Pharmacokinetics of amikacin in the horse following intravenous and intramuscular administration.

The pharmacokinetics of amikacin sulfate (AK) were studied in the horse after intravenous (i.v.) and intramuscular (i.m.) administration. Serum (Cs), synovial (Csf) and peritoneal (Cpf) fluid concentrations of the drug were measured. Doses of 4.4, 6.6 and 11.0 mg/kg were given. The concentrations at 15 min following i.v. injection were 30.3 +/- 0.3, 61.2 +/- 6.9 and 122.8 +/- 7.4 micrograms/ml, respectively, for the 4.4, 6.6 and 11.0 mg/kg doses. Mean peak Cs values after the intramuscular injections occurred at 1.0 h post-injection and were 13.3 +/- 1.6, 23.0 +/- 0.6 and 29.8 +/- 3.2 micrograms/ml, respectively. The t 1/2 of amikacin was 1.44, 1.57 and 1.14 h for the 4.4, 6.6 and 11.0 mg/kg doses, respectively. In this study, minimum inhibitory concentrations (MIC) of amikacin sulfate were determined for six pathogens. Based on the MIC and the pharmacokinetic parameters, it would appear that the usual therapeutic dose of amikacin would be between 4.4 and 6.6 mg/kg twice daily and, for the more serious life-threatening infections, dosing three times a day.

In vitro perfusion studies of the human placenta. VI. Evidence against active glucose transport.

Previous studies in our laboratory using "in vitro" perfusion have established that glucose transport across the human placenta is a carrier-mediated process. It is not known whether these carriers require the expenditure of metabolic energy to function. In the experiments presented here we demonstrate in the perfused placenta that there is not reduction in the rate of glucose transport or its analogue 3-O-methyl-alpha-D-glucopyranoside (3MG) in the presence of 10(-4) M dinitrophenol (DNP), an uncoupler of oxidative phosphorylation. The presence of DNP, however, does cause an increase in the glucose utilization rate as well as increased lactic acid production. In order to test whether glucose transport depends on the functioning of a sodium pump system, the sodium in the perfusion system was replaced with choline chloride. The final sodium content was 30 mEq/L. In the presence of a low sodium concentration there was no decrease in the rate of 3MG transport compared to the control experiments run at normal sodium levels. Also "counter transport" of glucose was observed, a further indication that the glucose carrier mechanism does not require a sodium gradient in order to function. Since the transport rate of glucose or its analogue 3MG across the placenta is not reduced in the presence of 10(-4)M DNP and is not reduced in the absence of a sodium gradient, it is unlikely that the mechanism of glucose transport is an active process requiring the expenditure of metabolic energy.

The lecithin/sphingomyelin ratio in a high-risk obstetric population.

An experience with the lecithin/sphingomyelin (L/S) ratio in a population of high-risk obstetric patients is presented. A wide range of values in ralation to gestational age was found. A delayed rise in L/S ratio was found in Class A diabetes and Rh sensitization but was most striking in Class B through F diabetes. Chronic hypertension alone or in combination with diabetes is associated with an earlier rise in L/S ratio. A poor correlation of L/S ratio and neonatal pulmonary outcome with birthweight and gestational age was found. However, a good correlation between L/S ratio and neonatal pulmonary outcome was apparent. An L/S ratio of over 2 was universally associated with absence of serious RDS, but a low L/S ratio was less precisely predictive.

In vitro perfusion studies of the human placenta. IV. Some characteristics of the glucose transport system in the human placenta.

In vitro perfusion studies of glucose transport in the human placenta show saturation kinetics at high glucose concentrations and competitive inhibition of glucose transfer by the nonmetablizable glucose analog 3-O-methyl-alpha-D glucopyranoside. These characteristics provide further evidence that glucose is transported by a facilitated diffusion process in the human placenta.