Total Peripheral Vascular Resistance Index Research Articles

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.

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.

The long-term hemodynamic effect of fusaric acid in elderly hypertensive patients.

The hemodynamic effect of fusaric acid calcium salt (calcium salt of 5-butylpicolinic acid), an inhibitor of dopamine beta-hydroxylase, was studied in long-term administration of this agent in 10 elderly hypertensive patients. The hemodynamic items were measured by dye-dilution method before and 3 months, 6 months and one year after administration of fusaric acid calcium salt. The main hemodynamic changes observed were as follows: 1) Heart rate did not show any consistent change. 2) Systolic, diastolic and mean blood pressure decreased. The mean values of these pressures after fusaric acid calcium salt administration were significantly lower than the mean values before administration of this agent. 3) Total peripheral vascular resistance index decreased. The mean values of this index at 3 months, 6 months and one year after fusic acid calcium salt administration were significantly lower than the mean value before administration of this agent. 4) Cardiac index showed various changes throughout administration of fusaric acid calcium salt. The changes in this index might be secondary following the changes in total peripheral vascular resistance index, an inverse correlation being existed between them. 5) Stroke volume index showed almost a similar pattern of change as observed in cardiac index. An inhibitory action of fusaric acid calcium salt on the inotropism of the heart could be hardly found. 6) Plasma volume showed no tangible changes after fusaric acid calcium salt administration throughout one year. It might be concluded that fusaric acid calcium salt elicited the hypotensive response primarily through the reduction of total peripheral vascular resistance index.