Dissolution of phenytoin precipitate with sodium bicarbonate in an occluded central venous access device.

OBJECTIVE: To report a case of restored patency of a central venous access device occluded by precipitate of phenytoin sodium injection. CASE SUMMARY: A patient experienced total occlusion of an implanted subcutaneous port caused by precipitation of phenytoin. Phenytoin sodium injection was mixed inadvertently with dextrose 5% in NaCl 0.45% injection during intravenous administration. Dextrose 5% in NaCl 0.45% injection, which is acidic (pH 4.0), caused the phenytoin sodium injection, a basic solution (pH 12.0), to precipitate. Local instillation of sodium bicarbonate 8.4% injection to decrease the pH of the medium restored patency of the occluded port. DISCUSSION: There are reports of local instillation of solvent restoring central ports occluded by lipid-containing parenteral nutrient admixture, calcium phosphate salt precipitate, and coagulated blood. No report of local instillation into an occluded port to dissolve precipitate of phenytoin could be found. Several factors are involved in the precipitation and dissolution of phenytoin. The key factor in this case was the hydrogen ion concentration (pH) of the solution. Decreased pH caused the precipitation, but increased pH caused the dissolution of the precipitate of phenytoin. CONCLUSIONS: Sodium bicarbonate injection was a suitable agent for clearing precipitate of phenytoin in this case of an occluded implanted central venous access device.

Phenytoin concentration elevation subsequent to ranitidine administration.

OBJECTIVE: To report elevated phenytoin (PHT) plasma concentrations in a patient receiving ranitidine. CASE SUMMARY: A patient treated with PHT and ranitidine experienced elevated PHT plasma concentrations that persisted several days after PHT was discontinued. The PHT plasma concentration declined rapidly after withdrawal of ranitidine. DISCUSSION: This is an unusual case report of elevated PHT plasma concentrations associated with concurrent ranitidine use. Ranitidine has been reported to interfere with the hepatic metabolism of other drugs. The proposed mechanism of this interaction is similar to that of other histamine 2-receptor antagonists--by binding to cytochrome P-450 hepatic mixed-function oxidase. We postulate that a small subset of patients may be susceptible to this effect of ranitidine. CONCLUSIONS: This case was complicated by several variables that may have affected the changes observed in total PHT concentrations. However, an interaction between ranitidine and PHT should be considered, especially in a subpopulation of patients that are more susceptible to this effect. Patients using ranitidine and phenytoin concurrently should be routinely monitored.

Effects of cholinomimetic drugs on reptilian atrial muscles.

The effects of some cholinomimetic drugs have been examined on isolated atria of rainbow lizards (Agama agama Linn.) and land tortoises (Kinixys spp. Linn.). Acetylcholine (ACh, 10(-8) - 5 X 10(-5) M) caused concentration-dependent, atropine-sensitive, negative chronotropic or inotropic responses in isolated spontaneously-beating right or electrically-driven left atria of rainbow lizards and land tortoises. This prototype cholinergic drug (ACh, 10(-8) 5 X 10(-5) M) also induced atropine-sensitive, concentration-related negative chronotropic or inotropic responses in isolated atrial muscles taken from guinea-pigs. Histamine (10(-8) - 5 X 10(-5) M) produced concentration-related positive chronotropic or inotropic responses in isolated spontaneously-beating right or electrically-driven left atria of rainbow lizards and guinea-pigs without significantly affecting (P greater than 0.05) the tortoise atria. 5-Hydroxytryptamine (5-HT, 10(-7) - 5 X 10(-5) M) induced concentration-dependent positive chronotropic or inotropic responses in isolated, spontaneously-beating right or electrically-driven left atria of rainbow lizards, tortoises and guinea-pigs. Nicotine (10(-8) - 5 X 10(-5) M) had no effect on the rate of beating of the lizard or tortoise isolated right atria, but caused concentration-dependent positive chronotropic responses in spontaneously-beating isolated right atria of the guinea-pig. Furthermore, nicotine (10(-8) - 5 X 10(-5) M) had no effect on contractile tension of isolated, electrically-driven left atria of the tortoise; it induced a biphasic inotropic response in driven left atria of the rainbow lizard and produced a concentration-related positive inotropic response in electrically-driven isolated left atria of the guinea-pig.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sympathomimetic drugs on reptilian atrial muscles.

The effects of some sympathomimetic drugs on isolated atria of rainbow lizards (Agama agama Linn.) and land tortoises (Kinixys spp. Linn.) have been examined. Noradrenaline, adrenaline, isoprenaline, phenylephrine or dopamine (10(-9)-10(-5) M) induced concentration-dependent positive chronotropic and inotropic responses in spontaneously-beating right- and electrically-driven left atria of rainbow lizards or tortoises. These catecholamines produced similar responses in guinea-pig isolated atria. Phentolamine or propranolol (10(-10)-10(-6) M) competitively antagonised the positive chronotropic and/or positive inotropic responses induced by these sympathomimetic agonists in these reptilian (and mammalian) atrial muscles; probably suggesting the presence of alpha- and/or beta-adrenoceptors in reptilian atrial muscles (as in the mammalian myocardium). It is suggested that in reptilian atrial muscles, only one adrenoceptor subtype which is capable of converting its properties to either alpha- or beta-, or even alpha- and beta-adrenoceptor subtypes (as in the frog heart) depending on the environmental temperature, may exist. The use of rainbow lizard and tortoise atrial muscle preparations as laboratory models for routine pharmacological evaluation of adrenergic drugs, particularly in developing tropical African countries where these cheap, harmless reptiles abound, is strongly recommended.