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Biomedical subjects

R Kolloch

Publications and source records attributed to R Kolloch.

80 records · Page 5Linked to original sources
PubMed1975

[Infusion theraphy in disorders of the acid-base equilibrium].

The acid-base balance is primarily regulated by renal and respiratory mechanisms affecting concentration of carbonic acid and bicarbonate in the extracellular fluid. The most important indication for intravenous therapy is diabetic keto-acidosis, lactate acidosis and the acidosis following poisoning. Calculation of the required amounts of buffer as well as corresponding formulars for therapy are of limited value and have always to be considered in relation to the actual clinical status.

Acid-Base Imbalance↗
PubMedDate not supplied

Increased hypothalamic noradrenergic activity in one-kidney, one-clip renovascular hypertensive rats.

To further define central and peripheral sympathetic nerve activity in the one-kidney and two-kidney, one-clip models of renovascular hypertension, plasma catecholamines and regional brain norepinephrine of these models were compared with the activities of their brain biosynthetic enzymes: tyrosine hydroxylase (TYH) and dopamine-beta-hydroxylase (DBH). Findings in the groups of 20 one-kidney and 17 two-kidney female Wistar rats were compared with those in 10 sham-operated rats. Systolic blood pressure, measured indirectly, and the mean arterial pressure, measured directly from the femoral arteries, verified development of renovascular hypertension in both the one and two-kidney animals. Plasma norepinephrine increased from 248 +/- 46 to 401 +/- 66 pg/ml in the one-kidney group only (p < 0.001). Hypothalamic TYH and DBH activities of the one-kidney animals were 48 and 34% greater than those of the two-kidney animals and 28 and 39% greater than the sham-operated animals. The multiple t-test indicated significant differences between the mean hypothalamic THY of the one- and two-kidney groups and between the hypothalamic DBH of the one-kidney animals and those of the two-kidney and sham groups (alpha = 0.05). Moreover, the mean norepinephrine content of the hypothalamus in the one-kidney animals was 66% greater than that of the two-kidney and sham groups (p < 0.05). These findings suggest that central noradrenergic pathways of the hypothalamus may be involved in the genesis of one-kidney renovascular hypertension.

Animals↗
PubMedDate not supplied

Raised cerebrospinal fluid norepinephrine in some patients with primary hypertension.

To test whether central neurogenic factors participate in blood pressure elevation in primary hypertension, we studied the concentrations of: norepinephrine, epinephrine and dopamine-beta-hydroxylase (DBH) in cerebrospinal fluid (CSF); and norepinephrine, epinephrine, DBH and plasma renin activity (PRA) in plasma of 22 subjects (seven with primary hypertension, 11 normotensive patients with non-systemic neurological disorders, and four with secondary hypertension). Plasma and CSF norepinephrine (NE) were increased in primary hypertensives compared to normotensives. Cerebrospinal fluid norepinephrine was related to diastolic blood pressure, and systolic blood pressure when normotensive and primary hypertensives were taken together. The CSF norepinephrine of primary hypertensive patients was correlated with natural log PRA. The CSF norepinephrine was correlated inversely with age in primary hypertensive patients but not in the normotensive subjects. The low CSF norepinephrine and epinephrine, despite markedly increased plasma NE and epinephrine, in two patients with pheochromocytoma, indicate a blood-brain barrier for these neurohormones. The observations support the view that the central sympathetic nervous system is involved in the pathogenesis of primary hypertension, particularly in younger patients.

Adult↗
PubMedDate not supplied

Antihypertensive effect of orally administered glandular kallikrein in essential hypertension. Results of double blind study.

The antihypertensive effect of oral administration of pig pancreatic kallikrein was investigated in a double blind study of 20 patients with essential hypertension. Kallikrein treatment lowered the blood pressure (BP) significantly from 159.5/104.5 to 146.3/92.8 mm Hg in the supine and from 153/106.1 to 136.1/95.6 mm Hg in the standing position. Blood pressure remained unchanged in the placebo group. Urinary kallikrein, sodium excretion, and GFR increased with treatment, but these changes did not reach statistical significance, In the kallikrein-treated patients but not in the placebo group, urinary kallikrein was correlated both to GFR (r = 0.7, p less than 0.001) and sodium excretion (r = 0.5, p less than 0.01). The antihypertensive mechanism of kallikrein treatment remains unknown. It could be speculated that kallikrein may induce changes in local blood flow, mediated by kinin and prostaglandin release.

Administration, Oral↗