No abstract

The uptake, distribution and excretion of curcumin in Sprague‐Dawley rats has been studied. When administered orally in a dose of 1 g/kg, curcumin was excreted in the faeces to about 75%, while negligible amounts of curcumin appeared in the urine. Measurements of blood plasma levels and biliary excretion showed that curcumin was poorly absorbed from the gut. No apparent toxic effects were seen after doses of up to 5 g/kg. When intravenously injected or when added to the perfusate of the isolated liver, curcumin was actively transported into bile, against concentration gradients of several hundred times. The major part of the drug was however metabolized. In suspensions of isolated hepatocytes or liver microsomes 90% of the added curcumin was metabolized within 30 min. In view of the poor absorption, rapid metabolism and excretion of curcumin, it is unlikely that substantial concentrations of curcumin occur in the body after ingestion.

No abstract

Effects of norepinephrine (NE) and isoproterenol on simultaneously recorded electrical and contractile activity in rat portal vein were studied using a sucrose-gap technique. This vascular smooth muscle shows spontaneous phasic contractions correlated with bursts of action potentials. Norepinephrine (10" 9 to 10" 7 w/v) increases the duration of the bursts and shortens the interval between bursts after an initial period of continuous spike discharge. The tension response is greater than can be accounted for by the increase in electrical activity. High NE concentrations (10~3) produce depolarization, decrease of spike amplitude, or even abolition of spikes and maintained contractions. Norepinephrine increases contracture tension of K + -depolarized portal vein without changing membrane potential. Electrical and mechanical activity is reinitiated in preparations inactivated by elimination of Ca 2 + ; this may be due to release of bound calcium. Phenoxybenzamine abolishes the above NE responses. The typical response to isoproterenol (10" 9 to 10~7) in a normal ionic environment consists of moderate depolarization, decreased burst duration, but increased frequency of bursts and inhibition of tension development which is not simply correlated with the change in electrical activity. This pattern resembles that produced by lowering [Ca agent used and on the vascular bed studied. The cellular mechanisms responsible for these opposite reactions of vascular smooth muscle to adrenergic agents are insufficiently understood. A better understanding of these excitatory and inhibitory actions would require, among o:her things, a more complete knowledge of the electrophysiological events associated with the mechanical changes.In the previous article in this issue (4), we have described the technique used here for simultaneous recording of electrical and mechanical activity of the isolated rat portal vein and the responses of this preparation to changes in ionic composition of extracellular fluid. The present paper describes the electrical and mechanical responses to norepineph-

Wahlstrom, B. A. Ionic fluxes in the rat portal vein and the applicability of the Goldman equation in predicting the membrane potential from flux data. Acta physiol. scand. 1973. 89. 436–448. The sodium, potassium and chloride effluxes from the rat portal vein were measured using radioactive tracer ions. It was found that the sodium efflux attributable to an intracellular compartment was very slow, with a rate constant of 4.66×10‐4 s‐1, and the corresponding intracellular sodium only 3.0 mmol/kg wetweight. The intracellular potassium exchanged with a rate constant of 2.15×10‐4 s‐1 and contained 45.5 mmol/kg wetweight. The intracellular chloride content was 14.7 mmol/kg wetweight, exchanging with a rate constant of 10.55 × 10‐4 s‐1. From these data the permeabilities of Na, K and CI were calculated to 0.130, 3.81 and 3.11 ×10‐8 cms‐1 respectively. The relative permeabilities PK: PNa: PC1 were 1: 0.034: 0.816, and from these values the Goldman equation predicted a membrane potential of ‐42.3 mV. The actual membrane potential, measured by glass microelectrodes, was ‐ 45 mV. It was concluded that the membrane potential in the rat portal vein in normal solution can be predicted from the permeabilities and distribution of K and CI, while Na plays an insignificant part.