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Biomedical subjects

J Brod

Publications and source records attributed to J Brod.

At least 55 records · Page 3Linked to original sources
PubMed1977

Phenacetin abuse and chronic pyelonephritis.

A history of phenacetin abuse has been found almost three times more frequently among subjects diagnosed on clinical and functional grounds as suffering from chronic pyelonephritis than among those suffering from other renal diseases or among non-renal controls. The chronic pyelonephritis in subjects admitting phenacetin abuse has been usually characterized by a more frequent intense bacteriuria and leucocyturia, by a slightly more frequent haematuria, history of renal colic, presence of stones and more rapid downhill course of glomerular filtration rate than in subjects without phenacetin abuse. A sterile lesion also without any past evidence of infection was observed only in subjects with the heaviest analgesic abuse. The discontinuation of the abuse in 5 subjects led to an improvement of the renal function.

Chronic Disease↗
PubMed1977

Central and peripheral haemodynamic effects of angiotensin.

In 10 normotensive subjects intravenous infusion of angiotensin was followed by a significant increase in the arterial pressure, total peripheral resistance, central venous pressure and by a marked reduction of the intravascular forearm volume and venous distensibility. Forearm circulation time was shortened. The cardiac index, heart rate, forearm vascular resistance and the forearm blood flow did not change significantly.

Adolescent↗
PubMed1976

[Water and potassium metabolism changes].

The disturbances of water and electrolyte metabolism in the body can be subdivided into three large groups: 1) disturbances of free water which are related to the whole body water and are always coupled with changes in the osmolality of the internal environment and also of the interior of the cells (hypertension due to loss of water, hypotension in water intoxication); 2) isotonic changes of the volume of the extracellular fluid-oedema or extracellular dehydration. The latter are always coupled with a hypovolaemia and with a danger to the circulation which may end in shock. There is also a cumulative loss of potassium as a result of the dehydration reaction; 3) disturbances of the intracellular water metabolism which are associated with disturbances of the potassium metabolism. These may have grave consequences for the function of striated and smooth muscles, for the function of the nerves and various enzyme systems. Since the disorders of the extracellular water balance are generally best known, the attention is principally drawn in this paper to the hypertonic dehydration and the status of the potassium metabolism. The symptomatology of both conditions is discussed, and also their diagnosis with the simplest laboratory effort not associated with great loss of time (which is essential if valuable time is not to be lost before the laboratory results can be obtained). The theoretical considerations are supplemented with clinical examples and explanations of the treatment.

Adult↗
PubMed1976

[Disturbances of Free Water and Electrolyte Metabolism: Three large groups are differentiated].

1. Disturbances of free water which are related to the whole body water and are always coupled with changes in the osmolality of the internal environment and also of the interior of the cells. 2. Isotonic changes of the volume of the extracellular fluid- edema or extracellular dehydration. The latter is always coupled with a hypovolemia and with a danger to the circulation which may end in shock. There is also a cumulative loss of potassium as a result of the dehydration reaction. 3. Disturbances of the intracellular water metabolism which are associated with disturbances of the potassium metabolism. These may have consequences for the function of striated and smooth muscles, for the function of the nerves and various enzyme systems.

Adult↗
PubMed1976

The effect of intravenous angiotensin II on the peripheral circulation with particular reference to its bearing on general haemodynamics.

1. Central and peripheral haemodynamic effects of intravenous infusion of angiotensin II have been investigated in ten normotensive subjects. Angiotensin II was given at the rate of 0-12-5-0 microng/min. 2. The pressor response to angiotensin II was accompanied by a significant increase in the total peripheral resistance, central venous pressure and by a marked reduction of the intravascular forearm volume and venous distensibility. Forearm circulation time was shortened. 3. Cardiac index, heart rate, forearm vascular resistance and the forearm blood flow did not change significantly in the whole group but in the individual subjects some of the variables changed markedly in either direction. 4. Direct action of angiotensin II on the vessels and its central and peripheral sympathomimetic aciton as well as the role of the baroreflex as responsible causes for haemodynamic changes after angiotensin II are discussed.

Adolescent↗
PubMed1976

Clinical and haemodynamic study of a new vasodilator drug L6150 (3-[bis-(2-hydroxyethyl)amino]-6-hydrazinopyridazine) in man.

1. L6150 is a highly effective vasodilator which produces an acute reduction of blood pressure when administered intravenously. 2. This is due entirely to a decrease in total peripheral vascular resistance. 3. On oral administration it can effectively lower blood pressure in mild hypertension and is effective in combination with other hypotensive agents with different mechanisms of action.

Administration, Oral↗
PubMed1975

[Kidney in heart failure (author's transl)].

The adaptability of the kidney in heart-failure is restricted. This is due to a sympathetically mediated renal vasoconstriction, forming part of a sympathetically induced general rearrangement of haemodynamics. This is reflected in a rise of the total peripheral vascular resistance and of the right auricular pressure and can be normalized to a large extent by sympathetic gamma-blockade. The renal vasoconstriction reduces the glomerular filtration rate and, thus, the tubular sodium load. Simultaneously, possibly by the same sympathetic stimulus, more renin is liberated from the juxtaglomerular apparatus. This increases the production of angiotensin and in turn, raises the production of aldosterone. By the combined effect of the reduced glomerular sodium load and aldosterone-mediated increase in tubular reabsorption of sodium, sodium and water will be retained in the body. During the night-rest the load on the circulatory system diminishes. In the early stages of heart-failure this emergency circulatory reaction, therefore, subsides and the rise of the renal fraction of the cardiac output leads to the excretion of the retained fluid and is the basis of nocturia.

Blood Proteins↗
PubMed1975

General and regional hemodynamics in hypertension in chronic renal disease.

Cardiac output, total peripheral vascular resistance, renal, extrarenal, forearm muscle and skin hemodynamics and an indicator of the splanchic vascular resistance were estimated in 20 subjects with chronic renal disease without signs of chronic renal failure and without anemia. The data were compared with a group of subjects with essential hypertension. The high blood pressure of chronic renal disease of mild or moderate severity was maintained in the first place by a high cardiac output, this being due to a rise of the stroke volume, while the heart rate was only slightly increased. The total peripheral vascular resistance was within the normal range in most of the subjects. The vascular resistance in the skin was slightly raised, that in the splanchnic area and muscle unchanged in renal hypertension. The possible pathogenic mechanisms are considered.

Adolescent↗