The metabolic clearance of progesterone in the pregnant rat: absence of a physiological role for the lung

The metabolic clearance rate (MCR) of progesterone is among the highest for all steroid hormones studied, yet it is difficult to apportion this high MCR to specific organ contributions. The isolated lung has been shown to metabolize progesterone, and since this tissue receives the entire cardiac output, potentially it could make a major contribution to the overall MCR. This possibility was examined in the present study by measuring lung extraction of [3H]progesterone under steady-state conditions in the intact pregnant rat. Anesthetized rats (n = 6) were infused with [3H]progesterone via a femoral vein for 100 min on Day 16 of pregnancy. After the onset of steady state (40 min), four blood samples were obtained at 20-min intervals from the right ventricle and from the aorta, and the concentrations of [3H]progesterone and its metabolites were determined. Throughout the sampling period, mean arterial pressure and heart rate remained stable (two-way analysis of variance), as did the production rate (3.76 +/- 0.35 mg/day; mean +/- SEM) and the MCR (34.8 +/- 3.5 ml/min) of progesterone. Despite this high rate of clearance, there was no difference between the concentration of [3H]progesterone in arterial and right ventricular blood, indicating no net extraction of progesterone during passage through the lung. Furthermore, there was no change in the concentration of either lipid-soluble or aqueous-soluble [3H]progesterone metabolites during trans-lung passage. These observations demonstrate that the lung does not contribute to the MCR of progesterone when measured under physiological and steady-state conditions. Therefore, the relationship, MCR (ml/min) = whole-body extraction (%) x cardiac output (ml/min), is upheld for progesterone in the rat.     

Effects of ambulance transport in critically ill patients.

Two groups of critically ill patients were transferred by ambulance from other hospitals to a central intensive therapy unit. The effect of transport was reviewed retrospectively in 46 patients and prospectively in 20 patients. Of the 46 patients reviewed retrospectively six became hypotensive, six became hypertensive, and seven developed delayed hypotension. One patient developed fits and six out of 13 patients had a rise in arterial PCO-2 of 1-6-4-1 kPa (12-31 mm Hg). Of the 20 patients reviewed prospectively, one patient became hypertensive due to overtransfusion, one had a fit, but none became hypotensive. Three out of four cases of delayed hypotension were related to starting intermittent positive pressure ventilation. Arterial PCO-2 fell in one patient and arterial PCO-2 rose in two, each change being related to changed oxygen therapy or narcotics. There were no changes in other cardiovascular or respiratory indices, body temperature, or urine production. Earlier transfer, resuscitation before transfer, continuing medical care during the journey, and hence a slower smoother journey seemed to be important factors in the management of these patients. Our findings, may have important implications in the future regional organization of the care of critically ill patients.     

Identification of the human hepatic microsomal glucose-6-phosphatase enzyme

The glucose-6-phosphatase enzyme protein of the human hepatic microsomal glucose-6-phosphatase system was identified as a 36.5 kDa polypeptide. The 36.5 kDa glucose-6-phosphatase enzyme protein was shown to be absent in the microsomes isolated from a patient previously diagnosed as having a type 1a glycogen storage disease.