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Biomedical subjects

J Castenfors

Publications and source records attributed to J Castenfors.

At least 19 recordsLinked to original sources
PubMed1991

A study of exercise-induced microalbuminuria in type I (insulin-dependent) diabetes mellitus.

Microalbuminuria is thought to be an important prognostic factor in diabetes mellitus. To study the influence of changes in blood pressure on the development of microalbuminuria during exercise, two exercise tests were carried out. A total of 32 insulin dependent diabetic men whose age at onset was less than 30 years, mean duration of diabetes 14 years (range 7 to 21) and mean age 29 years (range 21 to 40), and who did not have albuminuria (N-labstix negative) were studied. The diabetic patients were compared with a total of 29 age-matched male control subjects. Urinary albumin excretion was measured during two exercise tests: at a standardised workload (150 W) for 30 min, and at a standardised heart rate for 25 min. The diabetic patients had higher albumin excretion rates during both exercise tests compared with the control subjects. Blood pressure and heart rate during exercise were significantly higher in diabetic patients compared with control subjects in the standardised workload test. If the test was individualised to achieve the same standardised heart rate there was no significant difference in blood pressure between the diabetic patients and the control subjects. These results indicate that the diabetic kidneys were more sensitive than the healthy kidneys to similar degrees of haemodynamic stress induced by exercise.

Adult↗
PubMed1979

Hemodynamic changes during sequential ultrafiltration and dialysis.

Seven patients on regular dialysis were studied to elucidate the hemodynamic changes during ultrafiltration and dialysis, performed sequentially, the period of ultrafiltration (1 hour) either preceding or following dialysis (3 hours). During dialysis ultrafiltration was prevented by applying positive pressure in the dialysate compartment. Cardiac index (dye dilution: indocyanine green), heart rate, stroke volume index, blood pressure, and total peripheral vascular resistance index were measured. During ultrafiltration, cardiac index and stroke volume index decreased, but heart rate was not significantly changed. Total peripheral vascular resistance increased, resulting in unchanged blood pressure. During dialysis, the total peripheral vascular resistance decreased, but cardiac index and heart rate increased. BP decreased when the increase in cardiac index was insufficient to compensate for the decrease in total peripheral vascular resistance. PRA increased during ultrafiltration due to hypovolemia and decreased during dialysis, presumably due to decreased sympathetic activity which may also be a cause of dialysis-induced vasodilation.

Adult↗
PubMed1979

[Hemodynamic changes during ultrafiltration and hemodialysis in uremia].

1. The ultrafiltration causes a reduction of blood pressure and minute output of the heart which is compensated by vasoconstriction and thus a decrease of blood pressure is prevented. 2. Changes in the salt concentrations with reduction of the osmolarity during the dialysis without simultaneous ultrafiltration lead to vasodilation and hypotension despite increase of the minute output of the heart. 3. During a usual haemodialysis (i.e. dialysis with simultaneous ultrafiltration) the vasodilating effect of the dialysis may abolish the vasoconstrictive effect of the ultrafiltration and thus may be the cause of the hypotension.

Adult↗
PubMed1978

Angiotensin effect in the human kidney.

The renal effect of angiotensin has been recorded in patients by determination of variations in the length of the kidney and by selective injection of contrast medium into the renal artery with special angiographic techniques. The experiments demonstrate the rapid onset of the angiotensin effect on the renal vessels. The effect on kidney length was considerably prolonged compared with the vascular effect.

Aged↗
PubMed1978

The influence of dialysis fluid composition on the blood pressure response during dialysis.

To elucidate the relative role of osmolar (sodium) and acetate shifts during dialysis, 6 patients with problems of overhydration underwent rapid ultrafiltration for 1 hr (mean weight reduction 2.0 kg), using the 1 m2 RP 6 dialyzer. Ultrafiltration was carried out at the beginning of each of 5 dialysis treatments at weekly intervals. Ultrafiltration was undertaken without dialysis (controls) and with simultaneous dialysis using acetate (40 mmoles/1) or bicarbonate (25 mmoles/1) in the dialysis fluid with dialyzate sodium concentration of 133 and 145 mmoles/1. The systolic blood pressure and mean arterial pressure which were stable with ultrafiltration only fell slightly when a high dialyzate sodium concentration was used and much further when the dialyzate sodium concentration was kept low. These changes were apparently related to the changes in plasma osmolality. Acetate had no effect on blood pressure at the higher sodium concentration, but a slight (insignificant) additive effect when used in the low-sodium dialyzate. Shifts in osmolality (sodium concentration) seem to be more important than the effect of acetate in inducing dialysis-associated hypotension.

Acetates↗
PubMed1977

Haemodynamic effects of four months' mefruside therapy in hypertensive patients.

The haemodynamic changes after 4 months' mefruside therapy in 13 patients with essential hypertension have been studied. Intraarterial BP was significantly reduced both at rest supine and during standardized leg exercise in sitting position. The reduction was caused mainly by a decrease in cardiac output in about half of the patients and mainly by a decrease in total peripheral vascular resistance in the remainder. Thus, for the total material there was no significant change in either cardiac output or total peripheral vascular resistance. At rest, however, there was a significant decrease in storke volume (p less than 0.05) and an increase in heart rate (p less than 0.05). On changing from supine to sitting position, the average systolic and diastolic pressures increased before and decreased after therapy, the differences being significant. The results indicate that the hypotensive effect of long-term saluretic therapy is accomplished by a decrease in cardiac output and/or peripheral vascular resistance, with large interindividual variations.

Adult↗
PubMed1977

Haemodynamic effects of saluretic treatment and beta-receptor blockade in patients with essential hypertension.

The long-term haemodynamic effects of treatment with mefruside alone or in combination with alprenolol have been studied in nine patients with essential hypertension. After four months of mefruside therapy alone there was a significant decrease in intraarterial BP both at rest and during standardized leg exercise. Cardiac output and calculated total peripheral vascular resistance (TPVR) showed only minor mean decreases which were not statistically significant. Stroke volume tended to decrease and heart rate to increase. After another four months' treatment with addition of alprenolol there was a further significant decrease in intraarterial BP, related mainly to a further mean decrease in cardiac output which was not statistically significant. Heart rate decreased significantly, stroke volume was not significantly changed. Compared with the pretreatment levels, combination therapy induced a substantial decrease in intraarterial BP and a significant decrease in cardiac output both at rest in supine position and during standardized leg exercise. TPVR decreased slightly both at rest and during exercise but the change was not statistically significant. The results suggest that the decrease in BP after combined therapy with mefruside and alprenolol is mainly related to a decrease in cardiac output, the changes in TPVR being not significant. The additive hypotensive effect of alprenolol seems to be related in part to blocking of the increase in sympathetic activity that was found after treatment with mefruside alone.

Adult↗
PubMed1977

The effects of four months' treatment with spironolactone on systemic blood pressure, cardiac output and plasma renin activity in hypertensive patients.

The effect of spironolactone on BP, cardiac output, plasma renin activity and urinary excretion of electrolytes has been studied in 12 hypertensive patients. After 1 month of spironolactone therapy there was a significant decrease in arterial BP. Urinary sodium excretion was significantly decreased and plasma renin activity increased. After four months of spironolactone therapy there was no further decrease in arterial BP. Cardiac output, heart rate and stroke volume were unchanged in the supine position, but the calculated total peripheral vascular resistance (TPVR) was reduced, indicating that the lower BP was mainly a result of dilatation of the resistance vessels. During exercise there was still a significant decrease in arterial BP but this was related to a decrease in both cardiac output and TPVR.

Adult↗
PubMed1977

Effect of saluretic therapy on muscle content of water and electrolytes in relation to hemodynamic variables.

Muscle content of water and electrolytes (needle biopsy), intraarterial BP and cardiac output (dye dilution technique) were measured in 12 patients with essential hypertension before and after 4 months of mefruside therapy (25 mg/day). Before therapy there were no significant differences in muscle tissue electrolyte and water content compared with normotensive subjects. No correlation was found between central hemodynamic variables and the electrolyte and water content of muscle tissue either before or after therapy. After 4 months of mefruside therapy, muscle tissue water showed a mean decrease which was not significant. Serum potassium and muscle potassium content decreased significantly but there was no significant change in intracellular potassium concentration. Intracellular sodium concentration increased significantly, while muscle sodium content showed a mean increase which was not statistically significant. The change in intracellular sodium concentration showed a significant negative correlation with the decrease in mean arterial BP. The change in total cellular water content showed a significant negative correlation to the changes in total peripheral vascular resistance. Saluretic therapy seems to induce counterregulatory mechanisms that interfere with the hypotensive effect.

Adult↗
PubMed1977

Effect of changes in blood volume distribution on circulatory variables and plasma renin activity in man.

In 8 healthy subjects the pressure around the lower body was changed to 40 mmHg above (LBPP) and below (LBNP) atmospheric, thereby altering the amount of blood pooled in the lower body. Heart rate, intraarterial blood pressure, central venous pressure, cardiac output (dye dilution technique) and forearm blood flow (venous occlusion plethysmography) were measured. Plasma renin activity was determined with a radioimmunological method. 6 subjects maintained a relative circulatory steady state during LBNP. LBNP caused significant decrease in central venous pressure (CVP), stroke volume and cardiac output (Q) with an unchanged mean arterial pressure (MAP). Heart rate (HR) increased significantly. Calculated total peripheral vascular resistance (TPVR) and regional vascular resistance (RVR) in the forearm were significantly increased when measured 5-9 min after the onset of LBNP, whereas plasma renin activity (PRA) showed a definite increase only after 19 min of LBNP stimulation. No correlation was found between the changes in PRA and TPVR or RVR. Increasing the pressure around the lower body (LBPP) resulted in a slight but significant increase in MAP as well as a significant but transient increase in CVP. No significant changes were found in HR, Q or TPVR. In the forearm a decrease in RVR was demonstrated. PRA was not significantly changed. The results demonstrate that peripheral vascular resistance and PRA are both influenced by changes in blood volume distribution, possibly elicited via intrathoracic receptors sensitive to changes in central blood volume and/or CVP. The results also suggest that PRA does not play any significant part in the vasoconstriction during LBNP stimulation.

Atmospheric Pressure↗
PubMed1977

Blood pressure and heart rate regulating capacity of the carotid sinus during changes in blood volume distribution in man.

The influence of changes in blood volume distribution on the carotid baroreflex was studied in 18 subjects. Blood volume distribution was changed by varying the pressure around the lower body above and below ambient, thereby varying the amount of blood pooled in this region and exerting a secondary influence on the central blood volume. The carotid arterial stretch receptors were stimulated by varying the pressure in air-tight box enclosing the neck. To obtain a standardized carotid sinus stimulus (SCS) the pressure in the box was varied sinusoidally between - 10 and - 40 mmHg with a fixed freqency of 0.03 Hz. The effects on heart rate and blood pressure were assessed by harmonic analysis performed off-line on a digital computer. During lower body negative pressure of -40 mmHg (LBNP -40), i.e. during a procedure known to reduce the central blood volume, SCS induced an augmented effect on the blood pressure regulating capacity but not on the heart rate response. Expressing the blood pressure regulating capacity as peak-to-peak changes in systolic arterial pressure, the response during LBNP -40 mmHg was almost twice the control value. The opposite stimulus-lower body postive pressure-influenced the SCS-induced effects only slightly but on the average a minor reduction in both blood pressure and heart rate regulating capacity was found compared with the control condition, though the difference did not reach significant levels. The results support the hypothesis that changes in blood volume distribution modify the function of the carotid baroreflex, possibly via intrathoracic receptors sensitive to changes in central blood volume and/or central venous pressure.

Adult↗
PubMed1977

Carotid baroreceptor function in hypertensive patients.

Carotid baroreceptor function has been studied in twenty-five patients with essential hypertension and in ten normotensive control subjects of corresponding age. The carotid baroreceptors were stimulated by increasing the transmural pressure over the carotid arteries by the application of negative pressure in a box enclosing the neck. Stimulation elicited significant decreases in intra-arterial blood pressure, heart rate and cardiac index in both hypertensive and normotensive subjects. Both groups also showed a significant decrease in stroke index and a significant increase in total peripheral vascular resistance index. The response to carotid sinus stimulation did not differ significantly between the two groups. In fourteen of the hypertensive subjects, carotid baroreceptor function was studied after 4 months of saluretic therapy, mefruside, and in nine of these patients after additional treatment with a beta-receptor blocking drug, alprenolol, for another 4 months. Both mefruside and alprenolol induced a significant decrease in mean arterial blood pressure but the response to the carotid baroreceptor stimulation was not significantly altered. The findings indicate that the carotid baroreceptor is re-set to the actual blood pressure level, with little or no change in gain in hypertensive subjects both without and during hypotensive therapy.

Adult↗
PubMed1976

Cardiac effects of amitriptyline in rats.

The effect of intravenous amitriptyline (0.5-2 mg/kg) on heart rate, blood pressure, ECG, and electrolytes in plasma and heart muscle was studied in rats. In addition, the effect on monophasic action potentials was studied in rats with open chest. Amitriptyline caused a significant decrease in blood pressure and heart rate and a significant prolongation of QRS and PQ duration. At the time of maximal QRS prolongation (mean +94%) the duration of monophasic action potentials was virtually unchanged. Beta-adrenergic blockade by means of pretreatment with 0.1 mg propranolol did not influence the amitriptyline-induced prolongation of QRS duration. Amitriptyline administration causing obvious QRS prolongation induced no detectable changes in plasma and heart muscle electrolytes. The results contradict adrenergic dominance or marked imbalance between intra- and extra-cellular electrolytes as a cause of the ECG changes. The present data indicate that the amitriptyline effect is compatible with a direct quinidine-like action on the heart, resulting mainly in a slowing of impulse propagation in the intracardiac conduction system.

Action Potentials↗
PubMed1976

Circulatory effects of dihydroergotamine in patients with disturbed sympathetic vasomotor control with special reference to postural hypotension.

In five patients with postural hypotension (disturbed sympathetic vasomotor control) the effect of intravenous and oral administration of dihydroergotamin (DHE) has been studied. The therapeutic effect of oral administration of DHE has also been compared to the effect of treatment with an antigravity suit. Following intravenous administration of DHE, systemic and central venous pressure increased in all cases. The effect on cardiac output was negligible and consequently the calculated total peripheral vascular resistance increased. Orthostatic tolerance increased in all cases. During long-term oral administration the effect was comparable to that obtained with an antigravity suit. The increased orthostatic tolerance is explained by a constrictive effect on both capacitance and resistance vessels. In order to analyze the influence of a functional denervation on the effect of DHE on peripheral circulation, a study has also been performed during epidural anaesthesia of the lower body in 11 patients. In the legs which were deprived of sympathetic tone intravenous administration of DHE caused constriction of resistance vessels. In the intact forearm there was a decrease of tone in the resistance vessels. The results indicate that DHE - apart from its well-known venoconstrictive effect - also may constrict resistance vessels when they are subjected to a low sympathetic nervous outflow.

Administration, Oral↗
PubMed1975

Effect of dihydroergotamine on perpheral circulation during epidural anaesthesia in man.

The effect of intravenous administration of dihydroergotamine (DHE) on regional blood flow in the forearm and calf after pharmacological nerve blockade of the lower body induced by epidural anaesthesia has been studied in 13 subjects. After anaesthesia, DHE induced a significant increase in blood flow in the forearm with intact innervation and a significant decrease in blood flow in the nerve-blocked calf. On the average, the arterial blood pressure increased slightly. The calculated local vascular resistance increased in the nerve-blocked calf, probably due to a direct myogenic constrictive effect of DHE. In the intact forearm, local vascular resistance decreased. The results indicate that DHE exerts a complex effect on resistance vessels in addition to its well-known effect on the capacitance vessels.

Anesthesia, Epidural↗