the decrease in the activity of leptin and endothelin-1 in both groups; upward trend of the adiponectins activity under the influence of zofenopril. Conclusion. Zofenopril and nebivolol in obese hypertensive patients in addition to the antihypertensive action reduce negative cardiometabolic effects of the activation of adipocytes and endothelin-1.


1978 ◽  
Vol 55 (s4) ◽  
pp. 77s-80s ◽  
Author(s):  
O. Kuchel ◽  
N. T. Buu ◽  
TH. Unger ◽  
J. Genest

1. Noradrenaline and adrenaline in the adrenal vein of essential hypertensive patients are almost exclusively (99%) unconjugated or free. However only 17% of dopamine is free, the rest is conjugated. The further the site of sampling from the adrenal vein the closer come the free catecholamines to their normal peripheral venous proportion (noradrenaline + adrenaline 20%, dopamine less than 1% of total catecholamines). Deviations from these patterns help to detect the site and type of secretion of phaeochromocytoma. 2. Essential hypertensive patients have, compared with control subjects, higher conjugated plasma dopamine, less urinary free and conjugated dopamine with blunted urinary free dopamine and sodium responsiveness to frusemide. Conjugated noradrenaline + adrenaline, mean arterial pressure and age are positively interrelated. 3. Patients with primary aldosteronism have elevated plasma and urinary total dopamine. After removal of the adenoma urinary dopamine excretion decreases to normal. 4. Elevated conjugated dopamine appears to reflect a compensatory activation of the dopaminergic vasodilator pathway in hypertension, the total urinary dopamine excretion an intrinsic deficiency or compensatory increase of a dopamine-modulated natriuretic mechanism.


2010 ◽  
Vol 30 (11) ◽  
pp. 1883-1889 ◽  
Author(s):  
Allyson R Zazulia ◽  
Tom O Videen ◽  
John C Morris ◽  
William J Powers

Studies in transgenic mice overexpressing amyloid precursor protein (APP) demonstrate impaired autoregulation of cerebral blood flow (CBF) to changes in arterial pressure and suggest that cerebrovascular dysfunction may be critically important in the development of pathological Alzheimer's disease (AD). Given the relevance of such a finding for guiding hypertension treatment in the elderly, we assessed autoregulation in individuals with AD. Twenty persons aged 75±6 years with very mild or mild symptomatic AD (Clinical Dementia Rating 0.5 or 1.0) underwent 15O-positron emission tomography (PET) CBF measurements before and after mean arterial pressure (MAP) was lowered from 107±13 to 92±9 mm Hg with intravenous nicardipine; 11C-PIB-PET imaging and magnetic resonance imaging (MRI) were also obtained. There were no significant differences in mean CBF before and after MAP reduction in the bilateral hemispheres (−0.9±5.2 mL per 100 g per minute, P=0.4, 95% confidence interval (CI)=−3.4 to 1.5), cortical borderzones (−1.9±5.0 mL per 100 g per minute, P=0.10, 95% CI=−4.3 to 0.4), regions of T2W-MRI-defined leukoaraiosis (−0.3±4.4 mL per 100 g per minute, P=0.85, 95% CI=−3.3 to 3.9), or regions of peak 11C-PIB uptake (−2.5±7.7 mL per 100 g per minute, P=0.30, 95% CI=−7.7 to 2.7). The absence of significant change in CBF with a 10 to 15 mm Hg reduction in MAP within the normal autoregulatory range demonstrates that there is neither a generalized nor local defect of autoregulation in AD.


1999 ◽  
Vol 276 (1) ◽  
pp. H27-H32 ◽  
Author(s):  
Jennifer M. Kulics ◽  
Heidi L. Collins ◽  
Stephen E. DiCarlo

Mean arterial pressure (MAP), the product of cardiac output (CO) and total peripheral resistance (TPR), is reduced below preexercise levels after a single bout of mild to moderate dynamic exercise. Thus acute, dynamic exercise may be used as a safe, therapeutic approach to reduce MAP. However, the mechanisms responsible for the postexercise hypotension (PEH) are unknown. We tested the hypothesis that PEH is associated with reductions in TPR and sympathetic nerve activity (SNA). Two experimental protocols were designed to test this hypothesis in male spontaneously hypertensive rats (SHR). In protocol 1( n = 9), CO and TPR were determined before, during, and after exercise. In protocol 2 ( n = 7), lumbar SNA (LSNA) was recorded before and after exercise. Rats in protocol 1 were chronically instrumented with left carotid arterial catheters and ascending aortic Doppler ultrasonic flow probes. Rats in protocol 2 were chronically instrumented with left carotid arterial catheters and electrodes around the lumbar sympathetic trunk. Dynamic treadmill exercise (9–12 m/min, 10% grade for 40 min) resulted in a postexercise reduction in MAP (from 143 ± 5 to 128 ± 4 mmHg, P < 0.05). Associated with the PEH was a reduction in TPR (from 28 ± 3 to 19 ± 2 mmHg/kHz; P < 0.05) and an elevation in CO (from 5.7 ± 0.4 to 7.2 ± 0.5 kHz; P < 0.05). The reductions in arterial pressure and TPR were associated with a decrease in LSNA (from 98 ± 3 to 49 ± 6%; P < 0.05). These results suggest that PEH is mediated by reductions in TPR and SNA.


1964 ◽  
Vol 19 (5) ◽  
pp. 919-927 ◽  
Author(s):  
Loring B. Rowell ◽  
Henry L. Taylor ◽  
Yang Wang

The predictability of maximal O2 intake (max Vo2) was studied in four groups of normal men, 18–24 years of age. Prediction of max Vo2 was made from pulse rate and Vo2 at a single submaximal workload at an ambient temperature of 78 F by use of the nomogram of Åstrand and Ryhming (1954) and underestimated actual max Vo2 by 27 ± 7% and 14 ± 7% in a sedentary group, before and after 2frac12–3 months of physical training, and by 5.6 ȁ 4% in a group of ten endurance athletes. Accuracy of prediction in all groups varied with approximation of pulse rate to 128 beats/min at 50% of max Vo2. Nonspecific stresses increased predictive errors in all groups. Constants b (slope) and A (intercept) in the regression equation Vo2 = bP – A (where P is pulse rate), were determined from Vo2 and pulse measured at four submaximal workloads requiring 13–28 ml O2/kg min. Prediction of max Vo2 by extrapolation of the slope to maximal pulse rate resulted in underestimation of 700–800 ml O2/min. Removal of 14% of circulating hemoglobin decreased max Vo2 by 4% but there was no change in pulse rates or predicted max Vo2. The relationship of RQ to V22 during work provided no reliable basis for prediction of max Vo2. exercise pulse rate, oxygen intake, relationship; pulse rate, oxygen intake relationship in exercise; metabolic rate, maximal aerobic prediction of; aerobic metabolic rate, maximal, prediction of; phlebotomy, effect on maximal oxygen intake, pulse rate; blood loss, effect on maximal oxygen intake, pulse rate; training, effect on maximal oxygen intake, pulse rates; physical conditioning, effect on maximal oxygen intake, pulse rates Submitted on October 4, 1963


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