EFFECT OF SIZE (MIS)MATCHING IN CLINICAL DOUBLE-LUNG TRANSPLANTATION
1995; 59 (5): 707-713
CYTOPROTECTIVE EFFECT OF PENTAGASTRIN AND EPIDERMAL GROWTH-FACTOR ON STRESS-ULCER FORMATION - POSSIBLE ROLE OF SOMATOSTATIN
ANNALS OF SURGERY
1985; 201 (3): 290-295
Current United Network for Organ Sharing policy requires listing lung transplant recipients with an acceptable donor weight range, but lung size is a function of height, age, sex, and race. Frequently, lung transplant recipients are underweight, which results in a large discrepancy between donor and recipient weights. We reviewed our experience with size discrepancy between donors (D) and recipients (R) of 49 double-lung transplant (DLTX) procedures since July 1990. Pneumoreduction procedures were performed in 11 recipients of lungs judged to be too large at the time of DLTX (right middle lobectomy, 2; lingulectomy, 2; both, 6; right middle lobectomy and bilateral apical resections, 1). Predicted forced vital capacity (FVC) and total lung capacity (TLC) of donors and recipients were calculated. Donors were larger than recipients in general (D:R height = 1.02; D:R weight = 1.46), and, as a result, recipient-predicted lung volumes were smaller than donor-predicted lung volumes (D:R FVC = 1.1; D:R TLC = 1.1). Recipients undergoing pneumoreduction procedures had a significantly greater size discrepancy between donors and recipients; thus, both the ratio of D:R and the difference between D and R predicted FVC and TLC were significantly greater among recipients who underwent pneumoreduction, compared with nonreduced recipients. For recipients in the pneumoreduction group, predicted FVC and TLC were recalculated, with a proportionate amount subtracted based on the number of pulmonary segments removed. When the "corrected" FVC and TLC of the donors were compared with recipient-predicted FVC and TLC, there was no longer any significant difference between reduced and non-reduced groups, which implies that visual estimate of size mismatch at surgery is an accurate measure of size discrepancy. Post-DLTX spirometry showed identical improvement in FVC in patients who had pneumoreduction and those who did not, and survival at 6 months was identical in both groups. We conclude that pneumoreduction had no adverse effect on survival or post-DLTX spirometry, allowing safe use of larger donors in small recipients. Also, because lung size is more a function of height than weight, this study challenges the United Network for Organ Sharing practice of listing recipients with an acceptable donor weight range.
View details for Web of Science ID A1995QM65600012
View details for PubMedID 7886797
EXPERIMENTAL-EVIDENCE FOR A VAGALLY MEDIATED AND CHOLECYSTOKININ-INDEPENDENT ENTEROPANCREATIC REFLEX
ANNALS OF SURGERY
1985; 202 (1): 69-74
This study was designed to test the effects of pentagastrin and epidermal growth factor (EGF) on stress-induced ulceration and on the antral content of gastrin and somatostatin (SLI) in rats. Four groups of 14 to 15 rats had been prepared for 7 days by one of the following methods: saline injection (control); injection of pentagastrin (250 micrograms/kg, 3 times/day); injection of EGF (10 micrograms/kg, 3 times/day); or injection of EGF plus pentagastrin. At the end of the treatment period, half of each group of rats were sacrificed (nonstress group). There were no ulcers in the nonstress control groups of rats. Stress was applied by water immersion in the remaining half of the rats. The injections of pentagastrin and/or EGF resulted in substantial increase in antral content of SLI. After 20 hours of stress, the ulcer index was 40.5 +/- 3.3 in the controls, compared to 6.4 +/- 1.2 and 16.2 +/- 2.3 in rats that received pentagastrin or EGF, respectively. Injections of both pentagastrin and EGF resulted in an ulcer index of 26.2 +/- 2.0, which was significantly lower than that in controls, but higher than that in rats treated with either peptide alone. The stress resulted in significant decrease in antral SLI in all groups of rats, whereas SLI content in rats treated with pentagastrin and/or EGF remained significantly higher than that of controls. Antral content of gastrin did not differ significantly in the four groups tested. The ulcer index was inversely correlated with antral SLI content. We confirm and extend previous observations that pentagastrin and EGF prevent stress ulcer formation, and suggest that endogenous SLI may account, at least in part, for their antiulcer activity.
View details for Web of Science ID A1985ACZ3800005
View details for PubMedID 2858183
PLASMA-CONCENTRATIONS OF CHOLECYSTOKININ IN PATIENTS WITH DUODENAL-ULCER DISEASE
1984; 95 (1): 27-33
Truncal vagotomy results in diminished pancreatic protein secretion in response to intraduodenal fat. This diminished secretion may be due, at least in part, to interruption of the vagal reflexes between the intestine and the pancreas that work independently of cholecystokinin (CCK). In five dogs with chronic pancreatic fistulas, plasma CCK concentrations and pancreatic protein secretion in response to an intestinal stimulant (intraduodenal oleate) and to two exogenous peptides (bombesin and CCK-33) were compared before and after bilateral truncal vagotomy. Vagotomy decreased integrated protein secretion by about 50% in response to intraduodenal oleate. In contrast, protein output in response to parenteral stimuli increased after vagotomy. Integrated output of CCK in response to intraduodenal oleate or to exogenous bombesin or CCK was not significantly affected by vagotomy, but release of pancreatic polypeptide was decreased significantly in response to all stimuli after truncal vagotomy. These data provide evidence that truncal vagotomy decreases pancreatic protein secretion in response to intestinal stimulants by interrupting enteropancreatic reflexes mediated by the vagus, while maintaining normal (or supranormal) sensitivity of the pancreas to endogenous and exogenous CCK.
View details for Web of Science ID A1985AKV2200011
View details for PubMedID 4015214
COMPARISON OF CHOLECYSTOKININ RELEASE AND GALLBLADDER EMPTYING IN MEN AND IN WOMEN AT ESTROGEN AND PROGESTERONE PHASES OF THE MENSTRUAL-CYCLE
1984; 95 (3): 284-289
Cholecystokinin (CCK) is structurally similar to gastrin and is known to competitively inhibit the action of gastrin on the parietal cell, but little information has been accumulated about circulating levels of CCK in patients with duodenal ulcer (DU). In a group of 18 healthy volunteers (controls) and 22 DU patients (13 with active DU, nine with inactive DU), we stimulated endogenous release of CCK with oral administration of Lipomul corn oil. Plasma concentrations of CCK were measured by radioimmunoassay; ultrasonographic measurements of gallbladder volume were used as a biologic correlate for CCK in control patients and in patients with active DU. No significant difference was found in fasting plasma concentrations of CCK between controls (107 +/- 8 pg/ml) and DU patients (123 +/- 15 pg/ml), or in their total integrated release of CCK during the first hour after Lipomul ingestion (3.7 +/- 0.7 ng-min/ml in controls, 2.8 +/- 0.4 ng-min/ml in DU patients). Furthermore, no significant difference was found in integrated release of CCK between patients with active DU (2.9 +/- 0.6 ng-min/ml) and those with inactive DU (2.8 +/- 0.6 ng-min/ml). Gallbladder volume was highly correlated with plasma concentrations of CCK in controls (r = -0.91) and in active DU patients (r = -0.98). Patients with active DU had significantly smaller volumes of their resting gallbladders, they emptied less of their resting gallbladder contents in response to fat, and they showed diminished sensitivity to endogenously released CCK compared to controls. In six patients with active DU who underwent truncal vagotomy and drainage, integrated release of CCK increased significantly, from 1.9 +/- 0.6 ng-min/ml before vagotomy to 9.3 +/- 3.0 ng-min/ml after vagotomy. We found no evidence to suggest that abnormalities in release of CCK contributes to the development of duodenal ulcers. We speculate, however, that the increased release of endogenous CCK after truncal vagotomy may possibly play an etiologic role in the syndrome of postvagotomy diarrhea.
View details for Web of Science ID A1984RZ72500005
View details for PubMedID 6691183
EFFECT OF ALCOHOL ON THE RELEASE OF CHOLECYSTOKININ AND PANCREATIC-ENZYME SECRETION
AMERICAN JOURNAL OF SURGERY
1984; 147 (1): 53-57
Why are gallstones more common in women than in men? To investigate this, we measured gallbladder emptying (by ultrasonography) and release of endogenous cholecystokinin (CCK) (by specific radioimmunoassay) in eight men and nine women in response to ingestion of corn oil (1 gm/kg). Each woman was studied on the fourteenth and twenty-first day of her menstrual cycle, estimated to be the estrogen (women [E] ) and progesterone (women [P] ) peaks, respectively. Fasting plasma concentrations of CCK were significantly higher in women (E) (135 +/- 7 pg/ml) than in men (99 +/- 13 pg/ml) but not significantly higher than in women (P) (113 +/- 11 pg/ml). The peak increase in CCK concentration over basal concentration and the integrated release of CCK were not significantly different from one group to another. Men had a larger fasting gallbladder volume (GBV) (21.4 +/- 3.2 ml) than did women (E) (12.4 +/- 2.1 ml) and women (P) (14.2 +/- 2.1 ml) and emptied more GBV in response to fat than did the women. The residual GBV and fractional emptying after ingestion of corn oil were not different among the three groups. Measurements of plasma CCK and GBV during the contraction phase were highly correlated in all groups. It appears, from these data, that the increased prevalence of gallstones in women relative to men cannot be explained on the basis of significant differences either in release of CCK or in gallbladder motility. Linear regression lines that were developed indicated that the mean change in GBV relative to a given change in plasma CCK was significantly higher in men than in women. Differences between men and women in this hormonal-motility relationship may contribute to the incidence of gallstones in premenopausal women.
View details for Web of Science ID A1984SG58500007
View details for PubMedID 6701785
PHYSIOLOGIC ROLE OF CHOLECYSTOKININ IN THE INTESTINAL PHASE OF PANCREATIC-POLYPEPTIDE RELEASE
ANNALS OF SURGERY
1984; 200 (5): 600-604
Ethanol is often implicated in the pathogenesis of acute pancreatitis, but the pathophysiologic processes of alcohol-induced acute pancreatitis remains poorly understood. We found that ingestion of alcohol by healthy volunteers did not stimulate release of cholecystokinin, which is the chief hormonal stimulant of pancreatic enzyme secretion, nor did it significantly alter fasting levels of pancreatic polypeptide, a hormonal inhibitor of pancreatic enzyme secretion. In conscious dogs prepared with chronic pancreatic fistulas, direct intraduodenal instillation of ethanol significantly reduced pancreatic protein output, and this reduction corresponded to a decline in plasma concentrations of cholecystokinin that was similar in the percentage of diminution and in duration. These data suggest that, in patients who do not have chronic pancreatitis, alcohol does not induce acute pancreatitis, either by stimulating cholecystokinin release or by stimulating enzyme secretion directly.
View details for Web of Science ID A1984RZ08000009
View details for PubMedID 6691552
RELEASE OF CHOLECYSTOKININ IN CONSCIOUS DOGS - CORRELATION WITH SIMULTANEOUS MEASUREMENTS OF GALLBLADDER PRESSURE AND PANCREATIC PROTEIN SECRETION
1983; 85 (5): 1113-1119
Release of pancreatic polypeptide (PP) after a meal is biphasic, with an early transient peak believed to be under cholinergic control, and a secondary, prolonged intestinal phase thought to be mediated by hormones. Endogenous release of PP was stimulated by intraduodenal oleate (6.8 mmol/hr) or by intravenous administration of pure cholecystokinin-33 (CCK-33, 0.1 micrograms/kg/hr) in five dogs. Radioimmunoassay measurements of plasma concentrations of PP and CCK-33 were compared by linear regression analysis before and after vagotomy. Correlations between plasma concentrations of PP and CCK-33 before vagotomy (r = 0.83 [oleate], r = 0.97 [IV-CCK-33]) and after vagotomy (r = 0.92 [oleate], r = 0.92 [IV-CCK-33]) were highly significant. Changes in plasma concentrations of PP relative to a particular increment in plasma CCK-33 (before vagotomy) were similar, whether stimulated by oleate or by exogenous CCK-33. After vagotomy, less PP was released relative to a change in plasma CCK-33 (stimulated by oleate or by exogenous CCK-33), but the PP response relative to a change in plasma CCK-33 induced by the two stimuli remained remarkably similar. These results provide evidence that the intestinal phase of physiologic release of PP is mediated to a large extent through release of CCK.
View details for Web of Science ID A1984TP47500008
View details for PubMedID 6486910
CORRELATION OF RELEASE AND ACTIONS OF CHOLECYSTOKININ IN DOGS BEFORE AND AFTER VAGOTOMY
1983; 93 (6): 786-791
We have used an antibody that cross-reacts with cholecystokinin-33/39 to measure cholecystokinin release into plasma; this release was correlated with simultaneous measurements of gallbladder pressure and pancreatic protein secretion in response to intestinal administration of fat. Nine conscious dogs were prepared with chronic gastric, pancreatic, and gallbladder fistulas. Plasma cholecystokinin, gallbladder pressure, and pancreatic protein output were measured simultaneously before, and at intervals during, a 2-h intraduodenal infusion of sodium oleate. This infusion resulted in significant (p less than 0.05) elevations of plasma cholecystokinin (from 64 +/- 7 to 181 +/- 27 pg/ml), in gallbladder pressure (from 13 +/- 1 to 27 +/- 3 cmH2O), and in pancreatic protein output (from 65 +/- 7 to 148 +/- 21 mg/15 min); all measurements are from the basal state to 120 min after the onset of duodenal perfusion. Plasma concentrations of cholecystokinin were significantly correlated with gallbladder pressure (r = 0.91, p less than 0.05) and pancreatic protein output (r = 0.84, p less than 0.05). These data provide evidence that release of endogenous cholecystokinin, as measured by radioimmunoassay, can be correlated with the classic biologic actions ascribed to cholecystokinin.
View details for Web of Science ID A1983RM64900017
View details for PubMedID 6618104
PANCREATIC PROTEIN SECRETION AND GASTROINTESTINAL HORMONE-RELEASE IN RESPONSE TO PARENTERAL AMINO-ACIDS AND LIPID IN DOGS
1982; 92 (5): 902-905
Pancreatic secretion of enzymes and gallbladder contraction in response to intestinal stimulants are thought to be mediated through the vagus nerve and by means of release of cholecystokinin (CCK). The effect of truncal vagotomy on the release of CCK, pancreatic protein secretion, and gallbladder pressure (all stimulated by intraduodenal instillation of oleate) was studied in five dogs. Each dog was prepared with chronic pancreatic and gastric fistulas and catheter cholecystostomies. Simultaneous measurements were made of plasma CCK (by radioimmunoassay), pancreatic protein secretion, and gallbladder pressure (by perfused catheter technique) before and during intraduodenal administration of oleate. Before truncal vagotomy, intraduodenal oleate caused increases in plasma CCK (from 82 +/- 6 to 208 +/- 32 pg/ml), pancreatic protein secretion (from 83 +/- 8 to 165 +/- 15 mg/15 min), and gallbladder pressure (from 11 +/- 2 to 27 +/- 2 cm H2O) (all measured from basal state to 120 minutes). Truncal vagotomy caused a 45% decrease in the output of pancreatic protein in response to oleate and completely abolished the increase in gallbladder pressure, but it caused no change in release of CCK. The correlations between plasma CCK and pancreatic protein secretion before truncal vagotomy (r = 0.86) and after truncal vagotomy (r = 0.77) were highly significant. The correlation between plasma CCK and gallbladder pressure was highly significant before (r = 0.91) but not after (r = 0.42) truncal vagotomy. This study demonstrates that truncal vagotomy inhibits pancreatic protein secretion and gallbladder pressure in response to fat but does not interfere with release of CCK. The effects may be due to interruption of vagus-mediated reflexes between the intestine and the pancreas and gallbladder. The good correlation between plasma concentrations of CCK and both pancreatic protein secretion and gallbladder pressure provides evidence that the radioimmunoassay measures biologically active CCK.
View details for Web of Science ID A1983QT48400007
View details for PubMedID 6857497
CORRELATION BETWEEN RELEASE OF CHOLECYSTOKININ AND CONTRACTION OF THE GALLBLADDER IN PATIENTS WITH GALLSTONES
ANNALS OF SURGERY
1982; 195 (5): 670-676
Parenteral nutrition has been advocated for and used in clinical situations in which provision of calories without stimulation of pancreatic secretion is desired. A recent report, however, provided evidence for substantial stimulation of pancreatic secretion after parenteral administration of amino acids and fat. We have studied the effect of intravenous administration of crystalline amino acids and lipid on pancreatic protein secretion and release of gastrointestinal hormones in five dogs with chronic pancreatic fistulas. The amino acids were given as a 4.25% solution in 5% glucose at 2 gm/hr. Parenteral fat was administered as Intralipid 10% at 3.5 ml/kg/hr. Plasma concentrations of cholecystokinin (CCK) and pancreatic polypeptide (PP) and serum concentrations of gastrin, measured by radioimmunoassay, were determined before, and at intervals during, infusion of amino acids and fat. Pancreatic juice was collected simultaneously with blood sampling, and volume and protein output were measured. Basal concentrations of CCK, PP, and gastrin were not affected by intravenous infusion of amino acids. Pancreatic protein secretion and volume were also unaffected by parenteral amino acids. Parenteral infusion of fat resulted in a significant inhibition of integrated gastrin release but had no effect on plasma concentrations or integrated release of CCK or PP. Neither the volume nor protein output of pancreatic secretion was affected by intravenous fat administration. In summary, no stimulation of pancreatic secretion or release of CCK, PP, or gastrin occurred as a result of parenteral amino acid or fat administration. There is, therefore, no contraindication to the use of parenteral nutrition in situations in which it is desirable to keep the pancreas at rest.
View details for Web of Science ID A1982PP70800019
View details for PubMedID 6813982
The role of endogenously released cholecystokinin (CCK) in mediating gallblader (GB) contraction was evaluated in 12 normal volunteers and 24 patients with gallstones (11 additional gallstone patients were excluded because of failure of adequate ultrasonographic visualization). CCK concentrations before and after oral administration of fat (Lipomul((R))) were measured by a specific radioimmunoassay. CCK release was correlated with changes in GB volume determined simultaneously by ultrasonography. On the basis of gallbladder contraction and operative findings, gallstone patients were divided into "contractors" (14), "noncontractors" (6), and "hydrops" (4). Lipomul caused prompt release of CCK in normal volunteers and all groups of gallstone patients. The changes (basal to peak) in plasma CCK (pg/ml) for the different groups were as follows: normal volunteers (108 +/- 9 to 200 +/- 16), contractors (77 +/- 10 to 128 +/- 13), noncontractors (59 +/- 7 to 159 +/- 38), and hydrops (43 +/- 5 to 113 +/- 47). The total integrated output of CCK (0-60 min) was greater in normal volunteers (3975 +/- 762 pg-min/ml) than in contractors (1530 +/- 567 pg-min/ml). Lipomul caused similar GB contraction in normal volunteers and contractors (from basal volumes to maximal contraction); these changes were from 19.5 +/- 2.3 ml to 5.6 +/- 1.0 ml in normal volunteers, and from 19.6 +/- 3.2 to 5.2 +/- 1.0 in contractors. Plasma concentrations of CCK and GB volume were highly correlated in the 12 normal volunteers (r = -0.89, p < 0.01) and in the 14 contractors (r= -0.99, p < 0.01)), but the GB was significantly (p < 0.01) more sensitive to changes in plasma CCK in the gallstone contractors than in the normal volunteers. The authors suggest that there may be two groups of gallstone patients, noncontractors and contractors. Stasis may be important in the pathogenesis of gallstones in the noncontractors, whereas in contractors, the authors speculate that an abnormality in the CCK-gallbladder relationship (characterized by diminished CCK release and increased GB sensitivity to CCK) may be involved in the evolution of the disease.
View details for Web of Science ID A1982NN35700017
View details for PubMedID 7073364