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Because of reduced health care funding it is becoming necessary for surgeons to take a greater interest in the costs of individual operations. This study reports costs directly measurable to the patient, and also the indirect costs of hospital overheads, an operating suite and teaching, which were 37, 10 and 15%, respectively (62%), of hospital budget. A scheme has been developed which could give surgeons a standard to report direct costs. Pre-admission, ward, operating room, recovery, intensive care and post-admission are defined as cost periods and the modalities of staff, equipment (capital, maintenance and replacement), imaging, laboratory and consumables apply to each. This strategy was applied to assess open cholecystectomy (OC) and laparoscopic cholecystectomy (LC) as an example. The direct costs for OC were $3706 and LC $2868, a difference of $838; the indirect and direct costs were OC $6004 and LC $4646, a difference of $1358. Thus indirect cost magnified the difference between the operations. Bed stay, density of nursing and use of disposable instruments were the major influence on direct costs. The individual cost advantage of a shorter bed stay may be countervailed by an increased hospital activity. The main patient benefit of new operations may be improved quality of life and more rapid return to work with prevention of salary losses. A method has been developed to define costs of a particular surgical operation with the purpose of stimulating surgeons' interest in this topic and developing a common style of reporting.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitonin gene-related peptide (CGRP) is a 37 amino-acid peptide, undetectable in the plasma in health but elevated in certain disease states such as medullary thyroid cancer, and potentially causes symptoms. The kidney is a major site of and influence on the clearance of exogenously infused CGRP. As CGRP might cause symptoms in renal dysfunction, this study was performed to determine the clearance of CGRP in humans and animals with altered renal function. In chronic renal failure patients, CGRP was not detected in plasma either before or after haemodialysis. In sheep, before and after bilateral nephrectomy, there was an approximate halving of plasma clearance and doubling of the circulating half-life of infused CGRP. This reduction in clearance was greater than that which could be accounted for by the reduction in degradation by renal substance alone. This renal influence on extra-renal CGRP metabolism was not due to the renal production of a circulating peptidase as evidenced by the absence of such peptidase in the plasma of normal and anephric sheep. Further, severity of uraemia had no influence on the extra-renal metabolism. The mechanism by which the kidney influences the extra-renal metabolism of CGRP remains obscure.

Calcitonin gene-related peptide (CGRP) is a potent vaso-active peptide. Typically, it is elevated in the plasma of patients with medullary thyroid cancer (MTC), but is undetectable in the plasma of healthy individuals. Some symptoms associated with MTC could be caused by elevated CGRP. The plasma level of CGRP was measured in patients with recurrent MTC at rest and again after intravenous pentagastrin to further elevate the CGRP. When normal subjects received pentagastrin the CGRP level still remained below the detectable threshold (< 4 pmol/L). The CGRP levels did not correlate with the patients' blood pressure but a rise in CGRP was associated with a rise in heart rate. As not all patients showed symptoms, further investigation examined the possibility of plasma elevation of somatostatin, a known inhibitor, preventing responses but no change was found. Similarly, examination of the patient plasma for CGRP fractions did not reveal any increased breakdown.

Background: Although several growth factors are known to be essential for liver regeneration, the role of gastrin remains controversial. Methods: Liver regeneration was examined in wild-type (WT) and gastrin-deficient (gastrin KO) mice at days 2 and 10 after partial (40%) hepatectomy by measurement of liver weight. Hepatocyte proliferation and circulating gastrin concentrations were measured at the same time points by immunohistochemistry and radioimmunoassay, respectively. Results: There was no significant difference in the rate of liver regeneration between gastrin KO and WT mice. Hepatocyte proliferation in both groups was increased at day 2 but had returned to baseline values by day 10. At day 2, hepatocyte proliferation in the gastrin KO mice was significantly higher than in WT animals, whereas at day 10, proliferation was significantly greater in the WT mice. The circulating gastrin concentration in the WT mice was significantly lower at day 10 than in unoperated WT animals. Conclusion: This study suggests that gastrin is not essential for liver regeneration after partial hepatectomy.

The gastrointestinal tract is the largest endocrine organ in the body. However, gastrointestinal hormones are not confined to the gut and many of them are delivered to their target tissue by neural and paracrine routes as well as the circulation. Regulatory peptide is therefore a more appropriate term than gastrointestinal hormone. The functions of these regulatory peptides include effects on intake, digestion and absorption of food, and changes in gut secretions, motility and growth. Since these peptides do not act alone but in concert it has been difficult to ascribe particular functions to individual peptides. However, the recent and on-going development of specific regulatory peptide agonists and antagonists has resulted in major advances in our understanding of the physiology of these peptides. In turn these findings are creating new therapeutic avenues providing some return from all the research on these gastrointestinal regulatory peptides. The somatostatin derivative (octreotide or sandostatin) is the most obvious example. Although only approved in Australia for treatment of carcinoids and VIPomas, the prospects include treatment of other gastroenteropancreatic tumours, acromegaly, idiopathic diarrhoea, fistula closure, dumping, and ERCP or post-operative pancreatitis. A new gastrokinetic agent, that acts via the motilin receptor, is undergoing trials for the treatment of impaired gastric emptying. The trophic effect of gastrointestinal peptides has clinical significance. For instance, gastrin antagonists inhibit cell proliferation of colon carcinoma cell lines. Furthermore the trophic effect of gastrin must be considered when potent gastric acid inhibitors, which cause a reflex increase in gastrin, are used. The outlook is for more mammalian regulatory peptides to be discovered adding further to the complexity.(ABSTRACT TRUNCATED AT 250 WORDS)

Although meal-stimulated neurotensin release from the small intestine is inhibited by cholinergic blockade, it is uncertain whether this cholinergic mechanism involves the vagus. This study examines the role of the vagus in neurotensin release by first determining the effect of vagotomy on meal-stimulated plasma neurotensin in man and second, the effect on plasma neurotensin of electrical stimulation of the vagus in sheep. Six volunteers were studied 6-8 weeks after truncal vagotomy and pyloroplasty. Basal plasma neurotensin at 32(15-67) pmol/l (median, range) was greater than in normal controls at 17 (9-52) pmol/l (P less than 0.05). Following a standard meal, plasma neurotensin rose significantly (P less than 0.05), but similarly in both post-vagotomy and control groups to maxima of 74 (43-76) pmol/l and 52 (35-65) pmol/l, respectively. Basal plasma neurotensin in the six sheep was below the detection limit of the assay and remained undetectable during electrical stimulation of the vagus. Significant rises in plasma pancreatic polypeptide and gastrin confirmed the efficacy of the electrical stimulation. It is concluded that although the vagus might have a tonic inhibitory effect on basal plasma neurotensin, meal-stimulated neurotensin release is vagally independent. The inhibitory cholinergic influence on meal-stimulated release is most likely therefore to be mediated by cholinergic nerves of the enteric nervous system.