Biomedical subjects

G Gomez

Publications and source records attributed to G Gomez.

At least 73 records · Page 4Linked to original sources

PubMed1991

Intracolonic fat inhibits gastric acid secretion independent of gastrin release in the dog.

The purpose of this study was to examine the effect of perfusion of the colon with a fatty acid (oleic acid) on peptone-stimulated gastric acid secretion and release of gastrin in conscious dogs. Gastric acid secretion was monitored by continuous intragastric titration. Perfusion of the colon with sodium oleate (24 mmol/hr) inhibited gastric acid secretion (14.2 +/- 2.6 meq/hr) stimulated by a peptone meal (1%) significantly (P less than 0.05) when compared to perfusion of the colon with saline alone (20.1 +/- 1.6 meq/hr). The serum elevation in gastrin in response to intragastric instillation of the peptone meal was not affected by the colonic perfusion of oleic acid. Plasma concentrations of peptide YY (PYY) increased significantly in response to perfusion of the colon with saline or sodium oleate, and the integrated release of PYY in response to sodium oleate [6.9 +/- 2.8 ng (60-120) min/ml] was significantly greater than the response to saline [3.1 +/- 0.7 ng (60-120) min/ml]. The results of this study indicate that inhibition of gastric acid secretion by perfusion of the colon with fat is not due to an inhibition of gastrin release. In addition, because PYY is an inhibitor of gastric acid secretion, it is possible that PYY participates as an inhibitor of gastric acid secretion by the colon.

Animals↗

PubMed1991

Characterization of secretin release in response to food and intraduodenal administration of fat and hydrochloric acid.

The development and validation of a radioimmunoassay that detects release of secretin in plasma in response to low doses of secretagogues [intraduodenal HCl (0.033 meq/min); intraduodenal sodium oleate (0.04 mmol/min)] or an oral mixed meal in conscious dogs is described. Plasma secretin levels increased significantly (P less than 0.05) in response to an oral mixed meal in conscious dogs from a basal level of 4.0 to a peak level of 12.3 pg/ml at 15 min. Infusion of graded doses of HCl (2, 4, 8, 16, meq/hr for 30 min) intraduodenally in six dogs resulted in significant elevation of plasma secretin levels in a dose-dependent manner. The pancreatic bicarbonate and volume outputs correlated with the dosage of HCl administered and with the elevations in plasma secretin concentrations. Intraduodenal infusion of increasing doses of sodium oleate (2.4, 4.8, 9.6, and 19.2 mmol in 15-min periods) resulted in a significant (P less than 0.05) elevation of plasma levels of secretin.

Animals↗

PubMed1991

Peptide YY, a new gut hormone (a mini-review).

This report describes our current knowledge of a new gut peptide hormone, peptide YY. The localization, action, and possible mechanisms that control release of peptide YY are described.

Amino Acid Sequence↗

PubMed1991

Intracolonic infusion of bile salt stimulates release of peptide YY and inhibits cholecystokinin-stimulated pancreatic exocrine secretion in conscious dogs.

The purpose of this study was to examine the effect of transanal (intracolonic) infusion of bile acid on release of peptide YY (PYY) and cholecystokinin (CCK)-stimulated pancreatic exocrine secretion in seven conscious dogs. CCK-8 (50 ng/kg/h) was given intravenously for 120 min and either taurocholic acid (TA, 1 or 2 mmol/h) or saline was infused transanally (150 ml/h) during the 0-60-min period of CCK infusion. Transanal infusion of TA (1 or 2 mmol/h) significantly inhibited output of CCK-8-stimulated pancreatic protein, compared to transanal infusion of saline during the first 60 min. On the average, the magnitude of inhibition was approximately 45%. Plasma concentrations of PYY increased significantly in response to intracolonic infusion of TA or saline. Transanal infusion of TA (1 or 2 mmol/h) significantly increased plasma levels of PYY when compared with transanal infusion of saline during the first 60 min. The magnitude of the increase of plasma PYY levels was approximately 50 pg/ml (p less than 0.05). Plasma levels of pancreatic polypeptide were not altered significantly by transanal infusion of TA. Our results suggest that release of endogenous PYY by TA in the colon plays a role in the inhibition of CCK-stimulated pancreatic exocrine secretion. Bile salts in the hindgut may participate in the physiologic regulation of pancreatic exocrine secretion by stimulation of release of ilealcolonic PYY.

Animals↗

PubMed1991

Role of cytosolic Ca in renal tubule damage induced by anoxia.

Cytosolic free Ca (Caf) was measured in three different preparations of freshly prepared proximal tubules from the rabbit kidney during energy deprivation using fura-2. Isolated perfused tubules, tubules immobilized on glass cover slips, and tubules in suspension were subjected to inhibitors of oxidative phosphorylation ("chemical hypoxia"); the latter two preparations were also subjected to 40 min of anoxia. During normoxia, Caf ranged from 100 to 180 nM in all three preparations, and chemical hypoxia caused either no change or a small (30-100%) increase in Caf values. Subsequent addition of Ca ionophores increased Caf to 300-500 nM in the first 2 min and to greater than 1 microM after 15 min. In individual experiments, anoxia produced similar responses to those of chemical hypoxia, eliciting no average significant change in Caf, despite clear evidence for impaired respiration and plasma membrane damage after 40 min of anoxia. This lack of change in Caf was unrelated to "Ca buffering" by fura-2 or inactivation of the dye, since Caf increased to 666 +/- 59 nM upon addition of Ca ionophore during anoxia. These data suggest that increased Caf is not a prerequisite for cellular damage during anoxia in proximal renal tubules. Furthermore, no apparent alteration in plasma membrane permeability to Ca occurs before membrane disruption. Decreased ATP seems to initiate a series of Caf-independent events that cause irreversible injury.

Animals↗

PubMed1990

Terbutaline, a beta 2-adrenoreceptor agonist, inhibits gastric acid secretion and stimulates release of peptide YY and gastric inhibitory polypeptide in dogs.

Terbutaline, a beta 2-adrenoreceptor agonist, inhibits pentagastrin-stimulated gastric acid secretion. The purpose of this study was to examine the effect of intravenous administration of terbutaline on plasma levels of peptide YY (PYY) and gastric inhibitory polypeptide (GIP), both of which are known to inhibit gastric acid secretion. Seven dogs with gastric and duodenal fistulas were given pentagastrin (1 microgram/kg/hr) intravenously for 150 min in combination with terbutaline (10 or 20 micrograms/kg/hr) or saline during the 60- to 120-min period of pentagastrin infusion. Pentagastrin-stimulated gastric acid secretion was significantly (P less than 0.05) inhibited by intravenous administration of terbutaline. Terbutaline significantly increased plasma PYY levels, 24% in response to terbutaline at 10 micrograms/kg/hr, and 59% at 20 micrograms/kg/hr. Plasma GIP levels were also increased significantly, 24% with terbutaline at 10 micrograms/kg/hr, and 39% at 20 micrograms/kg/hr. Our data suggest that terbutaline-induced inhibition of pentagastrin-stimulated gastric acid secretion is mediated, at least in part, by the release of PYY and GIP. The adrenergic nervous system may influence gastric acid secretion through the release of PYY and GIP.

Animals↗

PubMed1990

Stimulatory effect of pancreastatin on gastric acid secretion in conscious dogs.

Pancreastatin, a new 49-amino acid peptide, has recently been isolated and characterized from extracts of the porcine pancreas. The objective of the present study was to examine the effect of various doses of pancreastatin on gastric acid secretion in conscious dogs that were prepared with chronic gastric cannulas. Pancreastatin, administered IV at 400 pmol.kg-1 x h-1, enhanced peptone meal [peptone (5%), phenylalanine (90 mmol/L), glucose (12 g/dL)]-stimulated gastric acid secretion by 50%; pancreastatin at 800 pmol.kg-1 x h-1 enhanced peptone meal secretion by 165% (P less than 0.05). Intravenous administration of pancreastatin did not affect basal or peptone-stimulated release of gastrin. In addition, IV pancreastatin (400 pmol.kg-1 x h-1) failed to influence basal gastric acid secretion. Pancreastatin did not affect acid secretion stimulated by 2-deoxyglucose, histamine, or pentagastrin. The present study shows that pancreastatin can selectively enhance gastric acid secretion by a mechanism independent of cholinergic, histaminergic, or gastrin input.

Animals↗

PubMed1990

The use of segmental anatomy for an operative classification of liver injuries.

There is no universally accepted standard classification for liver injuries, and thus accurate comparison of reports on the subject is impossible. Most published reports on liver trauma suggest that both morbidity and mortality have a linear correlation with not only the amount of liver parenchyma injured but also with the magnitude of the surgical intervention. The exceptions are retrohepatic vein injuries, which have a mortality independent of associated parenchymal injury but should be integrated in any classification of liver injury. The classification proposed is based on the segmental anatomy of the liver (as defined by Couinaud): Grade I--Injuries requiring no operative intervention, or any injury that requires operative intervention limited to a segment or less. Grade II--Any injury that requires operative intervention involving two or more segments. Grade III--Any injury with an associated juxta- or retrohepatic vein injury. We reviewed all patients with isolated liver injuries during the past 5 years and prospectively reviewed all patients for the 6-month period from January to June 1988 and applied this classification. Sixty-nine patients had grade I injuries, with one death (1%); thirteen patients had grade II injuries, with six deaths (46%); and 13 patients had grade III injuries with nine deaths (69%). Postoperative morbidity was 7% for grade I, 57% for grade II, and 50% for grade III. This study supports the conclusion that morbidity and mortality from liver injury are directly related to the volume of parenchyma involved, and that segmental anatomy can be applied to define this volume. Mortality from retrohepatic vein injuries is independent of associated parenchymal injury. We believe that this proposed classification will provide a simple, reproducible, and accurate means for reporting and comparing liver injuries.

Adult↗

PubMed1990

Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts.

The effects of luminal bile salts on plasma levels of cholecystokinin (CCK) and growth of the pancreas in mice were studied. Nonfasting levels of plasma CCK in control mice were 8.1 +/- 1.5 pM. Feeding mice a 0.5% (wt/wt) sodium taurocholate-supplemented diet for 1 wk significantly lowered nonfasting levels of plasma CCK to 4.1 +/- 0.5 pM and decreased the total contents of pancreatic DNA by 22%, RNA by 25%, and protein by 24%. All of the inhibitory effects of taurocholate on pancreatic growth were completely reversed by the simultaneous administration of CCK-8 (3 micrograms/kg, 3 times daily). In contrast, intraluminal neutralization of endogenous bile salts by feeding a 4% (wt/wt) cholestyramine-supplemented diet for 1 wk significantly elevated nonfasting levels of plasma CCK to 14.7 +/- 1.5 pM and increased the total contents of pancreatic DNA by 34%, RNA by 40%, and protein by 35%. All of the stimulatory actions of cholestyramine on pancreatic growth were completely abolished by the administration of the highly potent and specific CCK-receptor antagonist L364,718 (1 mg/kg, twice daily). These findings, therefore, indicate that bile salts appear to play a physiological role in pancreatic growth by regulation of plasma levels of CCK.

Animals↗

PubMed1990

Intravenous amino acids stimulate human gallbladder emptying and hormone release.

Gallbladder stasis during prolonged total parenteral nutrition (TPN) has been documented. We have examined the effect of intravenous amino acid infusion on human gallbladder contraction and release of cholecystokinin (CCK). Five healthy adult volunteers were given amino acid infusions at different rates (65, 125, 240, and 600 mg.kg-1.h-1). The volume of the gallbladder was calculated by means of ultrasonographic measurements. Plasma samples were analyzed for CCK immunoreactivity. Gallbladder and hormone responses after intravenous amino acids were compared with responses after a fat meal, after a protein meal, and after ingestion of an oral amino acid mixture. We found that intravenous amino acids stimulated human gallbladder contraction in a dose-related manner. The mechanism of stimulation may be through the release of CCK although significant correlation was not demonstrated. The magnitude of response is similar to that seen after meal stimulation. To compare the delivery of amino acids during a standard meal and during each dose of intravenous amino acids, peripheral plasma levels of dietary amino acids were measured after a standard commercially prepared enteral supplement meal and after each dose of intravenous amino acids. Our lower doses of amino acid infused resulted in levels of circulating amino acid comparable to those after a meal. The induction of gallbladder contraction and release of CCK in human recipients of parenteral nutrition may be of value in some circumstances.

Adult↗

PubMed1990

Protective action of luminal bile salts in necrotizing acute pancreatitis in mice.

Bile salts in the intestinal lumen act to inhibit the release of cholecystokinin (CCK). Recent studies have shown that CCK may play a permissive role in the development of acute pancreatitis. In this study, the amount of luminal bile salts in female Swiss Webster mice was either decreased by feeding 4% (wt/wt) cholestyramine or increased by feeding 0.5% sodium taurocholate for 1 wk. Plasma levels of CCK were stimulated by cholestyramine and inhibited by taurocholate. Then, acute pancreatitis was induced either by caerulein injections, or by feeding a choline-deficient, ethionine-supplemented (CDE) diet. Feeding of cholestyramine significantly decreased survival from 25% to 0% in the CDE pancreatitis, and increased the magnitude of elevation of serum amylase levels and the extent of pancreatic necrosis in both models of pancreatitis; CCK-receptor blockade with CR-1409 completely abolished the adverse effects of cholestyramine. In contrast, feeding of taurocholate significantly increased survival to 100% and decreased the elevation of serum amylase and pancreatic necrosis; CCK-8 antagonized these actions of taurocholate. Luminal bile salts appear to provide a physiologic protection against necrotizing pancreatitis, at least in part, both by inhibiting the release of CCK and by promoting resistance of the pancreas to CCK excessive stimulation in vivo.

Acute Disease↗

PubMed1990

The use of serum amylase and lipase in evaluating and managing blunt abdominal trauma.

In order to determine the usefulness of serum amylase and lipase in the initial evaluation and subsequent management of blunt abdominal trauma (BAT) patients, we collected serum amylase and lipase on 85 consecutive BAT patients at admission, hospital day 1, hospital day 3, and hospital day 7. Only one patient had a pancreatic injury. A total of 45 patients (53%) had at least one enzyme abnormality during the study. There was no correlation between amylase or lipase values and age, sex, type of injury, diagnostic tests, operation, and outcome. In a control group of nonabdominal-trauma patients with admit studies only, all enzyme values were normal. We conclude that serum amylase and lipase are randomly elevated in patients with nonpancreatic-BAT both initially and during subsequent hospitalization and are not useful clinical tools in these patients.

Abdominal Injuries↗

PubMed1990

Trauma systems. Economic and political considerations.

Mounting morbidity and mortality from trauma should be viewed as a societal problem. Preventable trauma deaths can be reduced to less than 10% with a regionalized trauma system. Trauma systems, however, incorporating categorization, regionalization, registry data, and prevention efforts, are difficult to design and maintain. As of 1988, only two states had full coverage of all components deemed essential to such a system. Burdens such as uncompensated care, increased malpractice liability, and the need for uniform standards must be overcome to insure survival of trauma systems.

Florida↗

PubMed1990

Proglumide inhibits cholecystokinin and meal-stimulated pancreatic secretion and release of pancreatic polypeptide.

Exogenously administered cholecystokinin is a potent stimulant of pancreatic exocrine secretion and pancreatic polypeptide release. Release of cholecystokinin by amino acids and fats is strongly correlated with both pancreatic exocrine secretion and pancreatic polypeptide release. Despite this correlation, direct evidence that cholecystokinin is a physiologic mediator of these actions is not available. We have studied this problem in fasted dogs with chronic pancreatic fistulas by means of a specific cholecystokinin antagonist, proglumide, to inhibit the effect of cholecystokinin. Secretion, neurotensin (with secretin stimulation infusion), or cholecystokinin-octapeptide was infused intravenously, either with saline solution or with proglumide (300 mg/kg/hr). For endogenous release of cholecystokinin, intraduodenal infusions of phenylalanine and tryptophan or of sodium oleate were given with either intravenous saline solution or intravenous proglumide. Pancreatic secretion and release of cholecystokinin and pancreatic polypeptide were measured in plasma. Cholecystokinin-octapeptide stimulated pancreatic secretion of water and protein; both of these were significantly inhibited by proglumide. Intraduodenal amino acids and sodium oleate both caused significant release of cholecystokinin, which was not altered by proglumide; however, proglumide inhibited pancreatic secretion stimulated by intraduodenal amino acids and sodium oleate. Release of pancreatic polypeptide stimulated by amino acid and sodium oleate was also significantly inhibited by proglumide. Since proglumide appears to block actions of cholecystokinin, our results show that cholecystokinin is physiologically important for pancreatic secretion and for release of pancreatic polypeptide.

Amino Acids↗

PubMed1989

Contractile response of canine gallbladder and sphincter of Oddi to substance P and related peptides in vitro.

Substance P (SP) is a neurotransmitter peptide that is widely distributed in the body. Since SP has been demonstrated in the gallbladder (GB) and bile ducts of dogs, it may have a role in biliary motility. The objective of this study was to examine the effect of SP on the GB and sphincter of Oddi (SOD) of dogs in vitro, to evaluate the structure-activity relationship of SP, and to compare the contractile effect of SP with that of cholecystokinin octapeptide (CCK-8) and acetylcholine (Ach). Isolated longitudinal strips of GB and SOD from dogs were suspended in oxygenated Krebs buffer and the isometric tension responses to various doses of CCK-8, Ach, SP, and SP homologs [SP-free acid (SPFA), Octa-SP (O-SP), physalaemin (PHY)] were measured. We found that all the SP homologs, other than SPFA, stimulated GB and SOD contractions in vitro in a dose-dependent manner. The potency of SP and its homologs on GB and SOD was SP greater than or equal to PHY greater than O-SP; SPFA was without effect. CCK-8 was significantly more effective than SP on GB contraction, but unlike SP, CCK had no effect on SOD. The maximum contraction achieved by Ach was 1.3 (SOD) to 2.3 (GB) times greater than that achieved by SP, but the ED50 of SP was approximately 100- to 200-fold lower than that of Ach. The contractile effect of SP was partially blocked by 10(-5) M atropine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1989

Down-regulation of pancreatic growth and gallbladder contractility by bile salts.

Luminal sequestration of bile salts with cholestyramine and the oral administration of bile salts represent current forms of therapy for some diseases. We have recently reported that secretion of these salts exerts negative feedback control on the release of cholecystokinin (CCK). The purpose of this study was to examine the effects of long-term alterations of luminal concentrations of bile salts on CCK target organs, the pancreas and gallbladder. The bile salt pool in adult guinea pigs was either enriched by feeding 0.5 percent sodium taurocholate or depleted by feeding 2 percent cholestyramine. Pancreatic growth, gallbladder contractility, the concentration of cholecystokinin receptors in the gallbladder muscle, and meal-stimulated plasma levels of cholecystokinin were significantly stimulated by feeding the bile salt sequestrant cholestyramine to guinea pigs. Administration of the bile salt taurocholate produced the opposite effects. Inhibition of CCK release by bile salts and up-regulation of CCK receptors by CCK may be the mechanisms responsible for the actions of bile salts on CCK target organs.

Animals↗

PubMed1989

Endogenous cholecystokinin regulates growth of human cholangiocarcinoma.

Exogenous administration of cholecystokinin (CCK) or caerulein inhibits growth of SLU-132, a human cholangiocarcinoma that we have shown to possess receptors for CCK. Chronic administration of cholestyramine, a resin that binds bile salts, increases release of CCK and growth of the pancreas in guinea pigs. Feeding the bile salt, taurocholate, inhibits meal-stimulated release of CCK. The purpose of this study was to determine whether endogenous CCK affects growth of the human cholangiocarcinoma, SLU-132. We implanted SLU-132 subcutaneously into athymic nude mice. The bile salt pool was depleted by feeding 4% cholestyramine for 40 days, either alone or enriched with 0.5% taurocholate for 32 days. When the mice were killed, tumors and pancreas were removed. Cholestyramine significantly inhibited the growth of SLU-132 and stimulated growth of the normal pancreas. Feeding of taurocholate acted to stimulate tumor growth. These results demonstrate that endogenous levels of CCK regulate growth of this human cholangiocarcinoma. Our findings suggest that manipulation of levels of endogenous gut hormones may, in the future, play a role in management of patients with certain gastrointestinal cancers.

Adenoma, Bile Duct↗

PubMed1989

Pancreatic juice enhances fat-stimulated release of enteric hormones in dogs.

The presence of pancreatic juice in the intestinal lumen results in the hydrolysis of dietary fat. The hydrolytic products of dietary fat are potent stimulants of pancreatic exocrine secretion and potent inhibitors of gastric acid secretion. In this study, residual pancreatic enzyme activity in the intestinal lumen may account for the observed increase of triglyceride-stimulated pancreatic exocrine secretion and the release of peptides during diversion of pancreatic juice. The presence of pancreatic juice enhanced the pancreatic protein output that was stimulated by the intraduodenal administration of a triglyceride (corn oil, 2 g/kg/h) by 240% (p less than .05). The presence of pancreatic juice during the intraduodenal administration of a triglyceride nearly abolished the output of gastric acid as well as the release of gastrin (p less than .05) that had been stimulated by the intragastric placement of a 10% peptone meal. Pancreatic juice in the duodenum significantly enhanced the triglyceride-stimulated release of cholecystokinin-33/39, secretin, neurotensin, peptide YY, pancreatic polypeptide, and insulin (p less than .05) when compared with the release of these enteropancreatic hormones during the diversion of pancreatic juice. This study shows that the presence of pancreatic juice in the duodenal lumen enhances the fat-stimulated release of enteric hormones that have a stimulatory action on the enteroacinar and enteroinsular axis as well as an inhibitory action (enterogastrone-like activity) on the postprandial regulation of gastric function.

Animals↗