PubMed Health⌕ Search

Biomedical subjects

A Polese

Publications and source records attributed to A Polese.

At least 55 records · Page 3Linked to original sources
PubMed1985

Effects of exercise-heat acclimation on fluid, electrolyte, and endocrine responses during tilt and +Gz acceleration in women and men.

Plasma fluid, electrolyte, protein, renin, and vasoactive hormone (epinephrine, norepinephrine, vasopressin) responses were measured in six women (21-23 yr) and four men (21-38 yr) before and immediately following an orthostatic tolerance test (70 degrees head-up tilt) and a +Gz (head-to-foot) acceleration tolerance test (0.5 G X min-1 linear ramp to grayout). These tests were conducted before and after 12 consecutive days of exercise-heat acclimation when the subjects exercised on a cycle ergometer at a relative oxygen uptake of 44% to 49% peak oxygen uptake in a hot environment (Ta = 40 degrees C, 42% rh). During acclimation plasma volume increased by 10.6% (p less than 0.05) in the women and by 11.9% (p less than 0.05) in the men; in both groups exercise heart rate decreased significantly. After acclimation, acceleration tolerance was unchanged in both groups (range 3.1 to 3.4 G); the women's tilt tolerance was unchanged (range 33.6 to 39.5 min), but the men's tilt tolerance increased from 30.4 min before to 58.3 min (delta = 91%, p less than 0.05) after acclimation. Since the pattern of fluid, electrolyte, and protein shifts and acceleration tolerances in the women and men were virtually the same, the hormone responses were highly variable, and the men's tilt tolerance increased significantly after acclimation, it is clear that responses to tilting cannot be used to predict responses to acceleration. Analysis of data from the present study and the literature suggests that current exercise training regimes should be unrestricted for astronauts who have not previously been highly endurance trained.(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗
PubMed1982

Circulatory response to prenalterol in normal subjects and in patients with primary congestive cardiomyopathy.

Experimental pharmacology indicates that prenalterol is a selective beta 1-adrenoceptor activator. In 5 normal individuals, 15 minutes after the drug (infused at a dose of 15 micrograms/kg over 5 min) the following circulatory changes were seen: a) increase of cardiac index (+31%), heart rate, stroke index, systolic aortic pressure, left and right ventricular mean rate of ejection and mean rate of the pressure rise in either ventricle during the pre-ejection phase; b) reduction of systemic vascular resistance (-18%), appearance, built-up and disappearance times in the left ventricular dye dilution curves. Pulmonary systolic, diastolic and wedge pressures and vascular resistance did not vary consistently. The circulatory effects persisted almost unchanged 30 minutes after the infusion. In a group of 5 patients with heart failure due to primary congestive cardiomyopathy, refractory to conventional therapy, the haemodynamic response to prenalterol (infused at a dose of 30 micrograms/kg over 5 min) was qualitatively similar to that of normal subjects in 3 cases. In 2 other patients cardiac performance deteriorated. The reasons for this paradoxical effect were not identified. These preliminary results suggest that prenalterol is a potent selective inotropic agent in man, that may assist in the therapeutic management of refractory heart failure due to congestive cardiomyopathy. However, careful haemodynamic monitoring is advisable for its use in this dysfunction until broader clinical experience can be accumulated.

Adrenergic beta-Agonists↗
PubMed1982

Evidence of a shared mechanism of vasoconstriction in pulmonary and systemic circulation in hypertension: a possible role of intracellular calcium.

We investigated the hemodynamics of the greater and lesser circulation in 35 patients with primary hypertension, as well as the effects of calcium-channel blockade, to test whether a common factor may account for the excessive vascular resistance in the two circuits and whether intracellular calcium concentration ([Ca++]i) may be involved. We proved that (1) elevated pulmonary arteriolar resistance (PAR) is not related to pulmonary blood flow and volume, pleural pressure, arterial oxygen or carbon dioxide tension and pH, left ventricular filling pressure and function; (2) systemic vascular resistance (SVR) significantly correlates with PAR; (3) calcium-channel blockade with nifedipine reduces systemic and pulmonary arterial pressures toward normal and significantly lowers both SVR and PAR; (4) the percent decrease in vascular resistance after nifedipine is related to the baseline level of resistance in both the greater and the lesser circulations. Failure of the mechanisms currently indicated as responsible for pulmonary vasoconstriction to explain convincingly the increased PAR, the correlation between SVR and PAR, as well as the qualitatively similar response to calcium-channel blockade suggest that a common factor produces vasoconstriction in the two circuits. A pathogenetic role of a primary disorder in [Ca++]i cannot be excluded, but remains to be proved.

Blood Pressure↗
PubMed1980

Cardiac performance in hypertension re-evaluated through a combined haemodynamic ultrasonic method.

From echocardiographic measurements, 39 patients with established, uncomplicated primary hypertension (diastolic pressure > 100 mmHg) were classified as follows: normal-sized heart (group 1, 10 cases); concentric left ventricular hypertrophy (group 2, 18 cases); left ventricular hypertrophy and cavity enlargement (group 3, 11 cases). Eighteen age-matched healthy subjects were investigated as a control group. Systolic and diastolic arterial pressure increased progressively from group 1 to 2 to 3. Left ventricular function, assessed from the relation between diastolic diameter and stroke index, was maintained in group 1, increased in group 2 (in spite of the greater pressure load), and reduced in group 3, in comparison with controls. Similarly, the mean velocity of circumferential fibre shortening (VCF) was normal in group 1, significantly increased in group 2, and reduced in group 3. It was impossible to discern whether the different behaviour of VCF in group 2 and in group 3 reflected opposite changes in ventricular contractility, or in wall stress during ejection, or in both. At variance with previous conclusions (which were based on utilisation of electrocardiographic and chest x-ray criteria to define hypertrophy) it is suggested that left ventricular concentric hypertrophy in man consequent to sustained hypertension is associated with an improved function. Whether this feature depends upon an augmented contractility or a ventricular unloading effect related to hypertrophy remains uncertain.

Cardiac Catheterization↗
PubMed1979

Cardiac load and function in hypertension. Ultrasonic and hemodynamic study.

On the basis of echocardiographic measurements, 46 patients with established, uncomplicated primary hypertension (diastolic pressure = 100 mm Hg) were classified as: those with a normal-sized heart (Group I, 13 patients); those with left ventricular concentric hypertrophy (Group II, 19 patients); and those with left ventricular hypertrophy and enlargement (Group III, 14 patients). Eighteen age-matched healthy subjects were investigated as the controls. The function of both the left and right ventricle, evaluated by the stroke index-filling pressure relation and by the mean rate of ejection, was maintained in Group I, augmented in Group II and reduced in Group III, in comparison with the controls. Left ventricular mean rate of circumferential fiber shortening (Vcf) was normal in Group I, significantly augmented in Group II and definitely reduced in Group III. It could not be established whether the divergent variation from normal of the Vcf in Groups II and III reflected opposite changes in ventricular contractility or in afterload (wall stress during ejection), or both. However, the parallel functional pattern of the right and left ventricle in these two groups suggests a functional interdependence of the two sides which cannot be interpreted in terms of afterload but is best explained by changes in the contractile state of the whole heart.

Aging↗
PubMed1979

Clinical use of a calcium antagonistic agent (nifedipine) in acute pulmonary edema.

Nifedipine induces vascular smooth muscle relaxation through a calcium antagonistic action. The possibility of clinical use of the drug as a ventricular unloading agent has been explored in this study. In patients with hypertensive (seven cases), primary (seven cases) or rheumatic (aortic insufficiency five cases, mitral regurgitation five cases) cardiac disease, nifedipine, administered in a single sublingual dose (10 mg), relieved acute pulmonary edema. Circulatory variations from control were the following: decrease of systemic and pulmonary arterial pressures, and of vascular resistances, of pulmonary wedge pressure, of left ventricular diastolic and systolic dimensions (echocardiography); increase of cardiac and stroke index, of left ventricular mean rate of circumferential fiber shortening, of left and right mean pre-ejection delta P/delta t and mean rate of ejection; improvement of forward output in primary and rheumatic disease. Nifedipine benefits acute congestive heart failure by sustained fall of both preload and afterload and, possibly, by an enhanced contractility. It seems to have an appropriate indication in cases in which left ventricular afterload reduction is desirable.

Adult↗
PubMed1979

Treatment of hypertension with nifedipine, a calcium antagonistic agent.

Hemodynamic monitoring after a single dose (10 mg) of nifedipine in 27 primary hypertensive subjects (diastolic pressure greater than 110 mm Hg) documented that this calcium antagonistic agent exerts a potent arteriolar vasodilating action, which results in prompt (-21% of control at 30 minutes) and persistent (-16% of control at 120 minutes) fall in mean arterial pressure associated with a rise in cardiac output and pulse rate. The same patients received oral treatment for 3 weeks. Hourly pressure readings showed that 1) the antihypertensive response to each dose lasts 8--12 hours; and 2) nifedipine every 6 hours significantly reduced blood pressure throughout the 24 hours, without postural hypotension. Side effect were short-lasting (headache in five patients, palpitation without arrhythmias in eight patients, burning sensation in the face and legs in five patients and sporadic extrasystoles in five patients) and tended to disappear with continued treatment. Development of drug resistance, sodium retention, plasma volume expansion, renin release or angina pectoris were not observed during the study. Although these findings seem to differentiate nifedipine from other vasodilators currently used in the treatment of hypertension, broader experience and more prolonged trials with nifedipine as an antihypertensive agent will be needed before conclusions can be drawn on these particular aspects.

Administration, Oral↗
PubMed1979

Echocardiographic and hemodynamic correlates in Prinzmetal angina pectoris: a case report.

In a patient suffering from Prinzmetal angina pectoris, ischemic attacks of the anterior left ventricular wall were associated with the following changes: fall in cardiac output; increased left ventricular diastolic pressure (LVDP) and volume; flattening of the septal motion; marked reduction of the mitral valve early diastolic amplitude and rate of opening; and marked reduction of the systolic closure velocity. It is suggested that LVDP rise depends, at least in part, on variations in left ventricular diastolic volume and segmental wall motion, and that disruption of the mitral valve motion derives from changes in LVDP and flow through the mitral orifice.

Angina Pectoris↗
PubMed1978

Haemodynamic effects of a calcium antagonistic agent (nifedipine) in hypertension: therapeutic implications.

1. In 27 severe primary hypertensive patients nifedipine (10 mg), administered orally, induced prompt (-21% of control at 30 min) and persistent (-17% at 120 min) fall of mean arterial pressure mediated through reduction of peripheral vascular resistance with rise of cardiac output. 2. The sublingual route (nine cases) showed more rapid onset of action and equal antihypertensive effectiveness. 3. In five patients with hypertensive crisis and acute left ventricular failure, the drug strikingly reduced systemic and pulmonary arterial pressures and relieved pulmonary oedema. 4. Prompt efficacy, ease of administration, absence of important side effects indicate that nifedipine may be a useful therapeutic agent in severe hypertension and in critical conditions that require rapid lowering of blood pressure.

Hemodynamics↗
PubMed1978

Pulmonary hemodynamics and right ventricular function in hypertension.

Pulmonary and systemic hemodynamics in 16 hypertensive subjects (group I) with left ventricular (LV) hypertrophy (ECG and echo criteria) and in 17 hypertensive subjects with ECG signs of LV strain (group II), were compared with those in 14 normal individuals. An augmented pulmonary arteriolar resistance (PAR) in group I and to a larger extent in group II accounted for the pulmonary pressure elevation in both groups. Increase in PAR was unrelated to pulmonary blood flow and volume, pleural pressure, arterial PO2, PCO2 and pH, and could not be explained entirely by the left ventricular end-diastolic pressure changes. In group I, left (L.MSEJR) and right (R;MSEJR) mean systolic ejection rate, stroke index (SI) and mean velocity of circumferential fiber shortening (VCF) were enhanced in spite of the heightened pressure load on both sides of the heart. In group II, a large reduction of SI, L.MS.EJR, R.MSEJR and VCF, as well as the relationship between ventricular filling pressures and SI, documented a compromised performance of both ventricles, Findings indicate that: systemic hypertension is associated with elevation of pulmonary arterial pressure and of PAR which is not necessarily a consequence of impairment in LV function; LV hypertrophy is associated with enhanced performance of either ventricle; in coincidence with development of ECG signs of LV strain, the performance of both sides of the heart deteriorates. A functional interdependence of the two ventricles is suggested.

Blood Pressure↗
PubMed1978

Influences of the adrenergic nervous system on the repolarization phase of the electrocardiogram.

The following conclusions can be drawn : (1) The nervous outflow to the heart may be varied from the baseline to opposite directions by different stressful stimuli. (2) ST-T alterations may be induced and abolished by adrenergic activation and inhibition respectively. (3) These effects are dissociated from or not necessarily associated with an exaggerated responsiveness of the cardiac beta receptors. (4) The adrenergic influences on the ST-T abnormalities of myocardial ischemia and hypertension are limited.

Coronary Disease↗
PubMed1977

Nifedipine, a new antihypertensive with rapid action.

Oral (17 cases) or sublingual (9 cases) administration of nifedipine (10 mg), a new coronary dilator, induced a prompt and large pressure reduction in patients with severe primary hypertension. Pressure started to fall within 20 and 5 min after oral and sublingual administration, respectively, and reached the lowest levels in the next 10 min. Maximal mean arterial pressure reduction averaged 36 mm Hg; 120 min after the drug, mean arterial pressure was diminished by 19.5% of control. The hypotension was mediated through diminished peripheral resistance associated with rise of cardiac output and pulse rate. Nifedipine was also administered siblingually in 3 cases with hypertensive encephalopathy and acute left ventricular failure with average systemic and pulmonary arterial pressures from 307/164 and 91/55 mm Hg, respectively, which fell to 237/115 and 68/35 mm Hg 15 min after 10 mg of the drug, and were further reduced to 176/89 and to 47/19 mm Hg by an additional 10 mg.

Administration, Oral↗
PubMed1976

Antihypertensive action of propranolol in man: lack of evidence for a neural depressive effect.

The hypothesis that a neural depressive action is related to the antihypertensive effects of beta blockers has been evaluated in 14 essential hypertensive male patients through the circulatory response to noxious stimuli. The pressor reaction to mental arithmetic was primarily mediated by cardiac stimulation (beta receptors activation), that to cold by vasoconstriction (alpha receptors activation). Arithmetic and cold were tested to separate the effects of peripheral beta blackade from possible neural and other influences. After propanolol (320 mg per day for 3 wk): (1) The baseline pressure was reduced; (2) appearance, peak, and disappearance time of the circulatory reaction to either stimulus was not altered; (3) the pressor effect of arithmetic was decreased in an extent proportional to the reduced rise of cardiac output; and (4) pressure during cold reached the pretreatment levels through an augmented increase of vascular resistance. Our findings indicate that propranolol depresses only the circulatory reactions mediated through beta receptors activation and provide no evidence of effects other than beta blockade.

Adrenergic beta-Antagonists↗
PubMed1976

Repetitive myocardial ischemia of Prinzmetal type without angina pectoris.

In a patient with a normal electrocardiogram, normal treadmill exercise test, normal coronary arteriogram and no symptoms to suggest angina pectoris, continuous monitoring during several days exhibited repetitive (one to two per hour) S-T segment elevations in the precordial electrocardiographic leads and hemodynamic changes typical of Prinzmetal's angina (reduction in arterial pressure and cardiac index and increase in systemic peripheral resistance and pulmonary wedge pressure). This case demonstrates that electrical and dynamic cardiac alterations of Prinzmetal's angina can occur even in the absence of angina pectoris.

Angina Pectoris↗