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Biomedical subjects

L H Rees

Publications and source records attributed to L H Rees.

293 records · Page 17Linked to original sources
PubMedDate not supplied

Splanchnic and hepatic metabolism of somatostatin: a study in cirrhotic patients with a portacaval shunt.

Experimental data suggest that somatostatin is metabolized by both liver and kidneys. Results in humans are conflicting. By studying a group of cirrhotic patients with surgically induced end-to-side portacaval shunts, basally and during a somatostatin infusion, we have been able to analyze separately the hepatic and splanchnic metabolism of this peptide. After catheterization, samples were obtained from the pulmonary artery, portal and hepatic veins. Basal pulmonary artery immunoreactive somatostatin (IRS) was significantly higher (p less than 0.001) in the cirrhotic patients (96 +/- 11 pg per ml) than in a sex- and age-matched control group (31.4 +/- 5.8 pg per ml). During the infusion of exogenous somatostatin, IRS values were higher in arterial (12,269 +/- 1,198 pg per ml) than in hepatic venous blood (7,648 +/- 1,234 pg per ml), indicating hepatic extraction of the peptide; but there was also a substantial splanchnic extraction demonstrated by higher arterial (12,269 +/- 1,532 pg per ml) than portal values (6,754 +/- 1,040 pg per ml) of IRS. During the somatostatin infusion, at very high circulation IRS levels, the liver was able to extract 38% of the peptide. This suggests that the high basal IRS levels found in liver cirrhosis are not likely to be due to hepatic failure. Possible mechanisms may involve increased somatostatin secretion, predominance of high molecular weight moieties of IRS which may not be as effectively removed by the liver, and/or portal-systemic shunting.

Adult↗
PubMedDate not supplied

ACTH release during passive avoidance behavior.

ACTH was measured by radioimmunoassay during learning and retention of a passive avoidance response. Electric footshock, used during the learning trial, appeared to be a weaker stimulus for ACTH release than was the retention test. Moreover high latency scores during retention were associated with high plasma ACTH levels, whereas shorter latencies were associated with lower levels. The results indicate that psychological mechanisms organizing behavioral coping are important in the response of the pituitary-adrenocortical system to stimuli which are related to a previous adversive experience.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Corticotropin-releasing factor is a potent inhibitor of sexual receptivity in the female rat.

Corticotropin-releasing factor (CRF), the recently characterized and synthesized 41-amino acid polypeptide isolated from ovine hypothalami, has been shown to be a potent stimulator of adenohypophyseal beta-endorphin and corticotropin (ACTH) secretion both in vitro and in vivo. In common with other regulatory peptides, CRF has also been demonstrated to possess extra-hypophysiotropic roles. Indeed, intracerebroventricularly (i.c.v.) administered CRF elicits several endocrine and behavioural responses compatible with the concept that this peptide could be a key signal in coordinating the organism's endocrine and behavioural responses to stressful and other adaptive stimuli. We now provide the first evidence for neurally placed CRF in the control of a specific hormone-dependent behavioural response and unequivocally demonstrate an extremely potent suppressive effect of CRF on sexual behaviour in the female rat when microinfused into the arcuate-ventromedial area of the hypothalamus (ARC-VMH) and the mesencephalic central grey (MCG).

Adrenocorticotropic Hormone↗