[Follow-up monitoring of kidney transplants with color-coded duplex sonography]. / Verlaufskontrollen von Nierentransplantaten mit der farbkodierten Duplexsonographie.

Fifty patients were examined immediately after renal transplantation by colour-coded duplex sonography. This procedure is a further development of conventional duplex sonography and permits demonstration of soft tissues in real time, as well as simultaneous imaging of blood flow over the whole imaging area. Perfusion of the transplant could be demonstrated in all patients by this method. Colour-coded duplex sonography can replace scintigraphy and angiography for the demonstration of perfusion of renal transplants. It is, however, not possible to distinguish with certainty between acute tubular necrosis and acute rejection by performing spectrum analysis of blood flow in the renal arteries.

Beneficial effects of long-term prostaglandin E2 infusion on the course of postischemic acute renal failure. Long-term studies in chronically instrumented conscious dogs.

The effect of a continuous intra-aortal infusion of prostaglandin E2 (PGE2) (0.03 microgram . min-1 . kg-1) on the course of postischemic renal failure (180 min cessation of blood flow by inflation of a pneumatic cuff) has been investigated in 11 conscious sodium-replete dogs. The glomerular filtration rate (51Cr-EDTA: endogenous creatinine clearance) was less decreased in the PGE2 group (group B, n = 6) than in the control group (group A, n = 5; 13 ml . min-1 vs. 22 ml . min-1; p less than 0.05). Renal blood flow (electromagnetic flow probe) was markedly lower in the control group (82 ml . min-1) than in the PGE2 group (130 ml . min-1; p less than 0.05), even exceeding baseline levels in the latter group. Accordingly, the excessive rise in renal vascular resistance in the control group (+277%) was abolished in the PGE2 group (-20%) (p less than 0.05). Nitrogen retention was also markedly improved. Plasma renin activity, which was markedly raised initially (25.8 ng angiotensin I . ml-1 . h-1) was not significantly further increased during the subsequent 7 days. Urinary excretion of PGE2 was diminished in the control group and elevated following PGE2 infusion. It is suggested that the beneficial effects of PGE2 are mediated by preservation of renal perfusion. Additional effects of prostanoids on the ultrafiltration coefficient (KF) and cytoprotection by reduction of intracellular calcium accumulation must also be taken into consideration.

Effect of nifedipine and verapamil on alpha-receptor-activation in patients with essential hypertension.

The question of whether the hypotensive effect of calcium entry blockers involves an interaction with alpha-adrenergic receptors was examined. The effect of nifedipine subl. (20 mg, n = 9) and of verapamil p.o. (160 mg, n = 9) on the pressor effect of the unselective alpha-adrenergic agonist noradrenaline, as well as on 3H-yohimbine binding to platelet alpha 2-adrenoceptors was studied in patients with essential hypertension. In addition, the effect of nifedipine on reactivity to the selective alpha 1-adrenergic agonist phenylephrine was investigated (n = 9). Nifedipine caused a significant reduction of reactivity to noradrenaline (P less than 0.01), along with a significant decrease in binding sites (P less than 0.01). Affinity to the alpha 2-receptors was unchanged. Verapamil, although equally effective in lowering blood pressure, had no effect on the pressor response or binding sites. The pressor effect of the alpha 1-agonist phenylephrine was reduced (P less than 0.01) by nifedipine. Nifedipine may therefore affect both alpha 1- and alpha 2-adrenoceptors in patients with essential hypertension. Since verapamil did not affect the pressor response to noradrenaline or yohimbine-binding, the interaction with alpha 2-adrenoceptors does not appear to be a general prerequisite for the hypotensive action of calcium entry blockers.

Influence of prostaglandin A1 on renal filtration, hemodynamics and excretion. Investigations in chronically instrumented conscious dogs on a low- and high-sodium diet.

The effect on renal function of a 210-min infusion of PGA1 into the aorta of 10 conscious beagle dogs has been investigated. In the sodium-replete group, PGA1 caused an increase in the glomerular filtration rate (GFR) (24%), renal blood flow (17%) and sodium excretion (20%). By contrast, in the sodium-depleted group, PGA1 caused a considerable reduction of GFR (25%) and sodium excretion (51%). In this group, baseline renal blood flow was lower, and there was no further reduction during PGA1 infusion. Fractional sodium excretion was unchanged in the sodium-replete dogs, but was reduced in the sodium-deplete state. Plasma renin activity was markedly elevated and further increased in the sodium-deplete group, but it was nearly unchanged in the sodium-replete group. This difference in renal response to exogenous PGA1 might be due to interaction with the renin-angiotensin system, which was markedly stimulated by sodium depletion and additionally by prostaglandin infusion.