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Biomedical subjects

K M Flowe

Publications and source records attributed to K M Flowe.

4 recordsLinked to original sources

Thoracic aorta injuries: management and outcome of 144 patients.

Rupture of the thoracic aorta from blunt injury is often lethal. Methods of operative repair vary, based on the surgeon's preference and circumstances. The primary hypothesis of this study was that operative management choices would correlate with outcome. Data on demographics, injury mechanism, initial evaluation, diagnostic procedures, operative treatment, and outcome were obtained from chart review at the state's eight trauma centers. Rates of paraplegia and survival were compared for different methods of operative repair. Of 63,507 hospitalized trauma patients, 144 patients sustained thoracic aortic injury (incidence = 0.23%). Sixty-four died (44.1%), most of whom died in the emergency department (26) or the operating room (12). Eighty-six patients had complete operative data for analysis, including cross-clamp time and methods of repair. No patient in the group with a cross-clamp time of less than 35 minutes developed paraplegia (p = 0.02). For the patients with longer cross-clamp times, 6 of 14 patients (42.9%) undergoing clamp and sew repair developed paraplegia, as compared to 2 of 37 patients (5.4%) repaired on bypass (p = 0.005). This study suggests that the rate of paraplegia after repair of thoracic aortic injury can be minimized with short cross-clamp times or the use of bypass when long cross-clamp times can be anticipated.

Adolescent↗

Gastrin-releasing peptide stimulation of amylase release from rat pancreatic lobules involves intrapancreatic neurons.

Gastrin releasing peptide (GRP) immunoreactivity has been localized to nerve fibers innervating pancreatic acini and identified in nerve cell bodies within intrapancreatic ganglia. The role of intrapancreatic neurotransmission in GRP- and neuromedin C (NmC)-stimulated amylase release was investigated using rat pancreatic lobules in vitro. Lobule responsiveness to neuronal depolarization was demonstrated by amylase release upon exposure to 55 mM potassium (207 +/- 7% of control) or veratridine (294 +/- 12%). Both GRP and NmC produced dose-dependent increases in lobular amylase release, with ED50 values of 1.1 nM and 0.13 nM, respectively. Amylase release in response to submaximal concentrations of GRP were significantly inhibited by tetrodotoxin (78 +/- 5% of control) or hexamethonium (71 +/- 5% of control). GRP-stimulated amylase release was decreased to 71 +/- 5% of control by atropine coincubation. NmC-stimulated amylase release was not affected by tetrodotoxin, hexamethonium, or atropine. GRP (10(-10) to 10(-6) M) produced dose-dependent increments in [3H]acetylcholine release from pancreatic lobules. GRP stimulates amylase release from rat pancreatic lobules by a neurally mediated mechanism in addition to direct action on acinar membrane receptors.

Acetylcholine↗

Galanin inhibits rat pancreatic amylase release via cholinergic suppression.

The effects of galanin on pancreatic exocrine function were examined using rat pancreatic tissues. In anesthetized rats, galanin (40 micrograms/kg/h) decreased amylase secretion stimulated by 2-deoxy glucose (5.8 +/- 0.1 vs. 3.1 +/- 0.1 times basal) and cholecystokinin octapeptide (21.5 +/- 0.6 vs. 16.8 +/- 0.5), while not inhibiting bethanechol-stimulated secretion. In dispersed acini, there was no effect of galanin alone (10(-8) to 10(-13) M) on amylase release, nor did galanin (10(-6) or 10(-8) M) coincubation affect amylase release stimulated by bethanechol (10(-3) to 10(-7) M) or CCK-8 (10(-8) to 10(-13) M). Using pancreatic lobules, coincubation with galanin (10(-6) M) suppressed 75 mM KCl-stimulated amylase secretion and ACh release (10.1 +/- 0.6% vs. 7.3 +/- 0.4%). Veratridine-stimulated (10(-4) M) amylase secretion and ACh release (12.4 +/- 1.7% vs. 8.5 +/- 0.7%) were similarly diminished.

Acetylcholine↗