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A rapid method for the quantitative analysis of radiopaque contrast media HPLC is described. Method can greatly help in solving problems of clinical and forensic interest.
A double-blind randomized study was performed in 49 patients to compare the hemodynamic changes induced by two contrast agents: non-ionic low osmolar lomeprol 350 (IO, n = 25) and ionic high osmolar Diatrizoat 370 (DIA, n = 24). We observed significant changes in hemodynamic parameters after laevocardiography with DIA: a decrease in LVSP from 125 +/- 14 to 113 +/- 14 mmHg, a decrease in mean aortic pressure from 96 +/- 9 to 84 +/- 10 mmHg and in max dp/dt from 2086 +/- 628 to 1861 +/- 654 mm Hg/sec. LVEDP increased from 13 +/- 5 to 17 +/- 6 mmHg and cardiac output from 5.9 +/- 1.2 to 7.7 +/- 1.2 l/min. Heart-rate also rose slightly, but insignificant. IO did not alter these parameters. After selective coronary angiography both groups did not differ significantly in systolic aortic pressure, but DIA caused a drop in diastolic aortic pressure after 10 to 15 sec and a bradycardia in the first five sec, in contrast to IO. These effects can be explained by a cardiodepressive action of contrast agents on left ventricular function, an increase in circulating volume and a reduced peripheral vessel resistance. Differences between both agents are probably due to their different osmolality. IO is a safe contrast agent, compatible in contrast to DIA. In patients with borderline left-ventricular function, IO is preferable, it exerts only very slight effects on cardiovascular function.
Many treatments have been proposed to manage sudden sensorineural hearing loss. The University of Iowa has used a protocol of intravenous radiopaque contrast and volume expander for the last 10 years in the treatment of sudden sensorineural hearing loss. A retrospective analysis of these cases was performed to review the efficacy of this treatment with respect to the natural history of the disease, as reported in previous studies. Sixty-four percent of 39 cases showed audiometric improvement in their pure-tone averages, speech reception thresholds, and speech discriminations while receiving treatment. Forty-eight percent of these showed improvement after their first treatment doses. Eighty percent of patients who presented more than 7 days after the onset of their hearing loss showed audiometric improvement with treatment, whereas 71 percent of patients presenting before 7 days showed audiometric improvement. However, the patients who presented earlier showed more marked improvement. Speech discrimination with the W-22 word list was a predictor of early recovery. Patients with measurable speech discrimination scores on presentation uniformly improved with treatment, even if their pure-tone average was profound. Our findings were suggestive of a pathophysiologic mechanism for some cases of sensorineural hearing loss for which intravenous contrast is efficacious. Although our findings were far from conclusive in this uncontrolled study, these initial results support the use of these agents in a rigorous clinical trial.
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The effect of conventional high-osmolality contrast media (diatrizoate) and new low-osmolality contrast media (iopamidol) on plasma histamine, cyclic AMP and cyclic GMP levels have been examined in a group of 37 mongrel dogs. Plasma histamine levels have a tendency of elevation at five minutes after initiation of injection of diatrizoate and iopamidol in low dose (5 ml/kg). However, statistically no significant changes were found in either diatrizoate or iopamidol in low dose (5 ml/kg) or high dose (15 ml/kg). Plasma cyclic AMP levels have elevated significantly in twenty minutes after termination of injection of iopamidol in low dose (5 ml/kg) and in high dose (15 ml/kg). Also plasma cyclic AMP levels have elevated significantly in twenty minutes after termination of injection of diatrizoate in high dose (15 ml/kg). These findings indicate iopamidol has potential of elevating plasma cyclic AMP as compared with diatrizoate. Plasma cyclic GMP levels have elevated significantly in twenty minutes after termination of injection of diatrizoate in low dose (5 ml/kg) and in high dose (15 ml/kg). Also plasma cyclic GMP levels have elevated significantly in twenty minutes after termination of injection of iopamidol in high dose (15 ml/kg). These findings indicate diatrizoate has potential of elevating plasma cyclic GMP as compared with iopamidol. It is suggested that iopamidol has potential of elevation of plasma cyclic AMP that suppresses histamine release and diatrizoate has potential of elevation of plasma cyclic GMP that enhances histamine release. And so iopamidol is though to be minor histamine releaser than diatrizoate.
UNLABELLED: Pulmonary function (specifically, forced expiratory volume in 1 sec and forced expiratory flow at low lung volumes) was measured with maximal expiratory flow-volume curves during excretory urography in 70 patients and during sham procedures in 27 subjects. Forty-one patients received a 100 ml intravenous bolus of 60% methylglucamine diatrizoate and 29 patients received 100 ml of 50% sodium diatrizoate. Within 20 min, greater than 95% of patients had bronchospasm as indicated by asymptomatic decreases in pulmonary function. These decreases were significantly (p less than 0.001) greater than in the subjects undergoing sham procedures. Greater than 50% of patients had a maximum decrease in pulmonary function that exceeded the range of variability for consecutive repetitions of maximal expiratory flow-volume curves. These patients were classified as responders during excretory urography. The prevalence of responders was similar in methylglucamine diatrizoate and sodium diatrizoate patients. The magnitude of maximum decreases in pulmonary function did not differ significantly between methylglucamine diatrizoate and sodium diatrizoate responders. CONCLUSIONS: Sodium diatrizoate does not offer an advantage over methylglucamine diatrizoate with respect to asymptomatic bronchospasm during excretory urography.
RATIONALE AND OBJECTIVES: Diabetic patients frequently suffer contrast media-induced nephropathy. Hyperglycemia in diabetes mellitus causes gradual deterioration of glomerular mesangial cells (MCs) in the kidney. In this study, the authors investigated the response of rat MCs cultured in high-glucose medium to diatrizoate and iohexol, high- and low-osmolar contrast media, respectively. METHODS: Isolated rat MCs were precultured under basal-glucose (5.5 mmol/L) and high-glucose (30 and 55 mmol/L) conditions for 24 hours to mimic hyperglycemia in diabetes mellitus and then were exposed to diatrizoate (40 and 80 mg I/mL) and iohexol (80, 120, 160 mg I/mL) for 2 hours. The cytotoxic effects of diatrizoate and iohexol were monitored by neutral red uptake in MCs. The protective effects of an antioxidant, d-alpha-tocopherol (Toc), on cytotoxicity of the contrast media were determined when MCs were precultured with Toc under high-glucose conditions or were exposed to the contrast media together with Toc. Peroxide levels in the cells exposed to the contrast media were analyzed by flow cytometry using dichlorofluorescin diacetate. RESULTS: Exposure to both contrast media (diatrizoate and iohexol) induced a concentration-dependent decrease in viability of the cells precultured under basal-glucose conditions (5.5 mmol/L). Preculture under high-glucose conditions (30 and 55 mmol/L) augmented the cytotoxic effects of both contrast media. An increase in the intracellular peroxide level was detected after exposure to both contrast media. Preculture with Toc prevented augmentation of the cytotoxic effects of diatrizoate by the higher glucose concentration (55 mmol/L). The exposure to diatrizoate together with Toc also attenuated its cytotoxic effects. Toc showed no such protective effects against iohexol exposure. CONCLUSIONS: These findings suggest that high-glucose conditions enhance the susceptibility of MCs to the cytotoxic effects of both contrast media; the enhanced susceptibility was in part attributable to oxidative stress caused by high-glucose conditions; diatrizoate exerted the cytotoxic effects by means of oxidative stress; and iohexol appeared to exert its cytotoxicity in a manner different from diatrizoate.
Contrast media can induce both a decrease in renal blood flow and a reduction in glomerular filtration rate (GFR) when administered to both experimental animals and humans. In the present study we have examined the role of adenosine in mediating these effects using the isolated perfused rat kidney. Kidneys were perfused with a 6. 7%-(w/v)-albumin-based perfusate supplemented with glucose and amino acids (n=6 per group). They were exposed to diatrizoate [20 mg of iodine (mgI)/ml; osmolality 1650 mOsm/kg of water] or iotrolan (20 mgI/ml; osmolality 320 mOsm/kg of water) in the presence or absence of theophylline (10.8 microg/ml), or to diatrizoate in the presence or absence of a specific adenosine A(1) receptor antagonist (KW-3902; 2 microg/ml) or a specific A(2) receptor antagonist (KF17837; 6 microg/ml). Diatrizoate (n=6) produced a fall in GFR from 0.65+/-0.04 to 0.42+/-0.03 ml.min(-1).g(-1) (P<0.05); renal perfusate flow (RPF) also declined, from 36.5+/-3.8 to 22.0+/-3.2 ml. min(-1).g(-1) (P<0.05). Iotrolan (n=6) produced a fall in GFR from 0. 64+/-0.02 to 0.48+/-0.04 ml.min(-1).g(-1) (P<0.05) and in RPF from 33.3+/-3.8 to 24.0+/-3.0 ml.min(-1).g(-1) (P<0.05). Theophylline (10.8 microg/ml) prevented the fall in GFR caused by either diatrizoate (baseline, 0.63+/-0.05 ml.min(-1).g(-1); diatrizoate+theophylline, 0. 60+/-0.04 ml.min(-1).g(-1)) or iotrolan (baseline, 0.64+/-0.04 ml. min(-1).g(-1); iotrolan+theophylline, 0.67+/-0.05 ml.min(-1).g(-1)), but did not affect the decreases in RPF caused by either agent. KW-3902 (2 microg/ml) also prevented the fall in GFR produced by diatrizoate (baseline, 0.66+/-0.05 ml.min(-1).g(-1); diatrizoate+KW-3902, 0.61+/-0.05 ml.min(-1).g(-1)), while the fall in RPF remained unaffected. KF17837 (6 microg/ml) had no effect on the decreases in either GFR or RPF induced by diatrizoate (n=6 per group). The results suggest a role for adenosine acting at the A(1) receptor in mediating the decrease in GFR induced by contrast media. This effect is independent of a change in renal vascular resistance, and possibly secondary to mesangial cell contraction causing a decrease in the ultrafiltration coefficient.
1. The involvement of endothelin in the renal responses to radiocontrast media was examined in the rat in vitro and in vivo using BQ123, a selective endothelin (ETA) receptor antagonist, and phosphoramidon, an endothelin-converting enzyme inhibitor. 2. For experiments in vitro, an isolated perfused rat kidney was employed perfusing in closed circuit with an albumin-based Krebs-Henseleit solution. The effects of BQ123 and phosphoramidon on the renal responses to iotrolan (iso-osmolar radiocontrast media) and diatrizoate (high-osmolar radiocontrast media) were examined. In vivo, renal conductance was measured using a Doppler flow probe in the anaesthetized rat pretreated with indomethacin, and the effects of BQ123 and phosphoramidon on the renal response to intravenous diatrizoate were examined. 3. In vitro, iotrolan and diatrizoate both produced a biphasic effect on the glomerular filtration rate, characterized by a transient increase followed by a sustained fall. Pretreatment with BQ123 (10 mumol/l), but not phosphoramidon (1 mmol/l), prevented both the increase and the sustained fall in glomerular filtration rate induced by radiocontrast media. 4. In vitro, iotrolan and diatrizoate both produced a sustained fall in renal perfusate flow. An initial increase in renal perfusate flow was only observed with diatrizoate. Pretreatment with BQ123 (10 mumol/l), but not with phosphoramidon (1 mmol/l), markedly inhibited the sustained fall in renal perfusate flow produced by both iotrolan and diatrizoate. BQ123 (10 mumol/l), however, markedly potentiated the renal vasodilatation produced by diatrizoate.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Radiocontrast-induced nephropathy is a clinically important complication of invasive cardiological procedures. It has been associated with DNA fragmentation of renal tubular cells, which is a hallmark feature of programmed cell death (apoptosis). We investigated the mechanism of this DNA fragmentation in an in vitro model of radiocontrast cytotoxicity on renal epithelial cells. METHODS: Madin Darby canine kidney (MDCK) cell monolayers were incubated (for 2-8 h) with isoiodine doses (37-111 mg iodine/ml) of the highly hyperosmolal, ionic radiocontrast agent diatrizoate or of the less hyperosmolal, non-ionic substance iopamidol. Mannitol, urea, and NaCl control media of corresponding hyperosmolality were used to evaluate the contribution of hypertonicity, hyperosmolality and/or ionic strength to radiocontrast toxicity. DNA fragmentation was assessed using fluorescence-activated cell sorting (FACS), agarose gel electrophoresis and terminal deoxynucleotidyl transferase-mediated deoxyuridine nick end labelling (TUNEL), cell morphology was analysed in Giemsa-stained cytospins. RESULTS: Diatrizoate induced concentration- and time-dependent DNA fragmentation of MDCK cells which was associated with morphological signs of apoptosis. Cycloheximide (1 microg/ml) did not prevent diatrizoate-induced DNA fragmentation, indicating that it is not dependent on protein synthesis. Diatrizoate-mediated cell death was associated with cell detachment from the tissue culture matrix. However, the DNA fragmentation is not a consequence of cell detachment since the prevention of cell attachment on agarose-coated dishes induced significantly less DNA fragmentation than diatrizoate. Iopamidol caused no detectable DNA breakdown. In contrast, hypertonic mannitol and sodium chloride, but not hyperosmolal urea, induced DNA fragmentation in MDCK cells, albeit less than diatrizoate. CONCLUSIONS: The DNA fragmentation of MDCK cells induced by diatrizoate is related to its hypertonicity in this in vitro model of radiocontrast cytotoxicity. Nuclear disintegration with subsequent cell death may contribute to the pathophysiology of radiocontrast-induced nephropathy, particularly in the hypertonic/hypoxic environment of the renal medulla. The present results underscore the importance of avoiding hyperosmolal urine states in patients at high risk of radiocontrast-induced nephropathy.
Radiographic contrast media (RCM) cause histamine-dependent allergic-like reactions. The direct effects of diatrizoate (high osmolar ionic monomer), ioxaglate (low osmolar ionic dimer), iopromide (low osmolar non ionic monomer) and iotrolan (iso-osmolar non ionic dimer) at the concentration of 200 mgI ml-1 (60 min exposure) on the release of histamine from human basophils, human lung mast cells (HLMC), and human skin mast cells (HSMC) were investigated. Diatrizoate induced 48 +/- 4% histamine release in basophils, 15 +/- 3% in HLMC and 25 +/- 6% in HSMC. The remaining RCM were relatively ineffective activators of histamine release in both HLMC and HSMC (ioxaglate 4 +/- 1% and 4 +/- 1%, iopromide 5 +/- 1% and 7 +/- 2%, iotrolan 7 +/- 2% and 10 +/- 3%, respectively). Both iotrolan and ioxaglate were effective in basophils inducing 21 +/- 3% and 24 +/- 6% histamine release, respectively, whereas iopromide was relatively ineffective (7 +/- 4%). Diatrizoate induced histamine release from all three cell types with optimal levels of histamine release after a 2-4 h incubation although significant levels occurred within 15 min. Dose-dependent histamine release from HLMC occurred in all four types of RCM, the largest response (37 +/- 3%) being produced by diatrizoate. The effect of osmolality on histamine release was investigated using different concentrations of mannitol solutions (0.25, 0.5 and 1 M). Histamine release from HLMC, HSMC and basophils after 90 min exposure to mannitol (1 M) was 24 +/- 2% (p < 0.05), 9 +/- 3% (p = 0.06) and 49 +/- 1% (p < 0.05), respectively, suggesting that hyperosmolality per se can induce histamine release from basophils and mast cells. Diatrizoate-induced histamine release in all three cell types was significantly reduced by lowering the temperature to 0 degree C and partially attenuated by the metabolic inhibitors antimycin A (1 microM) and 2-deoxyglucose (5 mM), and by the omission of glucose from the buffer solution. Diatrizoate-induced histamine release was not dependent on extracellular calcium. These data suggest that diatrizoate induces histamine release at least in part by non-cytotoxic mechanisms.
In order to assess systemic absorption, serum diatrizoate levels were measured in 25 patients requiring endoscopic retrograde cholangiopancreatography (ERCP). Urinary diatrizoate was measured in the urine of seven of these. In five additional patients, diatrizoate was instilled into the duodenum during endoscopy. Blood was drawn before and after completion of the procedure in all patients and at intervals from 2 to 24 hr in nine. Eighteen-hour urine collections were obtained from seven patients. Increases in serum diatrizoate concentration were 7.10 micrograms/ml +/- 3.01 (mean +/- SE) in the duodenal-instillation patients, 230.68 +/- 53.24 micrograms/ml in 9 patients in whom only the pancreatic duct was visualized, 7.83 +/- 1.05 micrograms/ml in three patients in whom only the bile duct was visualized, and 77.67 +/- 28.22 micrograms/ml in 13 patients in whom both ducts were visualized. The mean total urinary excretion of diatrizoate was 3.05 +/- 0.98 g of diatrizoate. Endoscopists performing ERCP should be aware of the likelihood of systemic absorption and the possibility of reactions to iodinated contrast materials in sensitive patients.