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PubMedDate not supplied

Does glucagon enhance opacification of the bile ducts during intravenous cholangiography? An experimental study in dogs.

To determine the rational for the ability of glucagon to enhance opacification of the bile ducts during intravenous cholangiography, which has been claimed in recent clinical reports, experiments were performed in dogs which had had Thomas cannulas inserted. A constant step-wise infusion of iodipamide was administered with or without a bolus injection and constant infusion of glucagon. At every infusion rate of iodipamide the biliary concentration of the contrast agent was less when glucagon was administered. Glucagon caused a choleresis, but had no effect on the rate of excretion of iodipamide. It is concluded that the theory that glucagon is of value to improve opacification of the bile ducts during intravenous cholangiography is unlikely to be confirmed by further clinical trials.

Animals↗
PubMed1977

Steroids: theoretical and experimental basis for utilization in prevention of contrast media reactions.

In vitro and in vivo studies were done to examine the effects of methylprednisolone on the adverse reactions induced by contrast media. At very high concentrations, the steroid potentiated the complement-activating effect produced in vitro by iodipamide, but inhibited the immune and nonimmune mechanisms of hemolysis. Rabbits pretreated for 3 days with intramuscular methylprednisolone (at high or low dosages) were significantly protected against an LD47 challenging dose of iodipamide. Those treated once with a low intravenous dose immediately prior to iodipamide challenge were protected to a lesser degree. Rabbits treated once with a very high intravenous dose of steroid evidenced no protection. A hyper-responsive dog was consistently protected against adverse reactions to injected sodium iothalamate by a 3-day steroid pretreatment.

Animals↗
PubMed1976

Pharmaco-cholangiography with anticholinergic drugs in the dog.

The effect of atropine and pipenzolate bromide (PB) in different dosage levels was investigated in intravenous cholangiography with 0.6 ml/kg iodipamide infused over 30 minutes in six cholecystectomized dogs (20-36 kg) equipped with Thomas cannulas through which the common bile duct could be cannulated. Doses of 1 mg atropine and 20 mg PB, half the dose given intravenously just prior to the contrast agent and the other half with the iodipamide infusion, had the greatest effect in decreasing the bile flow (atropine-24% at 60, PB-23% at 30 minutes) and increasing the bile iodine concentration (atropine + 16%, PB + 14%). The biliary iodipamide excretion rate was not affected.

Animals↗
PubMedDate not supplied

Emptying the gallbladder prior to intravenous cholangiography: effect on gallbladder visualization.

Experiments were done to test the hypothesis that emptying the gallbladder prior to intravenous cholangiography (IVC) would result in earler and better opacification of the gallbladder. Five dogs were studied on two separate days in a crossover experiment. Each dog had a standard IVC (15-minute infusion of meglumine iodipamide) 2.5 cc/kg of following a 14-16-hour fasting period. On one of the days, 0.3 mcg/kg of Ceruletide was intramuscularly administered to each dog 30 to 45 minutes prior to the iodipamide infusion. Films obtained at the end of infusion and at 20, 40, 60, and 90 minutes were evaluated independently by three radiologists. The results indicate that pretreatment with Ceruletide produces a significant (p less than 0.05) improvement in the quality of gallbladder opacification during the first 90 minutes following iodipamide infusion. We conclude that earlier and better opacification of the gallbladder during IVC can be obtained by prior emptying of the gallbladder with a cholecystokinetic agent.

Animals↗
PubMedDate not supplied

Particulate contrast media for computed tomographic scanning of the liver.

A contrast agent that is selectively accumulated in the liver should greatly improve the diagnostic value of contrast enhanced CT scanning. The advantages and disadvantages of different classes of hepatographic agents are briefly reviewed. Experimental results obtained with the particulate contrast agents, iothalamate ethyl ester and iodipamide ethyl ester, are presented in more detail. Following intravenous infusion of iodipamide ethyl ester, approximately 60% of the injected dose is accumulated in the rat liver. CT scanning experiments involving iothalamate ethyl ester infusions in New Zealand White rabbits demonstrate significantly higher liver contrast enhancement at 10-30 minutes postinfusion than is observed with diatrizoate at a sixfold greater iodine dose. The selective accumulation of a particulate contrast agent in hepatic reticuloendothelial cells compared to virtually no accumulation in implanted VX2 carcinoma demonstrates the important potential value of these agents in improving detection of liver metastases.

Animals↗
PubMedDate not supplied

Effect of elevated C1-esterase inhibitor concentrations on white blood cell-endothelium interactions: a potential mechanism for steroid protection in contrast material reactions.

Purified human C1-esterase inhibitor (C1INH) infused into the circulation of rabbits caused an immediate drop in white blood cell (WBC) count and, simultaneously, a marked decrease in WBC adhesion to the endothelium in the microcirculation. Infusion of iodipamide caused a marked "carpeting" of the venous endothelium by WBC, and this condition was reversed by subsequent infusion of C1INH. The relationship of elevated C1INH to the protective effect of prednisolone on iodipamide toxicity in the rabbit is discussed.

Animals↗
PubMed1976

Inhibition of in vitro concentrative prostaglandin accumulation by prostaglandins, prostaglandin analogues and by some inhibitors of organic anion transport.

1. Incubation of rabbit choroid plexus, anterior uvea (iris-ciliary body complex) or slices of kidney cortex in a medium containing tritium-labelled prostaglandin F(2alpha) ([3H]PGF(2alpha) or E1 ([3H]PGE1) results in a four- to thirteenfold concentrative accumulation of 3H activity. 2. Addition of PGF(2alpha, PGF(1) or PGA(1), any one of five PG analogues or a PG precursor, arachidonic acid, at a concentration of 10(-4) M reduced the active accumulation of [3H]PGs by 47-97%. Octanoic acid, at the same concentration, had only a moderate effect on the choroid plexus and no significant inhibitory effect on [3H]PFG(2alpha) accumulation by anterior uvea or kidney cortex. 3. Inhibition was also obtained with 2 mM iodoacetate (under anaerobic conditions) and with 10(-4) M diploretin phosphate, probenecid, iodipamide, indomethacin or dinitrophenol. Perchlorate (10(-4) M) and iodide (10(-4) or 10(-3) M) had no inhibitory effect while 10(-4) M p-aminohippuric acid had a significant inhibitory effect on the kidney cortex at a concentration of 10(-4) M and on the anterior uvea at 10(-3) M. 4. It is concluded that the apparent carrier mediated PG transport systems of the choroid plexus, anterior uvea and kidney cortex are not related to the iodide transport system, but may represent a subcomponent of the iodipamide transport system of these tissues. 5. These results suggest that the systemic distribution and the rate of renal excretion of PGs could be altered by high concentrations of PGs, pharmacologically less active PG analogues, some inhibitors of organic acid transport, and by some inhibitors of PG synthesis and PG action.

Animals↗
PubMed1992

Radiation inactivation of multispecific transport systems for bile acids and xenobiotics in basolateral rat liver plasma membrane vesicles.

The functional molecular mass of the cholate, phallotoxin, iodipamide, and ouabain transport proteins in isolated basolateral plasma membrane vesicles was determined by radiation inactivation. Purified basolateral plasma membrane vesicles were irradiated (-90 to -120 degrees C) with high energy electrons from a 10-MeV linear accelerator at doses from 0 to 30 megarads. After each dose, the initial uptake, the equilibrium binding, and the binding of the substrates at 4 degrees C were checked. The size of the transporting function was, for cholate, 107 +/- 8.9 kDa; for phallotoxin, 104 +/- 7 kDa; and for ouabain, 120 +/- 4.7 kDa. The target size for the binding proteins was 56 +/- 4.2, 57 +/- 5, and 47.2 +/- 1.95 kDa for cholate, phallotoxin, and taurocholate, respectively. In the case of iodipamide, the functional molecular mass for both the transport and binding proteins was 54 +/- 4.8 kDa.

Amanitins↗
PubMed1977

[Anticoagulant activity of triiodinated x-ray opaque media (author's transl)].

The anticoagulant activity of the triiodinated X-ray opaque media iodipamide, iothalamate and diatrizoate on standardized normal human pool plasma was investigated in vitro. We found a dose dependent lengthening of the thrombin time, the reptilase time and the partial thromboplastin time together with a dose dependent drop of the calcium thromboplastin and factor V activity. Iodipamide proved to exert the most pronounced anticoagulant activity of the 3 contrast media tested. The results are interpreted as latent disseminated intravascular coagulation with hyperfibrinolysis following the direct interaction of contrast media with the coagulation enzymes.

Blood Coagulation↗
PubMed1991

Hepatocellular transport of cyclosomatostatins: evidence for a carrier system related to the multispecific bile acid transporter.

The uptake of the cyclopeptide c(Phe-Thr-Lys-Trp-Phe-D-Pro) (008), an analog of somatostatin with retro sequence, was studied in isolated hepatocytes. 008 is taken up by hepatocytes in a concentration-, time-, energy- and temperature- dependent manner. Since 008 is hydrophobic, it binds rapidly to liver cells. This is evident by the positive intercept at the gamma-axis in the uptake curves. At higher concentrations, a minor part of the transport occurs by diffusion at a rate of 8.307.10(-6) cm/s. This part of diffusion is measured at 4 degrees C and can be subtracted from the uptake at 37 degrees C resulting in the carrier mediated part of uptake which is saturable. Kinetic parameters for the saturable part of uptake are Km 1.5 microM and Vmax 40.0 pmol/mg per min. The transport is decreased in the absence of oxygen and in the presence of metabolic inhibitors. Uptake is accelerated at temperatures above 20 degrees C. The activation energy was determined to be 30.77 kJ/mol. The membrane potential and not a sodium gradient is the main driving force for 008 transport. Cholate (a typical substrate of the multispecific bile acid transporter) and taurocholate are mutual competitive inhibitors of 008 uptake. Phalloidin, antamanide and iodipamide, typical foreign substrates of the transporter, interfere with the uptake of 008. AS 30D ascites hepatoma cells, known to be unable to transport bile acids, phalloidin and iodipamide, are also unfit to transport 008. Interestingly, sulfobromophthalein (BSP) but not rifampicin, both foreign substrates of the bilirubin carrier, inhibits the transport of 008 in a competitive manner.

Animals↗
PubMed1980

In vitro effects of radiographic contrast media on the complement system.

The effect of several radiographic contrast media on the complement system in vitro was examined using quantitative crossed immunoelectrophoresis. Diatrizoate, iothalamate, metrizoate, and methiodal did not cause electrophoretic conversion of C3 or properdin factor B. In fact, the small degree of spontaneous conversion occurring when serum is incubated in polypropylene tubes was inhibited by these contrast media or by hypertonic sodium chloride. Metrizamide caused enhanced conversion of C3 and factor B that was only partially inhibited by ethylene glycol tetracetic acid (EGTA) but completely inhibited by ethylenediaminetetraacetic acid (EDTA). Iodipamide caused a unique electrophoretic alteration of C3 that was not affected by EDTA or several other inhibitors and that was not identical with the usual products of C3 activation. Iodipamide in very low concentrations inhibited complement activation through the classical pathway.

Citrates↗
PubMedDate not supplied

Serine proteases as mediators of radiographic contrast media toxicity.

Iodipamide, iodoxamine, iothalamate, diatrizoate, and ioxitalamate exhibit a dose-dependent prolongation of coagulation time of global and monospecific functional coagulation tests. This is due to an inhibition of fibrin polymerization induced by these contrast media. Furthermore, a dose-dependent generation of fibrinolytic split products by RCM was found. At low doses, biliary RCM cause hypercoagulation by binding to spontaneously existing fibrinolytic products. Biliary RCM cause a dose-dependent decrease of hemolytic complement activity and decrease of complement factors of C3, B, and, to a lesser extent, C4. Nephrotopic RCM do not show these effects. By crossed immunoelectrophoresis B and C3 split products were not detected after in vitro incubation of iodipamide in serum or EDTA-blood. In contrast, zymosan, inulin, and dextran sulfate incubation of sera readily resulted in Bb and C3b generation. The failure to demonstrate complement split products was not due to artifacts. As a working hypothesis unspecific binding of RCM to blood proteins followed by interference with antithrombin and antiplasmin inhibitor functions is proposed. Possibly other antiproteases might be involved too. This results in a lowering of the clinical manifestation threshold of coagulation and fibrinolysis. The mechanism of complement activation remains unclear, since it is not influenced by EDTA, aprotinin, steroids, or by specific sera depleted of prekallikrein, Hageman factor, C2, and gamma-globulins.

Animals↗
PubMed1976

Facilitated transport of prostaglandins across the blood-cerebrospinal fluid and blood-brain barriers.

1. Ventriculo-cisternal perfusions were performed on rabbits with artificial cerebrospinal fluid containing blue dextran and tritium-labelled prostaglandin F(2alpha) ([(3)H]PGF(2alpha)). In order to study the nature of prostaglandin (PG) transfer across the blood-brain barrier, high concentrations of PGF(2alpha) or potential PG transport inhibitors were added to the perfusion fluid after the normal rate of [(3)H]PGF(2alpha) clearance was established.2. The [(3)H]PGF(2alpha) clearance was inhibited by 10(-6) to 10(-3)M PGF(2alpha), PGF(2beta), probenecid, iodipamide or bromcresol green but not by perchlorate.3. The (3)H content of the brain, relative to the (3)H-activity in the ventricular system, was also increased by high concentrations of PGF(2alpha), iodipamide or bromcresol green.4. It is concluded that the removal of PGs from the extracellular fluids of the brain is mediated by saturable, facilitated transport processes across both the choroidal and extrachoroidal regions of the blood-brain barrier system. In the case of the mammalian brain, such facilitated PG transport appears to be the primary mechanism for the termination of the action of these potent, endogenously produced autacoids.

Journal Article↗
PubMed1978

In vitro histamine and serotonin release by radiographic contrast media (RCM). Complement-dependent and -independent release reaction and changes in ultrastructure of human blood cells.

Peripheral leucocytes and platelets from twenty healthy volunteers were incubated in vitro with radiographic contrast media (diatrizoate-Hypaque, iothalamate-Conray and iodipamide-Cholografin) under varying conditions. All radiographic contrast media (RCM) were able to induce histamine release from peripheral leucocytes and the release reaction was dose-dependent. There were individual differences in the sensitivity of leucocytes to different RCM. The highest values (up to 80% histamine release) were found with high concentrations (0.07-0.3 M) of diatrizoate. The addition of normal human serum (NHS) to the reaction mixture led to a further increase in histamine release (P is less than 0.01), probably due to complement activation. The mechanism seems to be mediated by proteins of the alternative pathway, because serum depleted of complement components (factor B, factor D, properdin) did not show this synergistic effect. IgG-depleted serum, however, was able to show the augmented release reaction. Washed platelets incubated with RCM released serotonin in a dose- and time-dependent reaction. The most powerful serotonin-releasing RCM was found to be iodipamide, which produced a release reaction in all people investigated at concentrations of 0.04-0.09 M, while diatrizoate and iothalamate were effective only in half of the tested individuals at high concentrations (0.3 and 0.2 M respectively). The addition of plasma proteins to the reaction mixture inhibited the serotonin release quantitatively. There was no difference in inhibitory potency between autologous and heterologous plasma or serum; sera depleted of various complement components showed similar effects as NHS. The serotonin release was not due to platelet lysis, as determined by the concentration of lactic dehydrogenase present in the supernatant during serotonin release. Incubation of the leucocytes with RCM produced ultrastructural changes, including degranulation of basophils, aggregation of platelets and infiltration of the aggregates by polymorphonuclear leucocytes. The most prominent changes were observed when complement was present in the reaction mixture.

Basophils↗
PubMed1996

Movement of carboxyfluorescein across retinal pigment epithelium-choroid.

The movement of carboxyfluorescein (CF) across the isolated retinal pigment epithelium (RPE)-choroid of the albino rabbit was studied using an Ussing chamber under short-circuit conditions with CF concentrations ranging from 15 to 300 microM. The inward (from the choroid to vitreous side) permeability of the tissue to CF showed no significant change over the concentration range tested, averaging 2.2 x 10(-6) cm sec-1. Neither ouabain (1.0 microM), low external sodium concentration nor probenecid (100 microM) had significant effect on the inward movement of CF. The outward (from the vitreous to the choroid side) permeability of the tissue to CF gradually decreased as the concentration increased (ANOVA, P < 0.01: Scheffe's test, P < 0.05), averaging 3.7 x 10(-6) cm sec-1 at 75 microM. Further, it was always significantly greater than the inward permeability at the corresponding concentration (unpaired t-test, P < 0.05-0.01). The outward movement of CF was significantly inhibited by 2,4-dinitrophenol (10 microM), ouabain (1.0 microM), probenecid (100 microM), iodipamide (5.0 mM), hippurate (30 mM) or low external sodium concentration (25 mM). The net outward movement of CF became saturated as concentration was increased and a Lineweaver-Burk plot gave an apparent Km of 237 microM and Vmax of 1.8 nmol hr-1 cm-2. The results indicated that part of the outward movement of CF across the RPE-choroid depends on carrier mediated active transport, but to a much lesser extent than that of fluorescein. The inward movement of CF was thought to occur almost exclusively by passive diffusion through the paracellular spaces.

2,4-Dinitrophenol↗
PubMed1980

Protective effect of anionic cholecystographic agents against phalloidin on isolated hepatocytes by competitive inhibition of the phallotoxin uptake. Comparison of the influence on the inward transport of 3H-demethylphalloin and of 14C-cholate.

Several anionic substances used for cholecystography inhibit the development of protrusions in isolated hepatocytes in response to phalloidin. Drugs from the iopodate family were equieffective with those of th iodipamide type. The above protective effect results from a competitive inhibition of the phallotoxin uptake as shown for iopodate. Cholecystographic agents similarly inhibit the inward transport of cholic acid in a competitive manner. The inhibition of the phallotoxin response is inversely correlated with the uptake of 3H-demethylphalloin (r = 0.94) and with the inward transport of cholate (r = 0.84) at various inhibiting concentrations of iopodate.

Alkaloids↗
PubMed1976

Consideration of hepatic factor influence on drip infusion cholangiography.

The plasma disappearance rate (K) and transfer rate constants for the two compartmental system of Indocyanine Green (ICG) were calculated in visualized and nonvisualized cases of the biliary tract with hepatobiliary disease using drip infusion cholangiography (DIC). In nonvisualized cases with hepatocellular disorder K and the fractional hepatic removal rate mainly decreased, and in nonvisualized cases with cholelithiasis the fractional biliary secretory rate significantly decreased by DIC-A, utilizing it as a screening test. Three methods (B,C and D) of drip infusion cholangiography were established according to the result of the I-CG test. Through DIC-B, C- or -D in addition to DIC-A the visualization of the biliary tract significantly elevated in patients with hepatocellular disorder and cholelithiasis. These results were confirmed using 131I-iodipamide. In some cases the serum transaminase activity elevated, but the elevation was temporary.

Biliary Tract Diseases↗
PubMed1982

Prostacyclin-induced hyperthermia: implication of a protein mediator.

Intracerebroventricular administration of prostacyclin (PGI2) at room temperature (21 degrees C) induced dose-related hyperthermia in rabbits and also produced hyperthermia at low (4 degrees C) and high (30 degrees C) ambient temperatures. The PGI2-induced hyperthermia was not mediated by its stable metabolite 6-keto prostaglandin F1 alpha. Of the three anion transport systems (iodide, hippurate and liver-like) present in the choroid plexus, only the liver transport system seems to be important to central inactivation of pyrogen, prostaglandin E2 (PGE2) and the PGI2. Iodipamide (an inhibitor of the liver transport system) augmented the hyperthermia produced by PGI2, PGE2 and pyrogen. Phenoxybenzamine and pimozide had no thermolytic effect on PGI2-induced hyperthermia. After norepinephrine (NE) and dopamine levels were depleted by 6-hydroxydopamine, PGI2 still induced hyperthermia. Indomethacin and SC-19220 (a PG antagonist) did not antagonize PGI2-induced hyperthermia. Furthermore, the hyperthermia due to PGI2 was not accentuated by theophylline. In contrast, the hyperthermic response to PGI2 was attenuated by central administration of the protein synthesis inhibitor, anisomycin. These results indicate that PGI2-induced hyperthermia is not mediated by NE, dopamine, PGS, cyclic AMP, but, rather, that a protein mediator is implicated in the induction of fever by PGI2.

Animals↗