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Biomedical subjects

L McHenry

Publications and source records attributed to L McHenry.

15 recordsLinked to original sources
PubMed1995

Adenosine A1 and A2b receptors coupled to distinct interactive signaling pathways in intestinal muscle cells.

Adenosine receptors and the signaling pathways to which they are coupled were examined in dispersed intestinal muscle cells. The receptors were characterized by their ability to induce contraction or relaxation, mobilize Ca2+ and stimulate or inhibit cAMP, in naive cells and in cells where only one receptor type was preserved by selective receptor protection. Adenosine elicited contraction and increased [Ca2+]i and cAMP; the contraction was mimicked by the A1 selective agonist, cyclopentyladenosine. A selective A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine, and pertussis toxin abolished contraction and the increase in [Ca2+]i and augmented the increase in cAMP. Conversely, a preferential A2 antagonist, 9-chloro-2-(2-furyl) [1,2,4]triazolo[1,5-c]quinazolin-5-amine augmented contraction and the increase in [Ca2+]i and abolished the increase in cAMP; a cAMP-kinase inhibitor, Rp-cAMP[S], had a similar effect, augmenting contraction and the increase in [Ca2+]i. Adenosine elicited also relaxation of maximally contracted cells that increased or decreased in parallel with cAMP. The selective A2a agonist, 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamido adenosine, was a very weak relaxant agent, and the selective A2a antagonist, 8-(3-chlorostyryl)caffeine, had no effect on adenosine-induced relaxation. In cells where only A1 receptors were preserved, the cAMP response to adenosine was abolished, although contraction and [Ca2+]i were increased to the same extent as when naive cells were treated with the A2 antagonist. Conversely, in cells where only A2 receptors were preserved, contraction and the increase in [Ca2+]i were abolished and the increase in cAMP was augmented to the same level as when naive cells were treated with the A1 antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

Implementing self-directed teams.

The "self-directed team" concept is an innovative approach in the healthcare setting. Long-term benefits of customer satisfaction and quality improvement are consistent with concepts of total quality improvement and patient-focused care. Initial investment of time and money pays off in low turnover and marked employee and patient satisfaction.

Decision Making, Organizational↗
PubMed1993

Pharmacological control of gastric acid secretion.

Gastric acid produced by the parietal cells has a significant role in a variety of gastrointestinal diseases, such as duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. We address acid production by the parietal cell and the pharmacological means to control gastric acid secretion. The physiology of parietal cell acid secretion is reviewed. The role of acid-suppressive therapy with histamine H2 antagonists and omeprazole in duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease is discussed. Pharmacology, side-effect profile, and dosage requirements of the histamine H2 antagonists and omeprazole are outlined.

Depression, Chemical↗
PubMed1993

Nonsteroidal antiinflammatory drug-induced gastroduodenal lesions: prophylaxis and treatment.

Nonsteroidal antiinflammatory drugs (NSAIDs) are one of the most commonly prescribed agents, especially for elderly patients. These drugs frequently produce mucosal petechiae and erosions in the stomach and duodenum, but these conditions are rarely of clinical significance. NSAIDs, however, cause considerable morbidity and mortality due to their ability to cause gastric and duodenal ulcers. NSAID-induced ulcers are most likely to develop in elderly women receiving multiple NSAIDs for prolonged periods. NSAIDs injure gastric and duodenal mucosa by both a topical and a systemic effect. The latter is responsible for the pathogenesis of NSAID-associated ulcers. These ulcers are particularly prone to perforation and hemorrhage. Both complications frequently occur in asymptomatic long-term users of NSAIDs. H2 antagonists prevent NSAID-related duodenal ulcers but are not effective for prevention of gastric ulcers. Misoprostol is the only agent proven to decrease the risk of gastric ulcers in patients receiving NSAIDs. Both H2 antagonists and omeprazole are highly effective for the treatment of established duodenal ulcers in patients receiving NSAIDs. H2 antagonists also heal gastric ulcers in these patients but at slower rates than in patients not receiving NSAIDs. The existing literature is reviewed, and guidelines for prophylaxis against NSAID-induced ulcers and treatment of established ulcers are provided.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Inhibition of muscle cell relaxation by somatostatin: tissue-specific, cAMP-dependent, pertussis toxin-sensitive.

The direct action of somatostatin on smooth muscle was examined in muscle cells isolated from the stomach and intestine of human and guinea pig. Somatostatin inhibited relaxation in gastric but not intestinal muscle cells of the two species, and its mechanism of action was explored in more detail in gastric muscle cells of the guinea pig. Somatostatin inhibited relaxation induced by vasoactive intestinal peptide (VIP, 83 +/- 7%, P less than 0.001) and isoproterenol (85 +/- 5%, P less than 0.001), as well as the concomitant increase in adenosine 3',5'-cyclic monophosphate (cAMP) production [81 +/- 25% inhibition with VIP (P less than 0.02) and 68 +/- 12% inhibition with isoproterenol (P less than 0.01)]. Inhibition of relaxation and cAMP production was abolished by pretreatment of the cells with pertussis toxin. Relaxation induced by the permeant derivative of cAMP, N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate, by sodium nitroprusside, which acts by increasing levels of guanosine 3',5'-cyclic monophosphate, or by ATP, which acts by opening of K+ channels, was not affected by somatostatin. The fact that inhibition by somatostatin and its reversal by pertussis toxin was confined to agonists that stimulate an increase in the levels of cAMP implied that somatostatin acts by inhibiting the generation and not the action of cAMP. It is concluded that somatostatin receptors on gastric muscle cells mediate inhibition via a GTP-binding, pertussis-sensitive regulatory protein, Gi, coupled to adenylate cyclase.

Adenosine Triphosphate↗
PubMedDate not supplied

Percutaneous endoscopic gastrojejunostomy: a dual center safety and efficacy trial.

Although jejunal tube placement through a percutaneous endoscopic gastrostomy (PEG) has not been proven to be preferable to PEG feeding, it would be theoretically advantageous for those patients prone to gastrointestinal aspiration. However, reliable placement of a small bowel feeding tube through a PEG has been technically difficult. We have previously reported successful placement of a percutaneous endoscopic gastrojejunostomy (PEG/J) with minimal complications. These results are in contrast to other series that report technical difficulty, frequent tube dysfunction and gastric aspiration. We describe an over-the-wire PEG/J technique performed by multiple operators at two medical centers. Gastrostomy tube placement was successful in 94% of patients. Initial placement of the jejunal tube was successful in 88% of patients. Second attempts were 100% successful. The average procedure time was 36 minutes. The distal duodenal and jejunal placement of the jejunal tube resulted in no episodes of gastroduodenal reflux. Complications included jejunal tube migration (6%), clogging (18%), and unintentional removal (11%). The majority of patients were ultimately converted to either oral or intragastric feedings. We conclude that the PEG/J system is a reliable, reproducible method of small bowel feeding and is associated with no episodes of tube feeding reflux when the jejunal tube is positioned in the distal duodenum or beyond. Furthermore, it provides a temporary nutritional bridge for those patients who are later transitioned to either PEG or oral feeding.

Adult↗