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1. Splanchnic extraction rates of adrenaline and noradrenaline were determined in seven normal subjects and in nine patients with cirrhosis of the liver using arterial-hepatic venous catherization. 2. Both catecholamines were effectively removed when the blood passed through the splanchnic area: splanchnic fractional uptake of adrenaline in normal subjects was 90 ± 3%, and lower for noradrenaline, 68 ± 4% (P < 0.001). Net splanchnic extraction rates were higher for noradrenaline (126 ± 16 ng/min) than for adrenaline (40 ± 10 ng/min, P < 0.001), probably due to the higher arterial plasma levels of noradrenaline. 3. Resting arterial adrenaline and noradrenaline levels were significantly higher in cirrhotic patients than in normal subjects (adrenaline: 121 ± 27 vs 54 ± 8 pg/ml, P < 0.05; noradrenaline: 678 ± 89 vs 251 ± 26 pg/ml, P < 0.005). Net splanchnic catecholamine uptake was increased in cirrhotic patients. 4. The results demonstrate that the splanchnic bed in normal and cirrhotic subjects extracts plasma catecholamines efficiently; they suggest that elevated plasma catecholamines in cirrhosis are not the result of impaired splanchnic catecholamine removal.

Abstract. The effect of previous exposure to glucose on subsequent glucose-stimulated insulin and somatostatin secretion has been investigated using the isolated perfused rat pancreas. As expected, when the pancreases of non-diabetic rats were exposed to 16.7 mM glucose on two occasions, 20 min apart, insulin secretion during the second period of exposure to high glucose was greater than that during the first period. By contrast, there was no potentiation of somatostatin secretion during the second glucose stimulation with respect to that of the first. Indeed, when the basal glucose concentration was low (1.4 or 2.8 mm) somatostatin secretion during the second glucose stimulation was lower than that during the first.Since exogenous insulin is known to inhibit glucoseinduced somatostatin secretion, it seemed possible that lack of visible potentiation of glucose-induced somatostatin secretion by glucose could have been due to partial D cell inhibition by simultaneously augmented insulin secretion during the second glucose stimulation. In an attempt to exclude such an interaction between B and D cells, somatostatin secretion was also studied in the pancreases of spontaneously diabetic, Wistar (BB) rats (these animals are insulin deficient and are maintained by daily injections of insulin). However, even though insulin secretion was not detectable from these pancreases, glucose potentiation of glucose-induced somatostatin secretion did not occur.Although the pancreatic B and D cells are known to respond in a similar manner to many secretagogues the present results show that glucose potentiation of glucosestimulated somatostatin secretion is not found under circumstances where potentiation of insulin secretion does occur. In addition, the absence of potentiated somatostatin secretion could not be attributed to partial inhibition of the D cell by insulin.