Thromboxane A(2) and prostacyclin in patients with chronic glomerulonephritis and coronary heart disease in contrast media nephrotoxicity. Protectiveeffects of calcium antagonists

Aim. To study pathological significance of circulating thromboxane A(2) and prostacyclin in mechanisms of impairment of intrarenal hemodynamics and re nal function due to contrast media (CM) in risk group patients and to study protective effects of calcium antagonists in CM nephrotoxicity. Materials and methods, To study plasmic concentrations of TxA(2) and prosta cyclin, we used radioimmunoassay to measure plasmic TxB(2) and 6-keto-prost aglandin F1a in patients with chronic glomerulonephritis (group 1), systemi c atherosclerosis and coronary heart disease (group 2). The control group c onsisted of 23 healthy subjects. Diatrizoate (verografin), a high-osmolar C M, was used (40-60 and 250-400 cc in groups 1 and 2, respectively). Results, Plasma TxB2 and serum creatinine concentrations were significantly elevated in group I after CM infusion compared to the preinfusion period a nd healthy controls. Plasma 6-keto-prostaglandin F1a in group 1 before CM i nfusion was lower than in controls after CM infusion. The data in group 2 w ere similar to those for group 1. Administration of nifedipine before and a fter introduction of CM prevented a rise in serum creatinine and had benefi cial effects on TxA(2) and prostacyclin synthesis. Conclusion, Ionic CM have a renal vasoconstrictive effects mediated by imba lance between vasoconstrictor TxA2 and vasodilator prostacyclin and may be nephrotoxic in risk group patients. The protective effects of calcium antag onists promote normalization of calcium dependent TxA22 and prostacyclin sy nthesis.