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Biomedical subjects

G M Larson

Publications and source records attributed to G M Larson.

At least 55 records · Page 3Linked to original sources
PubMed1987

Analysis of hyperamylasemia in patients with severe head injury.

To evaluate the influence of severe head injury (SHI) on amylase activity, we studied the amylase profile of 60 patients with SHIs and Glasgow Coma Scores less than 10. Fourteen additional multiple trauma patients without head injuries were studied as a control group. We excluded patients with pancreatic injury and abdominal trauma. Total serum amylase (TA), pancreatic isoamylase (PA), and nonpancreatic isoamylase (NPA) levels were measured on Days 0, 2, 4, 7, and 14 postinjury. Values greater than 2 SD above the normal mean were considered elevated. All SHI patients were comatose; 14 died. In the SHI group, TA increased in 23 patients, PA increased in 40, and NPA increased in 14. The source of hyperamylasemia was PA in 14, NPA in one, and mixed in 8 patients. While PA increases occurred throughout the study, NPA elevations occurred early. These increases did not correlate with shock (BP less than 80 mm Hg; 17 patients), facial trauma (24 patients), or associated injury (29 patients). On Day 7 postinjury, the mean TA (215 du%) and the mean PA (203.8 du%) were significantly elevated in the SHI patients compared to controls (122.1 du%, P less than 0.05, Wilcoxon's rank sum test). These data indicate that serum amylase is not a reliable index of pancreatic injury in patients with SHI. Severe head injury and multiple trauma activate pathways that increase amylase levels in the blood, suggesting a central nervous system regulation of serum amylase levels.

Amylases↗
PubMed1987

Liver abscess. Review of a 12-year experience.

Experience with liver abscess was reviewed to determine whether new trends in treatment have altered clinical outcome. Thirty-one cases of liver abscess were identified from 1973 to 1985. In this group there were ten deaths for a mortality rate of 32 per cent; the primary disease accounted for seven deaths. Significant predictors of liver abscess mortality were multiple abscesses, elevated bilirubin levels, and underlying disease. Percutaneous drainage was effective in three of four patients and should be attempted before operative intervention in selected patients.

Female↗
PubMed1986

Colonoscopy after curative resection of colorectal cancer.

Colonoscopy is generally considered to be an important part of the follow-up program for patients who have undergone curative resection of colorectal cancer. However, there are few data available concerning the frequency with which colonoscopy should be performed and for what length of time after operation. Since 1978, our policy has been to examine the colon annually in these patients using colonoscopy alternating with barium enema. We have evaluated the results in 100 patients over a four-year period. Based on size and histology, the significant colonoscopic findings were new colon cancers in three patients and 11 polyps demonstrating increased risk for malignancy in nine patients. This represents an interval yield of 3% per year. From these results and other reports, we recommend that these patients undergo total colonoscopy in the perioperative period to identify and remove synchronous lesions of the colon, and that examination of the remaining colon should be performed annually, preferably with colonoscopy, for at least the first four years after curative resection.

Barium Sulfate↗
PubMed1986

Radionuclide esophageal transit. A screening test for esophageal disorders.

Radionuclide esophageal transit (RET) is a noninvasive method of studying esophageal function. The purpose of this study was to evaluate RET as a screening test for motility disorders in symptomatic patients. Esophageal manometry and RET were performed in 16 volunteers and in 34 patients who were referred for motility evaluation. Each RET study consisted of two swallows of labeled water with the patient in the supine position under a gamma camera. Six patients had achalasia, two had scleroderma, two had diffuse esophageal spasms, and five had a nonspecific motor disorder. In each case the RET time was prolonged (greater than 15 s). Ten patients had reflux esophagitis; two of these had both abnormal manometry results and prolonged RET times. There were nine patients with upper gastrointestinal tract symptoms but normal manometry results and the RET test was positive in two patients. There were no false-negative RET results. The agreement between the RET and manometry results in this series was 96% (48/50). This preliminary experience suggests that RET is as sensitive as manometry for identifying motility disorders.

Adult↗
PubMed1986

Omeprazole-induced hypergastrinemia: role of gastric acidity.

The increase in gastrin caused by the gastric proton pump inhibitor, omeprazole, is presumably related to inhibition of gastric acid secretion (GAS). We investigated omeprazole's effect on gastrin release by studying two doses of omeprazole which produced marked acid suppression. Six gastric fistula dogs received omeprazole, 3 mumole/kg, daily for 20 days and, after a rest interval of 2 months, omeprazole, 10 mumole/kg again for 20 days. Both doses of omeprazole increased gastrin levels and produced a decrease in GAS which was still significant (P less than 0.05) 3 days postfinal dose. The increase in the integrated gastrin response by omeprazole, 10 mumole, was greater than by omeprazole, 3 mumole. Omeprazole, 10 mumole, also reduced GAS and gastric acidity, and increased gastric pH more consistently than omeprazole, 3 mumole. The magnitude of the gastrin response corresponded with the degree of acid inhibition and pH increase. Therefore, the data support the hypothesis that the hypergastrinemia caused by omeprazole is dependent on gastric pH and GAS suppression.

Animals↗
PubMed1986

Relationship of omeprazole-induced hypergastrinemia to gastric pH.

The increase in gastrin caused by the gastric proton pump inhibitor, omeprazole, is presumably secondary to inhibition of gastric acid secretion but could also be due to a direct effect on the gastrin cells. This experiment was designed to determine whether gastrin elevations caused by omeprazole are related to intragastric pH. We studied gastrin release and acid output in response to 10% peptone broth (400 ml) in five dogs with gastric fistulas. The broth, at pH 5.5 or 2.5, was instilled into the stomach through the cannula, and the desired pH was maintained by intragastric titration with 0.1N NaHCO3 for 2 hours. Studies at each pH level were performed on separate days before, during, and after omeprazole (10 mumol/kg daily for 20 days). Omeprazole increased intragastric pH to greater than or equal to 3.5 for 24 hours. At pH 5.5 omeprazole inhibited acid secretion and increased gastrin levels; however, setting the intragastric pH at 2.5 completely blocked omeprazole's effect on gastrin release. Therefore these data support the hypothesis that the hypergastrinemia caused by omeprazole is dependent on gastric pH and gastric acid suppression.

Animals↗
PubMed1985

Bleeding from stress gastritis. Has prophylactic pH control made a difference?

Control of intragastric pH with antacids or H2-receptor antagonists is a standard prophylactic treatment routinely used to prevent or control bleeding from acute erosive gastritis (AEG) in critically ill patients on trauma and surgical services. The incidence of bleeding from AEG was documented on these services retrospectively before and after the institution of standard prophylaxis treatment to determine the relative morbidity, mortality, and risk factors of each era. During the preprophylaxis and postprophylaxis era, the incidence of bleeding was the same, 2.3 per cent (13 of approximately 550 patients in each study period). Prior to prophylaxis, three times as many patients required operation (1 versus 3 patients) although the average transfusion requirement was the same (4.4 units of blood). During both eras the majority of patients were septic and showed other signs of organ failure. Inadequate prophylaxis (failure to prescribe or early discontinuation) was documented in over half of the patients who bled and in the patient requiring operation in spite of a departmental interest in stress gastritis prophylaxis. If antacids and H2-receptor antagonists are used routinely, complications from AEG should be reduced. Even with improved methods of pH control, it appears unlikely that this problem will be eliminated.

Adult↗
PubMed1985

Surgical sympathectomy increases pancreatic polypeptide response to food.

Numerous studies in man and animals suggest that beta-adrenergic receptors stimulate pancreatic polypeptide (PP) release whereas alpha-adrenergic receptors inhibit PP release. This study was undertaken to further clarify the role of the adrenergic nervous system in regulating PP release. We evaluated the effects of stellatectomy and celiacectomy on resting and meat meal-stimulated PP release in the dog. PP release was studied in three stages--control, poststellatectomy, and poststellatectomy plus celiacectomy in five dogs. The meat meal caused a prompt and prolonged increase in plasma levels of PP. Stellatectomy did not alter the control PP response. However, celiacectomy increased basal and peak PP levels and enhanced the early and late phases of delta-integrated PP release. The data suggest that the celiac and superior mesenteric ganglia are the main source of the adrenergic innervation of the pancreas and that this innervation is primarily an inhibitor of PP release.

Animals↗
PubMed1984

Gastric response to severe head injury.

We studied the gastric response to severe head injury and multiple trauma in 53 patients admitted to the surgical intensive care unit at the University of Louisville. Twenty-two of the 32 patients with severe head injury could have endoscopy. Each patient had gastritis or duodenitis. Patients with severe head injury had a slightly higher rate of gastric acid secretion than did the other trauma patients without severe head injury, but the difference was not significant. Serum gastrin levels were normal in both groups and did not correlate with intracranial pressure. Pancreatic polypeptide levels were significantly higher in patients with severe head injury compared with the control trauma patients without head injury. Elevations in pancreatic polypeptide may be linked to increases in intracranial pressure. We conclude that erosive gastritis occurs commonly in patients with severe head injury and that severe head injury is associated with a marked increase in pancreatic polypeptide levels in the fasted, nongut-stimulated state. Gastrin levels are within normal limits. Head injury appears to specifically increase pancreatic polypeptide release, probably by influencing autonomic centers in the mid brain. Because the cephalic phase of pancreatic polypeptide release is vagalcholinergic, the data are consistent with the hypothesis that severe head injury increases vagal activity. Participation of vagal adrenergic fibers in this process cannot be excluded.

Adolescent↗
PubMed1984

Omeprazole, a long-lasting inhibitor of gastric secretion.

Omeprazole is a potent inhibitor of gastric acid secretion (GAS). It has a unique mechanism of action within the parietal cell where it inhibits (H+-K+) ATPase in secretory membranes. The inhibitory effect of omeprazole was measured over a 24-hr period in the dog. Seventy-five minutes after start of pentagastrin-stimulated GAS, placebo or omeprazole (0.5-3.0 micrograms/kg) iv was given to six dogs and GAS was collected for another 2 hr. Twenty-four hours later, GAS was again measured. Omeprazole produced a prompt and dose-dependent reduction of GAS, and significant suppression (44%) was still present at 24 hr.

Animals↗
PubMed1984

Approaches to repair of ventral hernia and full-thickness losses of the abdominal wall.

This article describes the causes, course, and treatment options for surgical repair of umbilical epigastric and incisional hernias. Special attention is paid to the full-thickness abdominal wall defects, which are particularly difficult wounds to close. A method of closure with Marlex mesh, followed by myocutaneous flap coverage, is discussed.

Abdominal Muscles↗
PubMed1984

The effect of chemical and surgical sympathectomy on gastric secretion and innervation.

The purpose of this project was to evaluate the effects of chemical and surgical sympathectomy on gastric acid secretion (GAS) and mucosal innervation in the dog. Chemical sympathectomy was achieved with 6-OHDA and surgical sympathectomy was performed by excising the celiac and superior mesenteric ganglia. Gastric biopsies for fluorescence microscopy were taken before and after sympathectomy, as was pentagastrin (PPG) stimulated GAS. Each sympathectomy increased GAS in response to submaximal doses of PPG while simultaneously destroying adrenergic nerve terminals in the gastric mucosa. 6-OHDA caused a complete degeneration of nerve terminals at one week, but regeneration was complete by 9 weeks. The data support the concept that the sympathetic innervation of the stomach is an inhibitor of GAS.

Animals↗
PubMed1984

Esophageal motility: effects of injection sclerotherapy.

The purpose of this project was to evaluate the acute and chronic effects of sclerotherapy on esophageal motility and function. We studied motility in eight patients before and after injection sclerotherapy of esophageal varices. We injected the varices with 5% sodium morrhuate twice during the first week and then at 1, 2, 3, and 6 months. Lower esophageal sphincter pressure, contraction wave amplitude, and duration were not altered by sclerotherapy. However, the length of the high-pressure zone increased significantly from 3.6 +/- 0.3 cm to 4.2 +/- 0.2 cm during the first 3 days after initial treatment, and sclerotherapy caused considerable distortion of peristaltic wave form. Also, esophageal peristaltic velocity decreased in three patients who complained of dysphagia and subsequently developed esophageal stricture. The strictures have responded well to dilatation, and in two patients velocity has even returned toward the baseline value. Reflux esophagitis has not been a problem. Esophageal motility is altered by sclerotherapy of esophageal varices. Stricture formation seems to be reversible after sclerotherapy is stopped or discontinued.

Aged↗
PubMed1984

Effect of stellatectomy on acid secretion and gastric release.

The stellate ganglia give rise to adrenergic fibers in the subdiaphragmatic vagus nerve which innervate the gut. Since stellatectomy causes a degeneration of these vagal adrenergic fibers, the purpose of this experiment was to evaluate the effect of stellatectomy on gastric acid secretion (GAS). GAS was measured in 6 dogs with gastric fistula before and after stellatectomy was performed; also the gastrin response to a meat meal was studied before and after stellatectomy . Acid secretion increased significantly at submaximal doses of pentagastrin after stellatectomy , while basal and meal stimulated gastrin levels did not change. Horner's syndrome developed in each dog. These results suggest that the vagal adrenergic innervation of the stomach is an inhibitor of GAS in the dog.

Animals↗
PubMed1983

The effect of stellatectomy on gastric acid secretion in the dog.

The stellate ganglion is the major contributor of adrenergic fibers to the vagus nerve and stellatectomy causes a degeneration of vagal adrenergic fibers. The purpose of this experiment was to evaluate the effect of stellatectomy on gastric acid secretion (GAS) and gastrin levels in the dog. GAS in response to pentagastrin stimulation was measured in six gastric fistula dogs before and after stellatectomy. Likewise, blood was collected for basal and meat meal-stimulated serum gastrin levels before and after stellatectomy. After bilateral stellatectomy acid secretion increased in response to submaximal doses of pentagastrin stimulation whereas maximal secretion was unchanged. Resting and meal-stimulated gastrin levels did not change. A Horner's syndrome developed in each dog. It is concluded that bilateral stellatectomy increases GAS in response to submaximal stimulation while not altering gastrin release. These results suggest that the vagal adrenergic innervation of the stomach has an inhibitory role in the control of GAS in the dog.

Adrenergic Fibers↗