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J Widimsky

Publications and source records attributed to J Widimsky.

At least 19 recordsLinked to original sources
PubMed1991

High salt intake-induced changes in atrial natriuretic factor kinetics are mediated by clearance receptors.

We have reported a paradoxical plasma atrial natriuretic factor (ANF) decline following prolonged high salt intake that was attributed to an increased tissue uptake of circulating ANF, leading to its augmented distribution volume (Vas) and metabolic clearance rate (MCR) as compared with control rats on a standard diet. To explore this phenomenon further, we evaluated possible chronic salt-loading-induced changes in ANF clearance (C-ANF) receptors, which appear to play a major role in ANF removal from the circulation. We studied changes in plasma [125I]ANF(1-28) and its pharmacokinetics after preoccupation of C-ANF receptors by its specific ligand, C-ANF(4-23), in high-salt-treated rats and their controls. Following C-ANF(4-23) administration, we detected significantly higher circulating [125I]ANF levels throughout the study period (8 min) in high-salt-fed rats compared with the controls (280-470% vs 100-215% increase of basal values, P less than 0.05). C-ANF(4-23) infusion caused a significantly greater decrease of the metabolic clearance rate and distribution volume of [125I]ANF in high-salt-fed rats than in control animals (74 +/- 6% vs 41 +/- 6% and 75 +/- 4% vs 50 +/- 5% of basal values, respectively; P less than 0.05). These data suggest that a prolonged high salt diet may increase the availability of C-ANF receptors and, through this mechanism, may negatively modulate plasma ANF concentrations. C-ANF receptors may thus fulfill a regulatory function on circulating ANF during prolonged salt loading in rats.

Analysis of Variance↗
PubMed1990

Dissociation between right atrial pressure and plasma atrial natriuretic factor following prolonged high salt intake.

The influence of prolonged high salt intake on intravascular volume, right atrial pressure, plasma atrial natriuretic factor, and extra-atrial tissue (lung, kidney, and liver) COOH- and NH2-terminal atrial natriuretic factor content was investigated in normotensive rats. Despite prolonged high salt (8% NaCl) intake for 5 weeks, total intravascular volume was not impaired. However, right atrial pressure was increased by 54% (p less than 0.01) after salt loading. Although this increment in right atrial pressure should favor atrial natriuretic factor release after NaCl intake, plasma atrial natriuretic factor (COOH-terminal) concentrations markedly decreased from 97.8 +/- 27 to 38.9 +/- 8 pg/mL. Sodium and circulatory homeostasis was, however, well preserved. The lungs contained the highest levels of COOH- and NH2-terminal atrial natriuretic factor. Salt loading resulted in increased concentrations of low as well as high molecular weight atrial natriuretic factor in the lung but not in the kidney or the liver. Our study indicates a limited role of atrial natriuretic factor in adaptation to prolonged salt consumption in rats. Dissociation between right atrial pressure and plasma atrial natriuretic factor after salt intake implicates other factors regulating circulating peptide levels. Prolonged salt intake increases lung generation of atrial natriuretic factor.

Animals↗
PubMed1990

ANF disappearance and tissue distribution in rats.

The disappearance of [125I]atrial natriuretic factor (ANF; Ser99-Tyr126) from the circulation and its tissue distribution with or without nonlabeled ANF pretreatment were investigated in normotensive Sprague-Dawley rats. Preadministration of the cold peptide increased plasma radioactivity levels for over 8 min following labeled ANF injection but did not change the half-life of circulating labeled ANF. The metabolic clearance rate (MCR) and volume of distribution in the first, second, and steady state phase were significantly decreased after cold ANF pretreatment. Circulating iodo-labeled ANF was taken up by several organs, even by tissues such as fat or bone, but its urinary excretion was very low. The highest uptake was found in the liver (16 +/- 1% of the injected dose), lung (14 +/- 1%), and kidney (12 +/- 1%), diminishing by 21, 89, and 59%, respectively, after cold ANF preinjection. The brain radioactivity was negligible implying an inability of [125I]ANF to cross the blood-brain barrier. Our data underscore the importance of the uptake-mediated, cold ANF preadministration suppressible clearance of ANF from the circulation, probably one of its basic elimination mechanisms. The liver, lung, and kidney are probably the most important participants in the MCR of ANF.

Animals↗
PubMed1985

Pressures.

Explore the source record for details and available documents.

Aorta↗
PubMed1984

The diagnosis of pulmonary embolism.

Pulmonary embolism is poorly diagnosed and therefore not treated in patients with chronic diseases, whereas it is overdiagnosed in formerly healthy patients. The diagnostic level is not satisfactory even in departments of cardiology. Insufficient use of auxiliary laboratory tests constitutes one of the main reasons for the unsatisfactory state of pulmonary embolism diagnostics. The clinical picture of pulmonary embolism depends on a) the size of pulmonary embolism, b) the previous state of the cardiopulmonary system. A massive pulmonary embolism can lead to a) sudden death, b) shock, c) acute cor pulmonale. The most typical diagnostic sign is suddenly developed or deteriorated dyspnea (present in 94% of patients). The presence of venous thrombosis and the appearance of sudden dyspnea always support the diagnosis very strongly. Dyspnea or tachypnea occur in more than 90% of patients. Dyspnea, tachypnea or deep venous thrombosis occur in 99% of patients with acute pulmonary embolism. Electrocardiographic signs of acute pulmonary embolism were present in 67% of our patients with hemodynamically significant pulmonary embolism. Electrocardiographic signs are most marked in cases in which pulmonary embolism originates suddenly, in patients with a normal cardiopulmonary system, if the pulmonary embolism is extensive and the electrocardiogram is carried out early and repeatedly. The electrocardiographic signs of pulmonary embolism in cardiac patients, however, are not specific and only rarely present. The principal advantages of the chest X-ray are simplicity, safety and low costs. A negative chest X-ray was found only in 16.6% of our patients with pulmonary embolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1983

Plasma concentration and urinary excretion of arginine-vasopressin in primary aldosteronism during the fluid deprivation tests.

Plasma concentration (PAVP) and urinary excretion (UAVP) of arginine-vasopressin were studied in 8 patients with primary aldosteronism (PA) during a 36 hour period of fluid restriction in relation to the disturbances of their maximal renal concentrating capacity. The results in untreated patients suffering from PA were compared with the findings in patients after a successful treatment of PA as well as with the results in 9 control subjects. The reduction of maximal renal concentrating ability in PA before the treatment was accompanied with a high excretion of UAVP and the physiological reaction of PAVP to dehydration. Together with the shift of the regression line of the dependence of UOsm on UAVP to higher values of UAVP this indicates a decrease of the sensitivity of the nephrons to the sufficiently high concentrations of endogenous AVP. The increase of renal AVP clearance in PA participates in the high urinary excretion of AVP. The disturbance of the renal concentrating ability as well as the changes of urinary AVP in PA are mostly reversible. After the successful treatment of PA and the completion of potassium stores in the body as well as the healing of the kaliopenic nephropathy, the maximal renal concentrating capacity and AVP gradually return to values close or equal to those in healthy subjects.

Adrenalectomy↗
PubMed1982

Longterm follow-up of patients with pulmonary thromboembolism. Late prognosis and evolution of hemodynamic and respiratory data.

Seventy-six patients with various forms of pulmonary thromboembolic disease were followed-up for 1 to 15 years. All were free of other cardiopulmonary disease at the time of the first examination which was performed at least two months after the last pulmonary embolism. Catheterization was repeated in all survivors on average 4.8 years later. Severe chronic pulmonary hypertension (mean pulmonary artery pressure (PPA greater than 30 mm Hg) did not occur after a single episode of acute embolism, was infrequent after single subacute or recurrent emboli (8 of 9 patients), and was common after occult emboli (12 of 13 patients). Mortality in all clinical groups correlated with PPA and with the presence of right heart failure. In survivors, no correlation was found between the longterm changes of PPA and age, duration of disease, interval between catheterizations, PaO2, or cardiac output. Pulmonary hypertension progressed further in patients with initial PPA greater than 30 mm Hg. In contrast, none of the patients with normal or borderline PPA at the initial examination developed severe pulmonary hypertension during the follow-up. Since the future course of patients could be predicted from the first examination, repeated hemodynamic investigation proved to be of minor prognostic value.

Adult↗
PubMed1980

Intermittent high altitude hypoxia.

The effect of intermittent high altitude (IHA) hypoxia on the myocardium and lesser circulation was investigated in adult male Wistar rats. IHA can induce intermittent pulmonary hypertension and right ventricular hypertrophy in a relatively short time. Even marked pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular changes can be normalized when rats are removed from the hypoxic atmosphere. At the beginning of the exposure to IHA acute myocardial necrotic changes were found; prolongation of IHA did not lead to further acute lesions. Experimentally induced CO polycythemia leads to mild pulmonary hypertension; IHA-induced pulmonary hypertension may, thus, be partly due to polycythemia. Beta blocking agents are able to decrease chronic hypoxic pulmonary hypertension, hypertensive changes in the pulmonary circulation, the degree of right ventricular hypertrophy, and necrotic myocardial changes.

Altitude Sickness↗
PubMed1975

Effects of physical training on central haemodynamics and working capacity in myocardial infarction.

Changes in central haemodynamics and physical working capacity were followed in 23 patients with myocardial infarction: in 12 of them, after six-month intense physical training, and in 11, after an equal control period without training. The haemodynamic indicators revealed after rehabilitation a significant decrease in the exercise heart rate in comparison with the unchanged value in the controls. The changes in the other haemodynamic values were not significant. The pulmonary arterial end-diastolic pressure, regarded as an indicator of the left ventricular filling pressure, sustained no significant change by the training. Some additional changes, such as decreases in the arterial and venous oxygen pressure both at rest and during exercise, were found in both groups of patients. The physical working capacity increased significantly after rehabilitation in comparison to the control group. It is emphasized that no adverse influence upon the central haemodynamics was revealed in patients with myocardial infarction after intense training according to WHO criteria.

Blood Pressure↗