Biomedical subjects

C Swartz

Publications and source records attributed to C Swartz.

At least 55 records · Page 3Linked to original sources

PubMed1976

Salt, frusemide and renin in severe experimental renal hypertension.

1. Sodium-deficient diet failed to alter development and maintenance of severe renal hypertension produced in the rat by ligation of the aorta between the renal arteries. 2. High sodium diet did not alter the early phase of this hypertension, but significantly decreased blood pressure elevation in the late phases. 3. The decrease in blood pressure produced by high sodium intake does not appear to be mediated by renin suppression. 4. Frusemide effectively reduced blood pressure and renin at all phases.

Animals↗

PubMed1976

The haemodynamic response to salt and water loading in patients with end-stage renal disease and anephric man.

1. Patients with end-stage renal disease and anephric patients underwent expansion and depletion of body fluids with salt and water. This resulted in four different sequential haemodynamic patterns: (i) no significant increase in blood pressure; (ii) increase in blood pressure associated with a rise in cardiac output and no effect on total peripheral resistance; (iii) increase in cardiac output followed by a rise in blood pressure and total peripheral resistance; (iv) increase in total peripheral resistance and blood pressure without significant changes in cardiac output. 2. It is concluded that an initial rise in cardiac output is not necessary to increase-blood pressure in either anephric man or patients with end-stage renaldisease.

Blood Pressure↗

PubMed1976

The interrelation of renin and iron binding capacity.

When rats are subjected to hypoxia, an increase in serum angiotensinogen concentration occurs which is accompanied by the appearance of serum erythropoietin (EP) during the first 24 h. Subsequent increases in EP reach maximum values 24 to 48 h after increases in packed cell volume (PCV) and serum renin levels. The current experiments were designed to determine if a decrease in iron stores is the stimulus for renin production when rats are rapidly expanding their red cell volume in a hypoxic environment. Young rats fed McCall's low iron diet were paired with rats fed the same diet supplemented with ferric citrate (6 g/kg diet). After two weeks at ambient pressure, they were subjected to hypoxia (0.48 atm) for 1 to 10 days. After 5 days at the reduced pressure, a fraction of the rats on the low iron diet were fed the iron-supplemented diet. At the time of sacrifice, serum was assayed for total iron binding capacity (TIBC) and renin. Rats that were fed the low iron diet showed an increase in TIBC, an increase in serum renin and a positive correlation between serum renin and TIBC. Rats that were fed a normal iron diet under the same conditions had lower TIBC, lower serum renin and no correlation between serum renin and TIBC. When low iron diet rats were supplemented with iron, TIBC and serum renin decreased. These experiments may have a clinical counterpart. The total iron binding capacity, renin and angiotensinogen were measured in the serum of women during the first 19 weeks of pregnancy. Women during early pregnancy showed an increase in TIBC, an increase of renin and angiotensinogen in the serum and a positive correlation between TIBC and renin concentration. It is suggested that the increased concentration of renin in the serum of women during the first 19 weeks of pregnancy and in the serum of rats that are rapidly expanding their red cell volume are related to a decrease in iron stores.

Angiotensinogen↗

PubMed1976

Experimental model of severe renal hypertension.

A simple technique is described for producing severe reproducible renal hypertension in the rat. Total ligation of the aorta between the renal arteries and just below the origin of the superior mesenteric artery resulted in sustained systolic and diastolic pressures in 90 per cent of 170 rats studied. Arterial pressure is then measured in the conscious unrestrained rat through a carotid cannula inserted no more than 48 hours before measurements are made. The mean arterial pressure increases to a peak of 180 mm. Hg at day 5 and then remains at a plateau of 160 mm. Hg through the 40 days of the study. Plasma renin increases to a peak at 5 days but returns to baseline at 30 days despite the persistence of severe hypertension. Infarction of the left kidney below the aortic constriction results in no increase in pressure or plasma renin. Infarctions of the right kidney by emboli originating from the indwelling carotid cannula are associated with greater increases in blood pressure and plasma renin than the standard preparation. Prolonged carotid cannulation must be avoided in order to prevent such emboli. This simple technique for producing renal hypertension allows studies on the pathogenesis of hypertension with an excellent degree of reproducibility and reliability.

Animals↗

PubMed1975

Cardiac effect of diuretic drugs.

Triamterene, amiloride, ethacrynic acid, and furosemide were studied to determine whether they modified the digitalis-induced egress of myocardial potassium which is thought to facilitate the development of digitalis arrhythmias. In a control group of 15 dogs, potassium was measured in samples obtained simultaneously from the femoral artery (FA) and the coronary sinus (CS) in a control period and at intervals after the administration of 1 mg. of acetylstrophanthidin. Acetylstrophanthidin caused a significant increase in cardiac A-V difference in the potassium concentration (CS-FA) averaging 0.47 mEq. per liter. In a group of 10 dogs, when 175 mg. of triamterene was infused prior to the acetylstrophanthidin, the rise in A-V differnece was abolished and the arrhythmias often aborted. In contrast, the infusion of potent diuretics (40 mg. of furosemide in five dogs and 100 mg. of ethacrynic acid in another five dogs) prior to acetylstrophanthidin, caused a doubling of the maximal A-V potassium difference. This study suggests that the clinical administration of antikaliuretic drugs may prevent the arrhythmias of digitalis toxicity not only by reducing kaliuresis and subsequent hypokalemia, but by a myocardial effect which antagonized the digitalis-induced loss of myocardial potassium. Contrariwise, potent diuretics may facilitate digitalis arrhythmias through a myocardial action causing a greater egress of myocardial potassium, thus explaining the development of arrhythmias despite normal serum potassium levels. These potent diuretics should be used cautiously, especially when given intravenously to patients receiving digitalis.

Amiloride↗

PubMed1975

Prazosin in the treatment of hypertension.

1. Prazosin decreases blood pressure in normotensive, renal hypertensive and spontaneous hypertensive rats. The effect is greatest in the last-named. 2. In spontaneously hypertensive rats the decrease in pressure is associated with a decrease in heart rate. 3. In hypertensive patients prazosin decreases blood pressure by decreasing total peripheral resistance with minor effects on cardiac output. 4. Prazosin is effective in the long-term therapy of hypertensive patients, alone and in combination with a diuretic. The effect on blood pressure is the same in the supine and standing position.

Animals↗

PubMed1975

Measurement of intra-arterial blood pressure and cardiac output through the bovine artegraft. Hemodynamic measurements through the bovine artegraft.

Serial hemodynamic studies have become increasingly important in hypertension research. These studies have been accomplished using the A-V shunt. The progressive decline in the number of A-V shunts in favor of the A-V fistula has limited the number of measure cardiac output, the intra-arterial blood pressure cannot be measured through it. The present paper describes a technique for measuring both the cardiac output and direct intra-arterial blood pressure using the bovine artegraft.

Animals↗

PubMed1975

Blood pressure regulation in end-stage renal disease and anephric man.

The hemodynamic pattern of response to bilateral nephrectomy was studied in 29 patients with end-stage renal disease on maintenance hemodialysis. Four patterns of hemodynamic response were seen. In 12 patients with nonmalignant hypertension, bilateral nephrectomy reduced blood pressure and total peripheral resistance with no effects on cardiac output. In 5 patients with malignant hypertension, bilateral nephrectomy reduced blood pressure, increased cardiac index, and reduced total peripheral resistance more markedly. In these two groups, at equivalent levels of total exchangeable sodium, before and after bilateral nephrectomy, mean arterial pressure and total peripheral resistance were invaribly lower in the absence of renal tissue. In 3 additional patients with nonmalignant hypertension, the decrease in blood pressure after bilateral nephrectomy was delayed from 3 to 12 weeks. When this occurred spontaneously, it was accompanied by a decrease in total peripheral resistance. The fourth hemodynamic pattern was seen in 6 normotensive patients with end-stage renal disease. After bilateral nephrectomy, there were no significant changes in mean arterial pressure, total peripheral resistance, or cardiac output. Salt and water loading failed to elevate blood pressure significantly. Renal transplantation was performed in 3 hypertensive patients before removal of the end-stage kidney. The functioning renal homograft did not result in normal blood pressure as long as the end-stage kidneys remained in place. Removal of the end-stage kidneys significantly decreased mean arterial pressure and total peripheral resistance. In the anephric state, a sharp difference was seen in blood pressure response to salt and water loading between previously normotensive and previously hypertensive patients. Previously hypertensive patients responded with a progressive increase in blood pressure that reached hypertensive levels. Previously normotensive patients failed to elevate their blood pressure significantly. It is concluded that the vasopressor function of the kidney is the most important factor in the pathophysiology of hypertension of end-state renal disease. Expansion of body fluid plays a role, but elevates the blood pressure only in patients who were previously hypertensive. The antihypertensive function of the kidney does not appear to be a major factor in the regulation of blood pressure in end-stage renal disease.

Adolescent↗

PubMed1975

A three-phase clinical evaluation of prazosin.

A preliminary study of cardiac hemodynamics with measurement in both supine and tilt positions showed that the antihypertensive effect of prazosin given intravenously is associated with a fall in total peripheral resistance, with minor effects on cardiac output and heart rate, and with no consistent orthostatic hypotension. The postural reflexes appear to remain intact. The results are entirely similar to those reported by Lund-Johansen. In a second, short-term study of ambulatory patients, prazosin alone exerted an antihypertensive effect somewhat less than that of methyldopa, but the difference in blood pressure reduction between supine and standing positions was less with prazosin than with methyldopa. Both drugs were well tolerated. In a third, long-term study, prazosin alone gave satisfactory antihypertensive results, and prazosin used in combination with polythiazide produced a satisfactory response in 80% of the patients.

Adult↗

PubMed1974