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Biomedical subjects

W Rascher

Publications and source records attributed to W Rascher.

At least 235 records · Page 13Linked to original sources
PubMed1986

[Continuous ambulatory peritoneal dialysis (CAPD) in children and adolescents].

Continuous ambulatory peritoneal dialysis (CAPD) is a relatively new blood purification method applicable as an alternative to intermittent hemodialysis in the treatment of end-stage renal disease. In this report we discussed the results of more than five years of CAPD in 32 children and adolescents aged 0.1 to 18 years treated for up to 22 months as well as the advantages and disadvantages of this technique in comparison to hemodialysis. Technical survival after one year of treatment increased from 48% in patients treated before 1983 to 84% in patients treated thereafter. Simplicity of technical procedure and lack of pain are considered the major advantages. Thus home dialysis can be performed even under adverse conditions (e.g. in infants). Infections of the abdominal cavity and the catheter tunnel are severe complications of CAPD. In the course of the last two years the frequency of peritonitis dropped to one episode per treatment year. We want to stress that successful treatment can be achieved by adequately training patients and their parents to perform home dialysis on their own and by surveying patients regularly according to standardized treatment guidelines in a pediatric nephrology unit.

Adolescent↗
PubMed1985

[Cardiovascular effect of the antidiuretic hormone arginine vasopressin].

The two major biological actions of vasopressin are antidiuresis and vasoconstriction. The antidiuretic action of low concentrations of vasopressin is well established and concentrations 10 to 100 times above those required for antidiuresis elevate arterial blood pressure. Antidiuresis is mediated by V2-receptors at the kidney, whereas vasopressin constricts arterioles by binding at V1-receptors. Pharmacological effects of specific antagonists of the vasoconstrictor activity of vasopressin (vascular or V1-receptor antagonists) are presented. Low concentrations of vasopressin do have significant hemodynamic effects. Physiological concentrations of vasopressin cause vasoconstriction and elevate systemic vascular resistance. In subjects with intact cardiovascular reflex activity, however, cardiac output falls concomitantly and blood pressure therefore does not change. In animals with baroreceptor deafferentation or in patients with blunted baroreceptor reflexes (autonomic insufficiency) a rise in plasma vasopressin causes vasoconstriction and an increase in blood pressure, because cardiac output does not fall under these conditions. Vasopressin contributes substantially via increase in systemic vascular resistance to maintain blood pressure during water deprivation. During hemorrhage and hypotension vasopressin has a major role to restore blood pressure. In experimental hypertension vasopressin contributes to the development and maintenance of high blood pressure in DOCA, but not in genetic hypertensive rats. The role of vasopressin in human hypertension is not yet clear. Vasopressin in extrahypothalamic areas of the brain affects circulatory regulation by interaction with central cardiovascular control centers. The exact mechanism of how vasopressin is involved in central regulation of blood pressure remains to be established. In contrast to our previous opinion vasopressin is a vasoactive hormone also at low plasma concentrations. Its cardiovascular action is more complex than previously assumed.

Animals↗
PubMed1985

Atrial natriuretic peptide in plasma of volume-overloaded children with chronic renal failure.

The effect of volume changes on the plasma concentration of atrial natriuretic peptide (ANP) in children with chronic renal failure was investigated by the use of a specific and sensitive radioimmunoassay. Predialysis plasma ANP was significantly higher in children with end-stage renal disease than in healthy children and children with advanced renal failure without evidence of volume expansion. During haemodialysis plasma ANP decreased significantly and plasma renin activity rose slightly, whereas plasma arginine vasopressin and aldosterone did not change. Plasma ANP correlated positively with volume status (body weight gain during the interval between two haemodialysis sessions). An expanded extracellular fluid volume thus seems to be a major stimulus for the rise in ANP in children with end-stage renal disease. The findings suggest that ANP may be important in volume homoeostasis.

Adolescent↗
PubMed1985

Congenital hypokalemia with hypercalciuria in preterm infants: a hyperprostaglandinuric tubular syndrome different from Bartter syndrome.

A congenital hypokalemic tubular disorder is described with many features resembling Bartter syndrome. Additional features include prenatal onset with polyhydramnios and premature labor; failure to thrive; episodes of fever, vomiting, diarrhea, and renal electrolyte and water wastage; hypercalciuria; nephrocalcinosis; and osteopenia. Unlike Bartter syndrome, there is no defect in tubular reabsorption of chloride. Urinary levels of prostaglandin E2 and 7 alpha-hydroxy-5,11-diketotetranorprosta-1,16-dioic acid are selectively elevated, indicating marked stimulation of renal and systemic PGE2 production. Chronic suppression of PGE2 activity by indomethacin corrects most of the abnormalities, and there is an immediate decompensation of the disease on indomethacin withdrawal. We conclude that these preterm infants have a distinct variety of hypokalemic tubular disorders rather than a variant of Bartter syndrome, because renal and systemic hyperprostaglandinism ranks high in the pathogenic chain of events, and the suppression of PGE2 hyperactivity is associated with significant improvement in the development (and probably in the prognosis) of the affected children.

Bartter Syndrome↗
PubMed1985

Hemodynamic effects of arginine vasopressin in conscious water-deprived rats.

By means of a specific antagonist [d(CH2)5AVP] of the vasoconstrictor activity of arginine vasopressin (AVP), we studied whether the vasoconstrictor effect of AVP contributed to the blood pressure control during water deprivation in conscious rats. After 24 h of dehydration plasma AVP rose from 3.5 +/- 0.5 to 11.2 +/- 2.0 fmol/ml. Intravenous injection of 5 micrograms/kg d(CH2)5AVP reduced total peripheral resistance. Since cardiac output rose simultaneously, mean arterial blood pressure remained unchanged. In rats with sinoaortic deafferentation (SAD) 4 wk before water deprivation, d(CH2)5AVP caused a reduction of total peripheral resistance and of mean arterial pressure, whereas cardiac output remained unchanged. Consequently, mean arterial pressure fell. No hemodynamic changes were observed in hydrated control rats with and without SAD. It is concluded that the vasoconstrictor activity of AVP plays an important role in maintaining blood pressure during water deprivation in conscious rats. After AVP blockade, arterial pressure fell only in SAD rats as intact rats maintain arterial pressure via acute increase cardiac output.

Animals↗
PubMed1984

The renal kallikrein-kinin system in spontaneously hypertensive rats.

In male spontaneously hypertensive rats (SHRSP) of the stroke prone strain (Okamoto) and in normotensive Wistar-Kyoto rats (WKY) urinary kallikrein excretion was investigated at different age and at drug-induced diuresis. In rats of both strains from 7th till 19th week of age urinary kallikrein excretion increased with age. In SHRSP of 7th till 11th week of age kallikrein excretion was higher than in WKY rats, while it was lower in the 48-week-old SHRSP. No correlation was found between urinary kallikrein excretion and systolic blood pressure. In SHRSP and WKY rats a similar daily rhythm of kallikrein excretion in urine was found being high in the early morning and low in the afternoon. Kallikrein excretion correlated significantly with urine volume. The loop diuretic bumetanide (4 and 40 mg/kg) induced diuresis and natriuresis in both strains, however more marked in the WKY rats than in the SHRSP. Urinary kallikrein excretion, however, showed in both strains the same biphasic course with a short lasting increase and a secondary decrease. Thus, in the average urinary kallikrein excretion was not effected by the drug. Prolonged treatment with furosemide over 5 days (125 mg/kg) resulted in an increase in kallikrein excretion in urine, more pronounced in the WKY rats than in the SHRSP. The observed results suggest that renal kallikrein-kinin system is not involved in the development of spontaneous hypertension as a pathogenetic factor, but rather is influenced by other factors like hormone interactions, i.e. mineralocorticoids and catecholamines, as well as renal function and acute changes in urine flow.

Angiotensin II↗
PubMed1984

Pathogenesis of hypertension in spontaneously hypertensive rats: definite evidence against a pressor role of vasopressin.

A number of experiments were performed in order to investigate the possible importance of vasopressin (AVP) in the pathogenesis of high blood pressure in spontaneously hypertensive rats of the stroke prone strain (SHRSP). Radioimmunological studies revealed reduced concentrations of AVP in the plasma and brain of SHRSP as compared to normotensive controls. Intravenous administration of an AVP pressor antagonist had no significant influence on mean arterial blood pressure, cardiac output and total peripheral resistance in SHRSP. Crossbreeding of SHRSP with rats homozygous for hypothalamic diabetes insipidus resulted in the development of a new strain of rats which show high blood pressure despite of a complete lack in AVP. These results argue strongly against a pressor role of AVP in the development or maintenance of hypertension in SHRSP.

Animals↗
PubMed1983

Effects of lesions in the paraventricular nucleus of the hypothalamus on vasopressin and oxytocin contents in brainstem and spinal cord of rat.

The effects of lesions of the paraventricular nucleus in rat hypothalamus (PVN) on the vasopressin (AVP) and oxytocin (OT) contents of the brainstem and spinal cord, as measured by radioimmunoassay, were studied. AVP decreased by 50% and 80% in brainstem and spinal cord of lesioned animals, whereas OT disappeared almost completely. Therefore, in contrast to OT, the PVN is not the only site of origin of AVP-containing nerve fibers projecting to the brainstem.

Animals↗
PubMed1983

Plasma arginine vasopressin concentrations in epileptics under monotherapy.

Plasma arginine vasopressin concentrations were determined by radio-immunoassay in 112 adult epileptics who were taking carbamazepine, phenytoin, primidone, or sodium valproate in long-term monotherapy, and in 19 controls. No significant difference was found between the groups, but some epileptics taking carbamazepine and primidone showed low values. Serum concentrations of carbamazepine did not correlate with the concentrations of plasma arginine vasopressin. In conclusion, there was no evidence of a stimulating effect of chronic carbamazepine medication or a special inhibiting effect of phenytoin on the release of vasopressin arginine from the posterior pituitary.

Adult↗
PubMed1983

Effect of prolonged indomethacin therapy on renal function and selected vasoactive hormones in very-low-birth-weight infants with symptomatic patent ductus arteriosus.

Renal function and changes in the activity of selected vasoactive hormones during prolonged indomethacin therapy (1 week) were studied in 11 very-low-birth-weight infants with symptomatic patent ductus arteriosus. The initiation of indomethacin therapy was associated with a reduction in diuresis, a transient decrease in creatinine clearance, and an increase in body weight (P less than 0.01). Furthermore, there was a transient trend toward hyponatremia and hyperkalemia. This acute renal dysfunction was compatible with a complex picture of renal hypoperfusion associated with a fall of plasma renin activity from high levels prior to indomethacin treatment, with a transient rise in the plasma level of arginine vasopressin and with suppressed renal and systemic prostaglandin synthesis. During treatment, an effective circulatory volume was restored by closing the ductus. In parallel, PRA and AVP plasma concentrations returned to nearly normal values. Subsequently, kidney function was not further impaired despite continued indomethacin therapy. These observations suggest that prolonged indomethacin therapy for prevention of sPDA relapse probably constitutes no further risk to kidney function after successful pharmacologically induced ductal constriction.

Arginine Vasopressin↗
PubMed1983

Oxytocin unlike vasopressin is a stress hormone in the rat.

The functions of oxytocin in the female are thought to be confined to the processes of milk ejection and parturition. In this study the role of oxytocin in the body's response to stressful stimuli has been examined. Physical immobilization of rats and forced swimming caused large increases in the secretion of the hormone, whereas vasopressin levels remained unchanged. These findings classify oxytocin, in contrast to vasopressin, as a so-called 'stress hormone' and suggest its importance in processes other than those related to reproduction.

Animals↗
PubMed1983

Vasoactive hormones in children with chronic renal failure.

Plasma renin activity (PRA), aldosterone, vasopressin and catecholamines were measured in 15 children (ages 7.3 to 16.2 years) with chronic renal failure (CRF) before and after one session of hemodialysis and in 15 control children. Basal levels of PRA and aldosterone in children with CRF did not differ significantly from control values, but showed a wider range. Uremic patients with nephronophthisis showed the highest basal PRA and aldosterone levels. In children with CRF, basal vasopressin levels were significantly higher (9.7 +/- [SEM] 2.0 ng/liter) than control values (3.2 +/- 0.8 ng/liter). Plasma noradrenalin and adrenalin concentrations were similar in children with CRF and controls. During hemodialysis, a fall in blood pressure and a rise in heart rate was observed in all children. PRA and catecholamines increased twofold to fivefold during dialysis while aldosterone and vasopressin showed a variable response. In contrast to reports in adults, there is no evidence for an insufficiency of vasoactive hormones or of the sympathetic nervous system in children on hemodialysis.

Adolescent↗
PubMed1983

Evaluation of adverse renal reactions to prolonged indomethacin therapy in preterm infants with persistent ductus arteriosus.

Adverse renal reaction during prolonged indomethacin therapy (1 week) was studied in 15 preterm infants with persistent ductus arteriosus (PDA), which was associated with an ineffective circulatory volume. Following the medication a decrease in diuresis and creatinine clearances together with an increase in urinary osmolality and body weight was observed. Determinations of selected vasoactive hormones, such as plasma renin activity (PRA), antidiuretic hormone (ADH), and renal and systemic prostaglandins, indicated a complex pathophysiological condition of renal hypoperfusion and antidiuretic excess. During the treatment with indomethacin an effective circulatory volume had been restored by closing the ductus, which was followed by hormonal normalization. Subsequently kidney function was recovering despite continued indomethacin therapy. Based on these observations, one may assume that prolonged indomethacin therapy for prevention of PDA relapses is probably of no further harm to kidney function once the ductus has been closed successfully.

Blood Volume↗
PubMed1982

Angiotensin stimulates oxytocin release: imparied response in rats with genetic hypothalamic diabetes insipidus.

Intracerebroventricularly (i.c.v.) administered angiotensin II (ANG II) at a dose of 100 ng caused a large increase in plasma oxytocin levels in Long Evans (LE) rats and in rats heterozygous for hypothalamic diabetes insipidus (HZ). In rats homozygous for diabetes insipidus (DI) even 100 fold higher doses of ANG II i.c.v. exerted only marginal effects on oxytocin release. The impaired responsiveness in DI rats was fully restored by prolonged treatment with a vasopressin (AVP) analogue. These data show that the decreased sensitivity of ANG II receptors in DI rats is due to the AVP defect and its metabolic consequences and can be reversed by AVP substitution.

Angiotensin II↗