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Biomedical subjects

K Hayduk

Publications and source records attributed to K Hayduk.

At least 19 recordsLinked to original sources
PubMed1992

[Fatal pulmonary embolism after lysis therapy in post-traumatic renal vein thrombosis].

A 30-year-old man was hospitalized because of increasing dyspnoea for 4 weeks. Chest X-ray demonstrated an infiltrate in the right upper lobe and enlargement of the central pulmonary arteries. Lung perfusion scintigraphy revealed, typical of embolism, absent perfusion of the entire right upper lobe, as well as segmental embolism in the left upper and basal lobes. Phlebography of the legs and pelvis was unremarkable. Intravenous heparin treatment was begun (initially 1,250 IU/h, then dosage adjusted according to the partial thromboplastin time). Nonetheless the patient's condition deteriorated the next day and the respiratory failure increased (pO2 61 mm Hg despite oxygen supply). Streptokinase was then infused in ultra-high dosage, 9 million units over 6 hours. But the patient died of cardiocirculatory failure 4 hours after the streptokinase infusion had been finished. Autopsy revealed fulminant recurrent pulmonary embolism with occlusion of the right main pulmonary artery. The emboli had their origin in renal vein thrombosis extending into the inferior vena cava, which had probably been caused by slight trauma to the flank during a game of squash 6 weeks previously.

Adult↗
PubMed1979

Regulation of aldosterone secretion in dehydrated babies.

The factors controlling aldosterone secretion were measured in 12 patients with moderate to severe dehydration during the first year of life. Secondary hyperaldosteronism was present in all cases (mean plasma aldosterone concentration 414.6 ng/dl), as well as increased plasma cortisol levels (mean 49.7 microgram/dl). Plasma cortisol, an indirect parameter of stimulation of the adrenal cortex by ACTH, showed the highest correlation with plasma aldosterone (r = 0.82). Despite a mean elevation of 168 ng AT/ml/h the plasma renin concentration did not seem to play the dominant role in the regulation of aldosterone secretion in these infants. High serum sodium concentrations have a clearly inhibiting effect on aldosterone secretion as shown by the negative correlation coefficient of r = 0.80.

Aldosterone↗
PubMed1978

[Saralasin-induced changes of blood pressure, renin and aldosterone in essential and renal hypertension (author's transl)].

In 34 patients saralasin was infused after variable degrees of sodium depletion in order to differentiate between essential and renin-induced hypertension. After sodium-depletion of short duration mean arterial pressure dropped more than 10 mm Hg in 9 of 25 patients with essential and in 7 of 9 patients with renin-induced hypertension. After long-lasting sodium depletion the fall of mean arterial pressure exceeded 10 mm Hg in 11 of 16 patients with essential and in 8 of 9 patients with renin-induced hypertension. Thus saralasin did not discriminate essential and renin-induced hypertension. Also, plasma renin concentration before and after saralasin did not allow to differentiate between the two forms of hypertension. The changes of renin during infusion of saralasin was negatively correlated to the change of blood pressure. Renal vein renin ratio in patients with renovascular hypertension was not modified by saralasin. Renin and aldosterone changed inversely during saralasin infusion.

Aldosterone↗
PubMed1978

[Side-effects on longterm treatment with antihypertensives (author's transl)].

Unspecific complaints as a result of lowering the blood pressure and substance-specific side-effects may occur during antihypertensive therapy. The frequency of the side-effects depends on the substance used (10 to 50%) and on the dose. An individual therapy, which in most cases involves the use of several substances, can reduce the frequency of side-effects decisively. With optimal therapy the ratio of benefits (= prevention of cardiovascular diseases) to side-effects (= sum of undesirable reactions) is completely acceptable in the treatment of high blood pressure.

Age Factors↗
PubMed1977

[Hemodynamic changes after angiotensin II blockade by saralasin (author's transl)].

Saralasin, an angiotensin II inhibitor was infused in 10 hypertensive patients. A blood pressure reduction was achieved after stimulation of the renin-angiotensin-system by salt depletion. Heart rate and cardiac output failed to compensate for reduction of blood pressure. Thus circulatory reflex-mechanisms are inhibited by saralasin. A direct influence on baroreceptor mechanism and/or catecholamines is probable. Failure of the hypotensive effect of saralasin in salt-depleted patients after administration of beta-blockers supports this hypothesis.

Adrenergic beta-Antagonists↗
PubMed1976

[Effects of longterm HCG administration on testicular function in hemodialysis patients (author's transl)].

Thirtheen male patients with chronic renal failure undergoing regular dialysis treatment (2 X 8-10 hours/week) were treated with gonadotropins (HCG, Primogonyl) primarily 2 X 2,000 IU/week and later 2,000 IU/week. Before HCG administration and during 4-months HCG-therapy testosterone, dihydrotestosterone, Androstandiol, LH and FSH levels were determined by RIA-methods in 7-14 days intervals. Before HCG-application plasma testosterone levels were low and did not increase in the course of regular dialysis treatment. Derivates from testosterone like dihydrotestosterone and Androstandiol were elevated in plasma, presumbably because of accumulation in renal failure. LH-levels were slightly elevated on the average. FSH-levels showed a high individual variation but also seemed to be elevated on the average. HCG stimulation by exogenous HCG administration for short time resulted in a insufficient rise of testosterone levels as compared to normals. During prolonged HCG administration plasma testosterone levels increased to normal but dropped immediatly after cessation of therapy or reduction to less than 2,000 IU HCG twice/week. Body weight, plasma proteins, haematocrite and fertility did not improve significantly. These results indicate that in chronic renal failure androgen synthesis by testicular tissue is seriously impaired and does not improve under usual dialysis treatment. Feedback regulation of testosterone levels by increase of LH levels seems not to be sufficient although pituitary response is found to be normal. This may be explained by elevated levels of testosterone derivates which exert negative feedback effects.

Adult↗