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At least 883 records · Page 49Linked to original sources
PubMed1994

Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat.

Human radiocontrast nephrotoxicity is predicted by the presence of multiple risk factors, often associated with compromised renal circulation. To produce a simple model of radiocontrast nephropathy, rats were pretreated with indomethacin and N omega-nitro-L-arginine methyl ester (L-NAME, to inhibit nitric oxide synthesis) before the administration of iothalamate. Acute renal failure consistently developed, with a decline in creatinine clearance from 1.05 +/- 0.10 to 0.27 +/- 0.05 ml/min (P < 0.001) associated with selective necrosis of 49 +/- 9% of medullary thick ascending limbs. Hemodynamic studies using laser-Doppler probes revealed that when injected alone, iothalamate increased outer medullary blood flow to 196 +/- 25% of baseline (P < 0.001). Pretreatment by L-NAME or indomethacin both reduced basal medullary blood flow and transformed the medullary vasodilator response to radiocontrast into vasoconstriction, with a prolonged reduction of medullary blood flow to less then half of baseline. Combined administration of indomethacin, L-NAME, and iothalamate lowered medullary blood flow to 12 +/- 4% of baseline. We conclude that prostanoids and nitric oxide have an important protective role in the renal response to radiocontrast material. Reduced synthesis of these vasoactive substances in renal/vascular diseases may predispose patients to radiocontrast nephropathy.

Acute Kidney Injury↗
PubMed1986

Nonionic contrast medium: effects on blood coagulation and complement activation in vitro.

A nonionic contrast medium was evaluated in vitro for its effects on coagulation and complement activation in comparison to a low osmolal contrast agent. In clotting assays each contrast medium was mixed with blood and clotting parameters were analyzed by using a thromboelastographic machine. Platelet function was studied by incubating platelet-rich plasma with individual contrast medium, and the subsequent challenge of a platelet aggregating agent. Complement activation was assessed by the hydrolysis of C3 protein into C3c fragment in contrast medium-incubated serum. Immunoelectrophoresis was used to detect C3c protein. Both the nonionic contrast medium and the low osmolal contrast agent acted as anticoagulant and antiplatelet agents, however, results with the low osmolal contrast agent were more pronounced compared to the nonionic contrast medium. Even at nonphysiologic concentration of contrast medium, no significant conversion at C3 to C3c was seen. Since these two agents caused hypocoagulable states in vitro, it is likely that patients with thrombocytopenia, severe liver disease and with clotting factor deficiencies may present hemostatic complications during angiographic procedures.

Blood Coagulation↗
PubMed1987

Variability in arteriographic assessment of the carotid bifurcation.

We evaluated interobserver and intraobserver variability in the arteriographic assessment of the carotid bifurcation. Two neuroradiologists evaluated area stenosis and lumen surface morphology for 60 biplane carotid arteriograms in two reading sessions. Absolute interobserver differences for area stenosis averaged 8.8%, and interobserver differences were statistically significant for arteries of at least 50% stenosis. Analysis of observations for lumen surface morphology revealed statistically significant interobserver differences, averaging 29.5% disagreement. Intraobserver differences were not statistically significant. Observer variability for arteriography should be considered in the process of evaluating patients for carotid endarterectomy.

Carotid Arteries↗
PubMedDate not supplied

Blocking effect of radio-contrast media on cochlear depression.

Furosemide injection was used in a total of 72 guinea pigs to induce a cochlear dysfunction similar to the sensorineural loss associated with sudden deafness. Prior to the furosemide administration, 38 of the animals were treated with an injection of one of four radio-contrast media; methylglucamine and sodium diatrizoate, sodium iothalamate, methylglucamine and sodium iodamide, and methylglucamine diatrizoate. In the control animals, receiving only furosemide, both endocochlear potential (EP) and cochlear microphonic (CM) underwent a severe depression followed by recovery and subsequent secondary depression. Animals pretreated with one of the first three compounds showed little or no EP or CM depression. Animals pretreated with the fourth, methylglucamine diatrizoate, showed the same EP depression as the control animals. The possible mechanism for this blocking effect and its significance in the clinical treatment of sudden deafness is discussed.

Animals↗
PubMed2004

Renal interaction between itraconazole and cimetidine.

Renal drug interactions can result from competitive inhibition between drugs that undergo extensive renal tubular secretion by transporters such as P-glycoprotein (P-gp). The purpose of this study was to evaluate the effect of itraconazole, a known P-gp inhibitor, on the renal tubular secretion of cimetidine in healthy volunteers who received intravenous cimetidine alone and following 3 days of oral itraconazole (400 mg/day) administration. Glomerular filtration rate (GFR) was measured continuously during each study visit using iothalamate clearance. Iothalamate, cimetidine, and itraconazole concentrations in plasma and urine were determined using high-performance liquid chromatography/ultraviolet (HPLC/UV) methods. Renal tubular secretion (CL(sec)) of cimetidine was calculated as the difference between renal clearance (CL(r)) and GFR (CL(ioth)) on days 1 and 5. Cimetidine pharmacokinetic estimates were obtained for total clearance (CL(T)), volume of distribution (Vd), elimination rate constant (K(el)), area under the plasma concentration-time curve (AUC(0-240 min)), and average plasma concentration (Cp(ave)) before and after itraconazole administration. Plasma itraconazole concentrations following oral dosing ranged from 0.41 to 0.92 microg/mL. The cimetidine AUC(0-240 min) increased by 25% (p < 0.01) following itraconazole administration. The GFR and Vd remained unchanged, but significant reductions in CL(T) (655 vs. 486 mL/min, p < 0.001) and CL(sec) (410 vs. 311 mL/min, p = 0.001) were observed. The increased systemic exposure of cimetidine during coadministration with itraconazole was likely due to inhibition of P-gp-mediated renal tubular secretion. Further evaluation of renal P-gp-modulating drugs such as itraconazole that may alter the renal excretion of coadministered drugs is warranted.

ATP Binding Cassette Transporter, Subfamily B, Mem↗