Search PubMed⌕ Search

Biomedical subjects

F Skrabal

Publications and source records attributed to F Skrabal.

At least 91 records · Page 5Linked to original sources
PubMed1976

[Haemodynamics at rest and exercise capacity of patients treated by intermittent haemodialysis (author's transl)].

The haemodynamics at rest of 10 patients (mean age 42.6 years) with terminal renal failure treated by intermittent haemodialysis were studied over a period of 8 to 22 months by non-invasive methods. Additionally bicycle exercise testing was performed. After 13 months there was a reduction in cardiac index from 3.37 +/- 0.75 L/Min./m2 to 2.94 +/- 0.51 L/Min./m2 (p less than 0.05) and of the left ventricular minute work index from 6.21 +/- 1.60 mkp/Min./m2 to 5.71 +/- 1.36 mkp/Min./m2 (p less than 0.02). The blood pressure, index of peripheral resistance, systolic time intervals, arm-ear time and the ejection fraction showed no significant variations. Left ventricular failure was not detectable at rest, but the work capacity on exercise testing was reduced during the entire period of investigation without significant variation.

Adult↗
PubMed1976

The immediate plasma renin response to propranolol: evidence for a different mode of renin release in essential and renal hypertension.

1. The immediate short-term effects of intravenous injections of propranolol on plasma renin activity were studied in thirty-one normal subjects, 102 patients with benign essential and sixty-six patients with renal hypertension. 2. In essential hypertensive patients and normal subjects a marked fall in plasma renin activity was observed within 15 min, which was directly proportional to initial plasma renin values. In contrast, in patients with renal hypertension the fall observed was much less pronounced, or totally absent. 3. These differences in response to propranolol, which were particularly pronounced in patients with high initial renin values, suggest a dominant role of sympathetic tone at the juxtaglomerular apparatus for basal renin release in normal individuals and essential hypertensive subjects only. 4. The observations also indicate that sympathetic activity plays no part in the control of basal renin secretion in patients with renal hypertension, in whom basal renin secretion may be maintained by the renal baroreceptors.

Adolescent↗
PubMed1975

[Nomogram for the relation between plasma renin activity and fasting urinary sodium creatinine ratio (author's transl)].

Based on repeat measurements in 11 male and 12 female normal subjects, aged 20 to 35 years, on normal, low and high sodium intake a nomogram for the relation between fasting urinary sodium creatinine ratio and plasma renin activity (PRA) is presented. The use of fasting urinary sodium creatinine ratio as index of sodium intake and hydration of the subject results in a better prediction of PRA as compared with 24-hour urinary sodium excretion. Although fasting urinary sodium creatinine ratio in normal subjects on a normal sodium intake varies between 0.2 and 1.6, a uniform increase of basal PRA is found only at a ratio of below 0.3. A ratio greater than 0.5 excludes any stimulation of PRA by low sodium intake and (or) dehydration of the subject. The shape of the nomogram should make it applicable independent of the method used for PRA assay, as soon as the variation of PRA in normal subjects with a urinary sodium creatinine ratio above 0.5 is established.

Adult↗
PubMed1975

[Different reaction of plasma renin activity after propranolol in essential and renal hypertension].

In 16 normal subjects, in 29 patients with essential hypertension and in 25 patients with renal hypertension plasma renin activity was measured together with pulse rate and blood pressure under resting conditions and 15 minutes after the intravenous administration of 5 mg d-1-propranolol subsequently. Basal plasma renin activity (PRA) was correlated significantly to resting pulse rate in normal subjects and in patients with benign essential hypertension but not in patients with renal hypertension from chronic parenchymatous renal disease. In the normal subjects and in the patients with essential hypertension the decrease of not stimulated "basal" PRA 15 minutes after the administration of 5 mg d-1- propranolol was closely ralated to the initial plasma renin activity. In contrast, in the patients with well established renal hypertension the decrease of PRA was generally less pronounced or absent. Whereas in normal subjects as well as in patients with essentail hypertension in the sympathetic nervous system appears to be the major determinant for basal renin release, other factors, possibly the renal baroreceptors, may determine basal renin release in renal hypertension. This difference could possibley provide the basis for a simple biochemical test to differentiate between essential and renal hypertension.

Adolescent↗
PubMed1975

[Plasma renin activity, plasma aldosterone and electrolyte balance in the postoperative period (author's transl)].

Plasma renin-activity and plasma aldosterone were measured by radioimmunoassay in 15 female patients before and 16 hours after intraabdominal surgery. Plasma renin was increased in all patients and plasma aldosterone in 12 patients after operation. Plasma renin and plasma aldosterone were correlated significantly (r=0.66, p less than 0.01) in the whole group. The increase of renin and plasma aldosterone was correlated inversely to urinary sodium-potassium-ratio. In 5 patients the increase of plasma renin and plasma aldosterone could not be prevented by the intra- and postoperative administration of 360 mEq of sodium, which was consequently retained. It is proposed that postoperative hyperaldosteronism is at least partly mediated through the renin-angiotensin-system. An absolute or relative sodium deficit appears to be an unlikely explanation for the stimulation of the renin-angiotensin-system in the postoperative period. The postoperative increase of plasma renin and consequently plasma aldosterone is possibly a consequence of anaesthetic induced impaired kidney perfusion and/or catecholamine mediated stimulation of renin release.

Adrenal Glands↗