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Biomedical subjects

I Gregorová

Publications and source records attributed to I Gregorová.

At least 19 recordsLinked to original sources
PubMed1991

[Hypertension in patients with polycystic kidneys--the effect of volume expansion].

Arterial hypertension is found in as many as 75% patients with autosomal dominant polycystic kidneys with normal renal function, its pathogenesis is however not quite clear so far. The authors examined 16 patients with polycystic kidneys with normal or only slightly reduced renal function (plasma creatinine lower than 140 umol/l), 8 of these patients were normotonic (N) and 8 hypertonic (H). In all examined subjects right-sided cardiac catheterization was performed with assessment of the minute cardiac volume by thermodilution. To all patients in the course of one hour 1500 ml saline per 70 kg body weight were administered and the haemodynamic examinations were repeated after termination of the infusion. In all subjects before and after expansion the plasma renin activity was assessed (PRA), as well as plasma aldosterone (PA), plasma catecholamines (PC) and the atrial natriuretic factor (ANF), the renal blood flow and glomerular filtration by means of clearance and extraction of PAH and inulin clearance. The authors did not find differences in plasma concentrations, cardiac output and splanchnic and renal ANF extraction in groups N and H, nor in PRA, PA and PC. Volume expansion led in both groups to a comparable rise of ANF and suppression of PRA and PA. Group H did not differ from group N in any of the investigated haemodynamic and renal parameters except for systemic vascular resistance. In hypertensive patients before expansion a close correlation was found between pressure in the pulmonary artery in a wedged position and diuresis (r = 0.935, p less than 0.01) and natriuresis (r = 0.895, p less than 0.01). The volume expansion was in both groups associated with a comparable rise of diuresis, the haemodynamic response of patients N and H was however quite different. While in patients of group N a decline of the systemic vascular resistance occurred as well as an increase of the minute volume without a change of the renal flow and glomerular filtration, in hypertonic patients the systemic vascular resistance and minute volume did not change but there was a significant rise of the renal flow and glomerular filtration. The relationship of diuresis and natriuresis of hypertensive patients with polycystic kidneys to volume parameters and the rise of the renal perfusion pressure during volume expansion indicates the importance of pressure natriuresis for ensuring the sodium and volume homeostasis in these patients.

Humans↗
PubMed1990

[Is it possible to predict the development of Nelson's syndrome in Cushing's disease after bilateral adrenalectomy?].

A detailed analysis of clinical and laboratory findings in a group of 66 patients with Cushing's disease treated with bilateral adrenalectomy, out of whom 15 developed Nelson's syndrome, gave evidence that Nelson's syndrome mostly affects children and young patients compared to older persons. Bilateral adrenalectomy performed in patients aged over 40 years was never accompanied by Nelson's syndrome. Basal plasma ACTH values prior to adrenalectomy (30.9 +/- 4.53 pmol/l in the absence of Nelson's syndrome and 31.3 +/- 5.41 pmol/l in patients with Nelson's syndrome) as well as the degree of their suppressibility with 8 mg dexamethane (to 18.8 +/- 3.43 pmol/l in Nelson's syndrome and 19.0 +/- 3.44 pmol/l in patients without it) did not provide sufficient evidence for the prediction of later development of Nelson's syndrome. The same is true of the plasma cortisol concentrations. A tendency to a significant plasma ACTH increase after adrenalectomy within a 6-month period, and especially its lesser suppressibility raises a strong suspicion of an incipient development of Nelson's syndrome. These findings will have to be taken into account when deciding on the surgical treatment of Cushing's disease.

Adolescent↗
PubMed1990

[The effect of dopamine on hemodynamic and hormonal parameters in liver cirrhosis].

To 11 patients with liver cirrhosis (5 with ascites) and 6 controls a one-hour dopamine infusion, 1.5 micrograms/kg/min., was administered. In all before administration of the infusion catheterization of the hepatic veins and lesser circulation was performed with concurrent assessment of the cardiac minute volume by thermodilution, and haemodynamic measurements were repeated also after the dopamine infusion. Before the dopamine administration and after termination of the infusion the plasma renin activity was assessed (PRA), plasma aldosterone, the atrial natriuretic factor (ANF), prolactin and in some patients also plasma catecholamines. Dopamine administration was not associated with an increase of the cardiac output, heart rate or peripheral resistance; the infusion had only purely dopaminergic effects. Plasma prolactin declined after dopamine administration significantly in controls (from 29.17 +/- 7.01 to 11.83 +/- 3.22, p less than 0.05, in patients with liver cirrhosis without ascites) from 18.16 +/- 2.44 to 8.64 +/- 2.01, p less than 0.01) in patients with ascites liver cirrhosis (from 23.5 +/- 9.3 to 15.2 +/- 7.47, p less than 0.05). In the controls after the dopamine infusion PRA suppression occurred (from 2.37 +/- 0.81 to 0.9 +/- 0.27, p less than 0.05), while in patients with compensated liver cirrhosis (from 0.97 +/- 0.41 to 0.85 +/- 0.34, n.s.) and in patients with decompensated liver cirrhosis the PRA did not change significantly either (from 4.56 +/- 1.67 to 5.065 +/- 2.29, n. s.). After the dopamine infusion in none of the investigated patient groups changes of plasma aldosterone and ANF were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1990

[The effect of clonidine on humoral factors in patients with arterial hypertension].

Clonidine, an agonist of central alpha-2-adrenergic receptors, reduced the peripheral sympathetic activity. With regard to the mutual pathophysiological relationship of blood pressure regulating mechanisms, the authors wanted to find out whether after clonidine administration, in addition to the known suppression of catecholamine levels (CA), also changes in the concentration of other pressor and depressor humoral substances will occur. They investigated therefore in 15 patients with essential hypertension (EH) and in three patients with pheochromocytoma the urinary excretion of free noradrenaline (NA), adrenaline (A) and dopamine (DA), the plasma renin activity (PRA), the aldosterone concentration (PAC) and atrial natriuretic factor (ANF) in plasma, using radioimmunoanalysis, always before and 24 hours after clonidine administration (Haemiton retardR) by the oral route. Its administration led in patients with EH to a decline of NA and DA. On the other hand, in pheochromocytoma their urinary excretion did not change in an unequivocal way, and when it declined, never normal NA and DA levels were reached. A excretion remained unaltered in both groups of patients. The drop of PRA after clonidine as a result of the drop of peripheral adrenergic activity was not associated with an expected parallel drop of PAC but by its rise. This effect can be explained by a reduction of the tonic inhibition of PAC output when the DA level declines. The rise of ANF after clonidine administration will be the subject of subsequent investigations. It cannot be ruled out that this effect is due to the direct action of clonidine on alpha receptors in the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗
PubMed1990

[Atrial natriuretic factor in liver cirrhosis. Relation to hemodynamic parameters].

In 12 patients with cirrhosis of the liver (six with ascites) and six controls the authors made catheterizations of the hepatic veins and portal circulation, assessing concurrently the in cardiac output by thermodilution. The patients with ascitic cirrhosis had, as compared with controls, a significantly higher portohepatic gradient, central venous pressure, mean pressure in the pulmonary artery and also pulmonary capillary wedged pressure and a significantly lower mean arterial pressure and systemic vascular resistance. These patients had also, as compared with controls, a significantly higher concentration of ANF (atrial natriuretic factor) in the pulmonary artery (15.89 +/- 2.26 vs. 8.04 +/- 0.97, p less than 0.01) and in the hepatic vein (7.44 +/- 0.44 vs. 3.91 +/- 0.63, p less than 0.01); the difference between ANF concentrations in the peripheral blood stream was not significant (9.52 +/- 2.46 vs. 5.71 +/- 1.24 n. s.). Patients with ascitic cirrhosis of the liver had a significantly higher calculated cardiac production of ANF than controls (24.36 +/- 3.44 vs. 8.12 +/- 2.9, p less than 0.01); the difference in the splanchnic extraction of ANF between patients with ascitic cirrhosis of the liver (0.46 +/- 0.1) and controls (0.51 +/- 0.06) was not significant. The ANF concentration in the pulmonary artery in patients with cirrhosis of the liver correlated significantly with the central venous pressure (r = 0.677, p = 0.02) and the pressure in the pulmonary artery in a wedged position (r = 0.639, p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1990

Humoral and renal response to acute volume loading in patients with essential hypertension.

The effect of acute volume expansion (2 liters of saline solution in 2 h) on plasma concentrations of atrial natriuretic factor (ANF), plasma aldosterone concentration (PAC), plasma renin activity (PRA) and their relationship to the renal excretion of urine, sodium and potassium were studied in 6 control subjects and 7 patients with essential hypertension (EH) WHO stage I. Saline infusion provoked comparable rise in plasma ANF in both groups (from 2.98 +/- 0.45 to 12.36 +/- 1.74 pmol/l in the control subjects and from 3.80 +/- 0.72 to 15.78 +/- 2.06 pmol/l in EH patients), significant drop in PRA (from 0.915 +/- 0.419 to 0.256 +/- 0.127 nmol/l/h in controls and from 1.711 +/- 0.324 to 0.714 +/- 0.128 nmol/l/h in EH) and in PAC (from 0.30 +/- 0.07 to 0.14 +/- 0.03 nmol/l in control subjects and from 0.53 +/- 0.13 to 0.24 +/- 0.07 nmol/l in EH). The increase of plasma ANF concentrations after volume expansion might be involved in the suppression of PRA and PAC found after this stimulus. Similar increase in plasma ANF after saline infusion in both groups was associated with significantly greater urine and sodium excretion in EH than in controls. From these results it may be suggested that the acute volume expansion during saline infusion evokes a comparable release of ANF into circulation in both EH patients and controls. In EH patients, however, the similar rise in ANF is accompanied by a more pronounced diuretic and natriuretic response. This exaggerated natriuresis after acute volume and sodium loading cannot be explained solely by a rise in ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Mutual interaction of the renin-angiotensin system and the atrial natriuretic factor in the renal response to acute volume loading].

The authors investigated dynamic changes and the interaction of the plasma renin activity (PRA), plasma aldosterone (PAC), i.e. the main representatives of sodium retaining systems, and of the atrial natriuretic factor (ANF) the decisive natriuretic substance in acute expansion of the extracellular volume (ECV) by infusion of two litres of saline in six controls, seven patients with essential hypertension and liver cirrhosis without ascites (6 patients) and with ascites (6 patients). The expansion evoked controversial changes of these systems. It led to a rise of ANF and suppression of PAC and PRA. Although ANF rose after infusion to the roughly similar range (12.4 to 15.7 pmol/l), the natriuretic response to expansion differed significantly in different groups of patients. It was most marked in hypertonic subjects (517.2 to 93.2 mumols/min) and practically zero in ascitic liver cirrhosis (54.2 +/- 44.2 mumols/min). The explanation of this finding may be the persistence of high activity of the renin-angiotensin-aldosterone system despite its partial inhibition by infusion of saline in cirrhosis of the liver (PRA 1.69 +/- 0.66 nmols/l/hr., PAC 1.12 nmol/l). For the renal response to acute expansion of the ECV thus not only the absolute plasma concentration of ANF is decisive but also its ratio to the activity of the sodium retaining renin-angiotensin-aldosterone system.

Aldosterone↗
PubMed1989

[Relation between atrial natriuretic factor and the renin-angiotensin-aldosterone system in the renal reaction to acute volume loading in patients with essential hypertension].

Investigation of changes of the atrial natriuretic factor plasma concentration (ANF), plasma renin activity (PRA) and the plasma aldosterone concentration (PAC) and their correlation with the renal excretion of urine, sodium and potassium before and after infusion of 2 1 saline in the course of 2 hours in 6 controls and 7 patients with essential hypertension (EH) revealed the same rise of ANF in plasma of both groups (from 2.98 +/- 0.45 to 12.36 +/- 1.74 pmol/l in controls and from 3.80 +/- 0.72 to 15.78 +/- 2.06 pmol/l in EH), a comparable decline of PRA (from 0.91 +/- 0.419 to 0.256 +/- 0.127 nmol/l/hr in controls and from 1.711 +/- 0.324 to 0.714 +/- 0.185 nmol/l/hr in EH), and PAC (from 0.30 +/- 0.07 to 0.14 +/- 0.03 nmol/l in controls and from 0.53 +/- 0.13 to 0.24 +/- 0.06 nmol/l in EH). The comparable rise of plasma ANF concentration during infusion of saline was associated with a significantly higher renal excretion of urine and sodium in EH, as compared with controls. The authors conclude from these results that the ANF release into the blood stream after an acute volume overload in EH does not differ from controls. Thus the raised natriuresis in EH after a volume overload cannot be explained solely by the rise of ANF. Its renal action depends obviously on the interaction with many other haemodynamic and renal mechanisms, and as regards humoral factors, in particular on the interaction with the renin-angiotensin-aldosterone system. The inhibitory action of elevated ANF concentrations might participate in the suppression of PRA and PAC after a volume overload.

Adult↗
PubMed1989

Atrial natriuretic factor in liver cirrhosis--the influence of volume expansion.

Plasma levels of atrial natriuretic factor (ANP) were examined in 12 patients with liver cirrhosis (6 with ascites) and 6 controls before and after the administration of the infusion of 2000 ml of saline solution per 70 kg of body weight during 2 hours. Basal concentration of ANF tended to be slightly, but nonsignificantly higher in patients with ascitic liver cirrhosis (5.5 +/- 1.3 fmol/ml) than in controls (3.0 +/- 1.0 fmol/ml) and in patients with non-ascitic liver cirrhosis (4.6 +/- 1.3 fmol/ml). Saline administration led to the comparable increase of plasma ANF in ascitic (14.2 +/- 4.0 fmol/ml) and non-ascitic cirrhotics (15.7 +/- 3.7 fmol/ml) and in controls (12.4 +/- 4.3 fmol/ml). The increase of plasma ANF was accompanied by the suppression of plasma renin activity (PRA) and plasma aldosterone (PA) in all groups; in ascitic patients, however, PRA and PA remained above the normal range. While in controls and non-ascitic cirrhotics saline administration led to the increase of urine flow rate /from 0.74 +/- 0.13 to 2.04 +/- 0.44 ml/min, P less than 0.01, in controls; from 0.83 +/- 0.05 to 1.28 +/- 0.07 ml/min, P less than 0.01, in non-ascitic cirrhotics) and urinary sodium excretion (from 110.7 +/- 21.3 to 364.8 +/- 74.4 umol/min, P less than 0.01, in controls; from 125.0 +/- 16.7 to 218.7 +/- 24.3 umol/min, P less than 0.01 in non-ascitic cirrhotics), in patients with ascitic liver cirrhosis neither urine flow rate (from 0.66 +/- 0.1 to 0.72 +/- 0.15 ml/min, n.s.), nor urinary sodium excretion (from 16.7 +/- 9.9 to 54.2 +/- 40.3 umol/min, n.s.) changed significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1987

Long-term results of surgical and conservative treatment of patients with primary aldosteronism.

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.

Adrenalectomy↗