[Thromboxane A2 and prostacyclin in patients with chronic glomerulonephritis and coronary heart disease in contrast media nephrotoxicity. Protective effects of calcium antagonists].
OBJECTIVE
To study pathological significance of circulating thromboxane A2 and prostacyclin in mechanisms of impairment of intrarenal hemodynamics and renal function due to contrast media (CM) in risk group patients and to study protective effects of calcium antagonists in CM nephrotoxicity.


METHODS
To study plasmic concentrations of TxA2 and prostacyclin, we used radioimmunoassay to measure plasmic TxB2 and 6-keto-prostaglandin F1a in patients with chronic glomerulonephritis (group 1), systemic atherosclerosis and coronary heart disease (group 2). The control group consisted of 23 healthy subjects. Diatrizoate (verografin), a high-osmolar CM, 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 1 after CM infusion compared to the preinfusion period and healthy controls. Plasma 6-keto-prostaglandin F1a in group 1 before CM infusion was lower than in controls after CM infusion. The data in group 2 were similar to those for group 1. Administration of nifedipine before and after introduction of CM prevented a rise in serum creatinine and had beneficial effects on TxA2 and prostacyclin synthesis.


CONCLUSIONS
Ionic CM have a renal vasoconstrictive effects mediated by imbalance between vasoconstrictor TxA2 and vasodilator prostacyclin and may be nephrotoxic in risk group patients. The protective effects of calcium antagonists promote normalization of calcium dependent TxA22 and prostacyclin synthesis.
Dzgoeva
F U
FU
Kutyrina
I M
IM
D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000097:blood; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D002908:Chronic Disease; D003287:Contrast Media / Q000009:adverse effects*; D003327:Coronary Disease / Q000097:blood* / Q000150:complications / Q000175:diagnosis; D018450:Disease Progression; D004342:Drug Hypersensitivity / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D011464:Epoprostenol / Q000097:blood*; D005260:Female; D005921:Glomerulonephritis / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000098:blood supply / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D012079:Renal Circulation / Q000187:drug effects; D013928:Thromboxane A2 / Q000097:blood*
D015415:Biomarkers; D002121:Calcium Channel Blockers; D003287:Contrast Media; D013928:Thromboxane A2; D011464:Epoprostenol