[Histometric and enzyme histochemical studies of the pathogenesis of the muscle changes following neurectomy in growing swine].
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Biomedical subjects
Publications and source records attributed to W Kaufmann.
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Calcium antagonists are increasingly used in the treatment of primary and secondary hypertension. A new substance of this group, isobutyl methyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinecarboxylate (nisoldipine, Bay k 5552) inhibits the calcium-induced contraction of arteries and veins in concentrations 5-20 times lower compared to those of nifedipine in vitro. The effect of nisoldipine (10 mg orally) on blood pressure and heart rate in supine and upright position, on serum electrolytes (Na+, K+, Ca2+) and on serum aldosterone and serum hydrocortisone (cortisol) was comparatively studied in patients with essential hypertension (n = 6, 57 +/- 7 years), in patients with hypertension and chronic renal failure (n = 6, 46 +/- 4 years, serum creatinine 2.1 +/- 0.5 mg/100 ml) and in 6 patients with unilateral renal artery stenosis. In patients with essential hypertension, systolic blood pressure (BP) dropped by 26 mmHg; diastolic BP was lowered by 17 mmHg after 150 min compared to placebo. In patients with chronic renal failure, decrement in BP was 25/16 mmHg (systolic and diastolic BP, respectively). In patients with renal artery stenosis, blood pressure declined by 31/18 mmHg after nisoldipine. Serum electrolytes (Na+, K+ and Ca2+) and serum aldosterone as well as serum hydrocortisone remained unchanged. The hypotensive action of nisoldipine seems to be independent of the type of hypertension. However, the hypotensive activity correlates with the level of the baseline blood pressure.
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The pattern of aldosterone excretion during high sodium intake in 100 patients with essential hypertension allowed the differentiation of two groups: in the majority of patients (group A, n = 64) aldosterone excretion was suppressed below 6 micrograms/day similar to the normotensive control group. In a second group (group B, n = 36), aldosterone remained above the control range despite forced sodium loading. In group B, serum potassium was significantly lower than in patients of group A (3.81 +/- 0.44 meq/l vs. 4.26 +/- 0.57 meq/l, p less than 0.001). The blood pressure lowering effect of spironolactone (200 mg/d) was more pronounced among patients in group B. Plasma renin values tended to be lower in group B compared to patients with suppressed aldosterone. Infusion of Angiotensin II (0.1 - 2 micrograms/kg/min) led to a similar relative rise of plasma aldosterone levels in both groups despite higher baseline values in group B. The exact mechanism of the impaired regulation of aldosterone in a subgroup of patients with essential hypertension remains to be elucidated.
The term "hypertensive emergency" includes all clinical syndromes which are triggered by a rapid rise in the arterial blood pressure and are improved by medicinal lowering of the blood pressure. Among them are hypertensive encephalopathy, acute rise in blood pressure with left heart failure and acute rise in blood pressure complicated by intracerebral hemorrhage or a dissecting aortic aneurysm. Parenteral application of dihydralazine, diazoxide and clonidine are suitable for immediate lowering of blood pressure medicinally and sodium nitroprusside under clinical supervision. In phaeochromocytoma Regitin is the drug of choice.
The mechanisms of renin release after furosemide (F) and ethacrynic acid (EA) in man were examined. We evaluated whether acute volume shifts within the low pressure system after F induce renin release via neural pathways. Immersion in a water-bath or beta-blockade reduced the increase of plasma renin concentration after F but not after EA. It is concluded that acute renin release after F but not after EA in man is partially due to neurally mediated reflexes originating from volume receptors in the cardiopulmonary area.
In postmyocardial infarction patients longterm aspirin treatment with 1.5 g/day led to a significant increase in systolic and diastolic blood pressure after 6 months. This could not be found in the placebo- and the phenprocoumon-treated patients. After one year the blood pressure behaviour was the same in all three treatment groups. As nonsteroidal antirheumatic drugs can produce hypertension in animals, probably due to inhibition of prostaglandin synthesis, blood pressure control in longterm aspirin treatment is advisable.
Duodenal tumors are rare. The symptoms are mostly uncharacteristic upper abdominal pain or chronic anemia on account of occult blood loss. Tumors of mesenchymal or neurogenic origin may lead to dangerous bleeding from ulceration of the mucosa. Malignant tumors of the duodenum are often histologically adenocarcinomas and should be treated by partial or total pancreatectomy. If located below the papilla or at the duodenojejunal flexure, sometimes partial duodenal resection with end-to-end anastomosis may be performed. Benign tumors should be removed by local excision. In cases of duodenal malignancy, early detection and radical resection should help to increase the survival rate of the patients.
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The Na-K-ATPase activity of erythrocyte ghosts was increased in 6 patients with Cushing's syndrome compared with 28 control subjects (0.986 +/- 0.291 versus 0.259 +/- 0.1 microM Pi . h-1 . mg-1, p less than 0.001). Ouabain insensitive Mg-ATPase activity was similar in both groups. These data support the concept of an activation of the Na-pump in patients with glucocorticoid excess.