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1.
Arch Surg ; 130(8): 874-7; discussion 877-9, 1995 Aug.
Article in English | MEDLINE | ID: mdl-7632149

ABSTRACT

OBJECTIVE: To evaluate the outcomes of patients undergoing laparoscopic splenectomy (LS) at a single institution. DESIGN: Case control. SETTING: University teaching hospital. PATIENTS: The medical records of the initial 25 consecutive patients who underwent LS at a single institution were reviewed. For comparison, a control group of 25 patients undergoing open splenectomy (OS) matched for age, diagnosis, and splenic weight were also reviewed. MAIN OUTCOME MEASURES: Data regarding operative time, blood loss, pathologic findings, complications, postoperative hospital stay, ileus duration, preoperative and postoperative hematocrit and platelet counts, blood and platelet transfusions, and hospital costs were collected. RESULTS: Twenty-five patients underwent attempted LS. Four procedures (16%) were converted to OS. Operative time averaged 3.3 +/- 0.2 hours for LS and 2.6 +/- 0.1 hours for OS (P = .001). In the LS group, a regular diet was tolerated 2.1 +/- 0.3 days after surgery (P < .001), and mean postoperative hospital stay was 5.1 +/- 0.6 days (P = .037), compared with 4.3 +/- 0.3 and 6.7 +/- 0.5 days, respectively, in the OS group. No differences were observed in blood loss, complication rate, transfusion requirement, or hospital cost. CONCLUSIONS: Compared with OS, LS requires more operative time, is comparable in blood loss, transfusion requirement, complication rate, and cost, and appears to be superior in terms of return of bowel function and hospital stay.


Subject(s)
Laparoscopy/methods , Splenectomy/methods , Adolescent , Adult , Case-Control Studies , Child , Child, Preschool , Female , Hospital Costs , Humans , Laparoscopy/adverse effects , Laparoscopy/economics , Length of Stay , Male , Splenectomy/adverse effects , Splenectomy/economics , Time Factors , Treatment Outcome
2.
J Surg Res ; 59(1): 127-34, 1995 Jul.
Article in English | MEDLINE | ID: mdl-7630115

ABSTRACT

The processes regulating the development of the fetal gastrointestinal tract are largely unknown, but are likely dependent, in part, on peptide growth factors. The purpose of this study was to determine the contribution of hepatocyte growth factor (HGF) to the development of the fetal gastric epithelium, with particular reference to the parietal cell. Fifty-six fetal rabbits from 18 time-mated pregnant New Zealand White rabbit does were divided into four groups at Day 23 of gestation (term is 31 days): (1) unoperated control littermates, (2) those prevented from swallowing amniotic fluid by esophageal ligation (EL), (3) those with EL plus intragastric carrier infusion, and (4) those with EL plus intragastric HGF infusion. At Day 28 of gestation, fetal stomachs were harvested and analyzed for gastric weight, DNA content, and H+/K(+)-ATPase expression. In control fetuses, gastric weight was 470 +/- 30 mg, gastric DNA content was 741 +/- 59 micrograms, and gastric H+/K(+)-ATPase expression was 25.4 +/- 2.7 micrograms. EL resulted in a 45% decrease in gastric weight (P = 0.001), a 34% decrease in DNA content (P = 0.04), and a 43% decrease in H+/K(+)-ATPase expression (P = 0.007). These inhibitory effects were not reversed by intragastric carrier infusion. Although intragastric HGF infusion did not significantly restore gastric weight or gastric DNA content, it restored gastric H+/K(+)-ATPase expression to levels no different from those of unoperated controls (23.9 +/- 2.8 micrograms), but significantly greater than those of the EL or carrier infusion groups (P = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Fetus/drug effects , Gene Expression Regulation, Enzymologic/drug effects , H(+)-K(+)-Exchanging ATPase/biosynthesis , Hepatocyte Growth Factor/pharmacology , Stomach/drug effects , Animals , Female , Fetus/enzymology , H(+)-K(+)-Exchanging ATPase/genetics , Organ Size/drug effects , Pregnancy , Rabbits , Stomach/enzymology
3.
Semin Pediatr Surg ; 4(1): 9-21, 1995 Feb.
Article in English | MEDLINE | ID: mdl-7728511

ABSTRACT

Gastrointestinal (GI) endocrinology has undergone rapid change during recent years. A greater appreciation has been gained for the role of gut peptides in the regulation of GI motility, secretion, blood flow, absorption, and immunity. Furthermore, it is increasingly recognized that these peptides function in both the brain and the gut as neurotransmitters. Many effects initially attributed to hormonal influences are now known to be neurocrine in origin. GI peptides can be classified into families based on their structural homology. In this article, the physiology of the major gut peptides is reviewed, and their role in the pathophysiology of GI disorders is highlighted.


Subject(s)
Gastrointestinal Diseases , Gastrointestinal Hormones/physiology , Child , Gastrointestinal Motility/physiology , Humans , Neurotransmitter Agents/physiology , Opioid Peptides/physiology , Peptides/physiology
4.
Gastroenterol Clin North Am ; 23(2): 261-79, 1994 Jun.
Article in English | MEDLINE | ID: mdl-8070912

ABSTRACT

This article reviews the current literature on the postgastrectomy syndromes of dumping and postvagotomy diarrhea. Pathophysiology, diagnosis, incidence, and treatment options are discussed. These syndromes present some of the most difficult treatment dilemmas seen after surgery. Specific recommendations for both medical and surgical treatments are included.


Subject(s)
Diarrhea , Dumping Syndrome , Vagotomy, Truncal , Diarrhea/etiology , Diarrhea/therapy , Dumping Syndrome/therapy , Humans , Postoperative Complications/therapy
5.
Yale J Biol Med ; 67(3-4): 145-51, 1994.
Article in English | MEDLINE | ID: mdl-7502523

ABSTRACT

The vagus nerve plays a central role in the regulation of gastric acid secretion and gastrin release. The current understanding of the mechanisms involved in vagal regulation of acid secretion and gastrin release is reviewed. Thyrotropin-releasing hormone from the medullary raphe nuclei appears to be the central excitatory mediator of vagal action in the dorsal motor nucleus. Vagal stimulation of the parietal cell occurs through M3 cholinergic receptors and via the release of histamine and gastrin from enterochromaffin-like cells and G-cells, respectively. Somatostatin exerts a tonic basal inhibition of both the parietal cell and the G-cell. Vagal stimulation suppresses somatostatin release from delta cells, thereby "disinhibiting" these cells.


Subject(s)
Gastric Acid/metabolism , Gastrins/metabolism , Stomach/physiology , Vagus Nerve/physiology , Humans , Neural Inhibition , Thyrotropin-Releasing Hormone/pharmacology , Vagotomy , Vagus Nerve/drug effects , Vagus Nerve/surgery
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