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Biomedical subjects

G Liebau

Publications and source records attributed to G Liebau.

At least 37 records · Page 2Linked to original sources
PubMed1982

Antidiuretic hormone in congestive heart failure.

In advanced heart failure, severe edema develops associated with hyponatremia. In 20 patients with severe congestive heart failure, we studied plasma antidiuretic hormone (ADH) concentrations related to hemodynamics and plasma osmolality. Prazosin was used to test the acute response to changes in atrial receptors and hemofiltration to test the response to changes in volume receptors. One group of the patients had inappropriately high ADH values (14.5 +/- 8.8 pg/ml) in relation to their plasma osmolality, which was well below normal values (276 +/- 23 mosmol/kg water) with no apparent osmoregulatory control. The other group showed a normal relationship of ADH and plasma osmolality (3.9 +/- 1.0 pg/ml; 289 +/- 8 mosmol/kg water), Only in the normal regulating group did lowering of left atrium pressure by prazosin result in a rise in ADH related to the decrease in pressure. Inappropriately high ADH secretion could be reversed by hemofiltration. This suggests that the syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli; however, it cannot be ruled out that associated hemodynamic effects in the kidney or other intrarenal or hormonal factors contribute to this mechanism.

Adult↗
PubMed1982

The renin-angiotensin-aldosterone system, antidiuretic hormone and sympathetic nerve activity in an experimental model of congestive heart failure in the dog.

1. Congestive heart failure was induced in dogs by rapid pacemaker stimulation of the heart (240-280/min) for 14 days. This represents a model of low output heart failure which permits the study of the development and reversal of congestive heart failure in an anatomically intact circulation in the unanaesthetized animal. 2. Cardiac output was reduced by 54%. Pulmonary artery pressure gradually increased by a factor of 2.4 and pulmonary capillary pressure rose to 4.6 times basal values. The animals retained a mean of 1.1 litres of fluid. 3. At the same time there was a gradual increase of plasma levels of renin, angiotension II, aldosterone, noradrenaline and adrenaline. After the pacemaker stimulation was discontinued all hormone levels returned to normal, the retained fluid was excreted, and intracardiac pressures and cardiac output returned to baseline values. 4. When heart failure was established at the end of the pacemaker stimulation period an inappropriately high secretion of antidiuretic hormone in relation to plasma osmolality was observed in five of six dogs. 5. It is concluded that beside the well-known non-hormonal renal factors, these hormone systems may be involved in the formation of oedema in congestive heart failure. The inappropriately high levels of antidiuretic hormone may cause hyponatraemia by water retention, representing a state of 'dilutional hypo-osmolality'.

Animals↗
PubMed1982

[Effect of intracoronary nifedipine on coronary sinus blood flow and myocardial oxygen consumption in patients with coronary artery disease].

UNLABELLED: Reflex sympathetic nerve activation obscures the direct myocardial effect of Nifedipine after intravenous administration. Consequently, in 10 patients with coronary artery disease 0.1 mg of Nifedipine were injected into the left coronary artery to evaluate its specific effect on coronary sinus blood flow (CSF), coronary vascular resistance (CVR), and myocardial oxygen consumption (MVO2). One minute after Nifedipine, CSF increased from 115 +/- 15 to 193 +/- 47 ml/min (p less than 0.001), and CVR decreased from 0.92 +/- 0.16 to 0,54 +/- 0.12 mm Hg X min X ml-1 (p less than 0.001). Mean aortic pressure dropped from 107 +/- 5 to 99 +/- 3 mm Hg (p less than 0.01). MVO2 was reduced from 14.6 +/- 2.6 to 11.7 +/- 2.8 ml O2 X min-1 (p less than 0.05). After five minutes CSF (113 +/- 18) and MVO2 (14.9 +/- 3.1) had returned to their preinjection level. Additionally, CSF and MVO2 were measured during rapid atrial pacing (mean rate 118 +/- 6 min-1). Average CSF and MVO2 values were 172 +/- 63 and 19.8 +/- 5.0 before and 177 +/- 69 and 20.6 +/- 7.3 approximately 6 minutes after Nifedipine injection. CONCLUSIONS: Intracoronary Nifedipine results in coronary vasodilation and subsequently in an increase in coronary flow. The concomitant reduction in MVO2 provides evidence for an oxygen sparing, negative inotropic effect of Nifedipine, which, however, is of very limited duration. A sustained oxygen-saving effect during periods with increased oxygen demand could not be shown.

Angina Pectoris↗
PubMed1981

Strong association of idiopathic membranous nephropathy (IMN) with HLA-DR 3 and MT-2 without involvement of HLA-B 18 and no association to BfF1.

The present study investigated the distribution of HLA-antigens and Bf alleles in a group of 21 patients suffering from biopsy proven Idiopathic Membranous Nephropathy (IMN). A statistically significant increase of HLA-DR3 (76.2%) was detected in the patient group as well as an increase of MT-2 (86%), which is a new supertypic specificity defined within the 8th International Histocompatibility Workshop 1980. No association between BfF1 and IMN can be deduced from this study. Only the common Bf alleles (BfFF, BfFS, BfSS) were found in the patient group presented here. Also the previously reported association between HLA-B18 and IMN was not corroborated by this study. Not a single IMN-patient typed positive for HLA-B18. Thus the presence of two different HLA-DR-Bf-B linkage groups (HLA-DR3/BfF1/HLA-B18 and HLA-DR3/Bf; all alleles/HLA-B8) may point to at least two different immunological mechanisms underlying IMN.

Adolescent↗
PubMed1980

[Variable acute effects of prazosin on left ventricular failure (author's transl)].

The effect of 2.5 mg prazosin orally was monitored for one hour by cardiac catheterisation in 11 patients with cardiac insufficiency as a result of primary cardiomyopathy. Mean pressures of the pulmonary capillary bed and pulmonary artery decreased on average by 9 mm Hg, of the right atrium by 2.5 mm Hg and systemically by 8 mm Hg. Judging by the increase of cardiac index patients were divided into a group of 7 "responders", all showing congestive cardiomyopathy, and a group of 4 "nonresponders" with various cardiomyopathies. During prazosin treatment cardiac index increased by 23% and pulmonary arteriole resistance decreased by 4% and pulmonary arteriole resistance increased by 41%. It is concluded that not all forms of left ventricular failure respond favourably to prazosin. Divergent effects of prazosin may possibly be caused by unequal effects on pre- and after-load of both ventricles and on variable behaviour of lung arteriole resistance.

Adult↗
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↗
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↗