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B P Setchell

Publications and source records attributed to B P Setchell.

At least 127 records · Page 7Linked to original sources
PubMed1976

The restricted penetration of iodinated rat FSH and LH into the seminiferous tubules of the rat testis.

The penetration of 125I-iodinated rat follicle-stimulating hormone (FSH; labelled by three different techniques) and luteinizing hormone (LH) through the walls of the seminiferous tubules of the rat testis has been studied by injecting the labelled hormone into rats with the efferent ducts of one testis ligated 16 h before the collection of samples of blood and tissues. The concentration of trichloracetic acid-precipitable and immunoprecipitable radioactivity was measured in blood plasma and rete testis fluid and calculated for the total secreted fluid retained in the testis by the ligature, and for the additional tubular fluid from the ligated testis, separated by centrifugation after decapsulating the testis and dispersing the cells. Very little intact hormone penetrated into the testicular fluids, even 16 h after injection of the labelled hormone, and the volume of distribution in the unligated testis of the trichloracetic acid-precipitable radioactivity was only slightly greater than that for markers known to be confined to the extracellular interstitial fluid. This suggests that the labelled hormones do not penetrate readily through the walls of the semiferous tubules into their lumina. Injected inorganic iodiide and trichloracetic acid-soluble 125I-circulating after the injection of iodinated hormones penetrated more rapidly into the tubules, but had not reached equilibrium between the testicular fluids and blood plasma 16 h after injection. Labelled FSH was reasonably stable in the circulation after injection, but 80% of the 125I was not protein-bound 16 h after injection of labelled LH.

Animals↗
PubMed1976

The oxidation of glucose, ketone bodies and acetate by the brain of normal and ketonaemic sheep.

1. The utilization and oxidation of glucose, acetate and ketone bodies by the brain of sheep has been determined from measurements of arteriovenous (A-V) differences and cerebral blood flow, as well as by infusing 14C-labelled metabolites. 2. The A-V difference for glucose was generally more than one sixth, on a molar basis, that of oxygen. 3. The mean rate of glucose utilization by the brain of conscious sheep (0-508 +/- 0-063 mumole/g per minute) was maintained even when the capillary glucose concentration was below 1-4 mM. 4. The amount of 14CO2 produced from [U-14C]glucose by the brain was consistent with glucose being the only energy source for the brain, even during hypoglycaemia and hyperketonaemia. 5. There was no appreciable production of lactate or pyruvate by the brain. 6. There was no significant A-V difference for acetate across the brain in normal or undernourished pregnant sheep. The small A-V differences that were measured show that less than 5% of the CO2 produced could be derived from acetate, a conclusion that is supported by experiments using [U-14C]acetate. 7. No significant A-V difference was detectable across the brain for 3-hydroxybutyrate or acetoacetate in normal fed, pregnant ketonaemic or even anaesthetized sheep infused with acetoacetate. Experiments in which [U-14C]-D(-)-3-hydroxybutyrate was infused also showed that less than 5% of CO2 was derived from ketone bodies. 8. In anaesthetized sheep infused with acetoacetate, measurements were made simultaneously across brain, heart and skeletal muscle. In contrast to the non-significant uptake of ketone bodies by the brain, uptake by heart and skeletal muscle was sufficient to account for nearly 60% of their oxygen consumption. 9. Experiments using [14C]hydroxybutyrate confirmed that during infusion of acetoacetate most of the CO2 produced by the heart, but not by the brain, was derived from ketone bodies. 10. In anaesthetized sheep ketone bodies penetrate only slowly into cerebrospinal fluid. 11. It is proposed that mechanisms for the utilization of ketones by the sheep brain have not evolved because glucose utilization by the brain is a smaller fraction of whole body glucose utilization than in man and rats.

Acetates↗
PubMed1973

Cerebral glucose transport and oxygen consumption in sheep and rabbits.

1. Mechanisms underlying the ability of ruminants to tolerate severe hypoglycaemia have been investigated. Anaesthetized sheep and rabbits were compared with respect to cerebral glucose transport and oxygen consumption as a function of glucose concentration in cerebral extracellular fluids.2. Glucose in plasma was decreased by insulin or increased by I.V. infusion. Measurements were made of cerebral blood flow, arteriovenous concentration differences of glucose and oxygen and the concentration of glucose in c.s.f.3. Equations for carrier-mediated transport accurately described steady-state glucose flux across the blood-brain barrier as plasma concentration was varied from 0.2 to 30 mM. In sheep, the affinity constant (K(m)) was 6 mM and the maximum transport capacity (T(m)) was 260 mumole min(-1). 100 g(1) brain. In rabbits, K(m) = 5.5 mM and T(m) = 280 mumole min(-1). 100 g(1). Transport of glucose across the blood-brain barrier of rabbits is at least as efficient as that in sheep and in both species T(m) is 10-15 times greater than normal rates of glucose utilization.4. During hypoglycaemia the concentration of glucose in c.s.f. is less in sheep than in rabbits (Fig. 5). Steady-state utilization of glucose by sheep brain decreased to 50% of normal when steady-state concentration of glucose in c.s.f. (interstitial fluid) falls to 0.1 mumole ml.(-1); in rabbits the corresponding concentration is 0.7 mumole ml.(-1) (Fig. 6). We suggest that transport capacity of membranes separating cerebral interstitial fluid from the site of glucose phosphorylation is greater in sheep than in rabbits; this may be the principal adaptation which enables ruminants to withstand severe hypoglycaemia (Discussion II).5. Approximately 30 min were required to reach a steady state of glucose transport following a sudden increment of glucose concentration in plasma (Fig. 1). 80-100 min were required to reach a new steady-state concentration of glucose in c.s.f.6. The molar ratio of steady-state cerebral glucose utilization to oxygen consumption (6G:O(2)) is normally 0.93 (S.E. +/- 0.05) but is decreased to the range 0.1-0.5 during sustained hypoglycaemia in both sheep and rabbits (Figs. 2, 3). Continued low glucose: oxygen ratios could be explained by (a) utilization of non-carbohydrate substrates derived from blood or (b) utilization of stored lipid in brain. Only 0.1 g lipid/100 g brain would suffice to account for the observed rate of non-glucose oxidative metabolism during 3 hr of severe hypoglycaemia (Discussion IV).

Animals↗