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Showing papers in "Surgery gynecology & obstetrics in 1973"




Journal Article
TL;DR: The hepatotrophic factors previously reported to be in splanchnic venous blood are pancreatic hormones and specifically insulin and glucagon and the interrelationship of these hormones to others in the moment to moment regulation of nutrient and hepatic homeostasis is a central fact of liver physiology that should reconcile a number of previously divergent opinions about portoprival syndromes.
Abstract: SUMMARY The origin of hepatotrophic factors in splanchnic venous blood was investigated by modifyingthe portal venous inflow to different parts of the canine liver while leaving the arterial bloodsupply and biliary drainage intactIn one variety of experiment, termed partial transposition, the liver portion perfused with thetotal splanchnic venous blood underwent weight gain and hepatocyte hypertrophy, hyperplasia,and glycogenation compared with the portion perfused with venous blood from thehindquarters, kidneys, and adrenal glands, but the combined weight of the total liver remainedconstant in spite of the rapidly evolving regional disproportions The lobar changes were welldeveloped within one to two months At this time, the hepatic lobes supplied with splanchnicvenous blood had higher concentrations of glucokinase and lower concentrations of cyclic 3 ′,5′-adenosine monophosphate and active phosphorylase than the lobes receiving hindlimb andadrenorenal venous blood, indicating that the biochemical environment of the different liverregions was drastically different by virtue of being under specific hormonal controlThe dissociation was even more dramatically illustrated by dynamic studies in which thedestruction of cyclic 3 ′, 5′-adenosine monophosphate by phosphodiesterase was blocked withaminophylline thereby permitting estimation of the rate of formation of cyclic 3 ′, 5′-adenosinemonophosphate In addition, the modifying effect of tolbutamide-induced endogenous insulinupon exogenously administered glucagon was evaluated by serial determinations of cyclic 3 ′,5′-adenosine monophosphate These investigations with the aminophylline and tolbutamide-glucagon tests demonstrated the anabolic role of insulin and the opposing roles of bothglucagon and epinephrine in contributing to liver homeostasis Epinephrine and glucagoncaused striking increases in cyclic 3′, 5′-adenosine monophosphate, and insulin had theconverse effectAnother type of preparation involving partition of the splanchnic venous blood between theliver portions was termed splanchnic flow division The substances responsible for the hepatichypertrophy, hyperplasia, glycogenation, and weight gain were shown to emanate mainly, ifnot virtually exclusively, from the pancreatic-gastroduodenal-splenic venous drainage Incontrast, intestinal nutritional substrate and hormones from the intestine or adrenal gland werenot profoundly influential in either promoting or preventing the morphologic or glycogenconcentration changes The concentrations of cyclic 3′, 5′-adenosine monophosphate,phosphorylase, and glucokinase in the two sides of the liver did not follow as distinctive apattern as in the partial transposition experiments However, the aminophylline andtolbutamide-glucagon tests revealed the same type of major dissociation of cyclic 3′, 5′-adenosine monophosphate as with the partial transpositions Particularly impressive was theway in which trace doses of tolbutamide-induced endogenous insulin on the side nourished bypancreatic venous blood restrained the cyclic 3′, 5′-adenosine monophosphate response toexogenous glucagon, whereas the other liver fragment which was not so covered by insulinhad completely uninhibited rises in cyclic 3′, 5′-adenosine monophosphateThe conclusion from these experiments is that the hepatotrophic factors previously reportedfrom our laboratories and by other investigators to be in splanchnic venous blood are pancreatichormones and specifically insulin and glucagon Of these, insulin is anabolic and glucagon ismainly catabolic but not exclusively so, since glucagon also has the anabolic effect ofstimulating gluconeogenesis The insulin-glucagon relationship and the interrelationship ofthese hormones to others, such as epinephrine, in the moment to moment regulation of nutrient

353 citations












Journal Article
TL;DR: The surgical therapy of post-transplantation hyperparathyroidism which, in every one of the authors' 18 patients, has been due to diffuse and multiglandular hyperplasia is discussed.
Abstract: Secondary hyperparathyroidism has been reported by Stanbury and Lumb (21, 22) and Massry and his associates (14) to be present in most patients with chronic renal failure. After successful renal homotransplantation, it has been said by several investigators, including Alfrey and his colleagues (1) and Johnson and his co-workers (9, 10) that resolution of this hyperparathyroidism occurs almost universally. With conservative management, severe hypercalcemia after renal transplantation has been uncommon, and the dogma has become well established that parathyroidectomy is seldom required. This conservative attitude was based upon relatively short term observations of renal recipients. In our center, there has been a growing realization that occult persistent hyperparathyroidism can be a major cause of morbidity, even more than five years after renal transplantation and in spite of multiple normal serum calcium concentrations. This article was undertaken, therefore, in order that the diagnosis of this complication might be described. The second reason for this study is to discuss the surgical therapy of post-transplantation hyperparathyroidism which, in every one of our 18 patients, has been due to diffuse and multiglandular hyperplasia. Classic subtotal parathyroidectomy has been performed in half of our patients, and in the remainder, all the parathyroid tissue has been excised and a fraction of one gland returned as a free autograft. The advantages of both approaches for both long term and short term management will be mentioned.