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PubMed1978

Effects of graded doses of alcohol upon esophageal motor function.

Twenty-nine normal volunteers were subjected to manometric studies before and after intraesophageal infusion of 100-proof alcohol at doses of 80, 120, 160, and 200 ml, corresponding to 31.6, 47.4, 63.2, and 79.0 g, respectively, administered over a 15-min interval on separate days. Corresponding mean serum concentrations of alcohol were 58.9 +/- 2.8, 77.0 +/- 4.8, 97.0 +/- 13.9, and 117.3 +/- 5.0 mg per dl, respectively. Both esophageal and lower esophageal sphincter function were unaffected at serum concentrations of alcohol less than 70 mg per dl. In contrast, when the serum alcohol concentration was 117 mg per dl, esophageal and lower esophageal sphincter function was altered significantly. The amplitudes of esophageal peristaltic waves were probably decreased in the proximal and distal segments. The maximal lower esophageal sphincter pressure response to pentagastrin was reduced from 35.4 +/- 4.6 to 17.3 +/- 6.1 mm Hg (P less than 0.01). In addition, the lower esophageal sphincter pressure response to a protein meal was inhibited significantly. Neither propagation velocities or esophageal contractions nor resting lower esophageal sphincter pressures were changed by the administration of alcohol at any of the doses tested.

Adult↗
PubMed2000

Functional motor unit failure precedes neuromuscular degeneration in canine motor neuron disease.

Hereditary canine spinal muscular atrophy (HCSMA) features rapidly progressive muscle weakness that affects muscles in an apparent proximal-to-distal gradient. In the medial gastrocnemius (MG) muscle of homozygous HCSMA animals, motor unit tetanic failure is apparent before the appearance of muscle weakness and appears to be presynaptic in origin. We determined whether structural changes in neuromuscular junctions or muscle fibers were apparent at times when tetanic failure is prevalent. We were surprised to observe that, at ages when motor unit tetanic failure is common, the structure of neuromuscular junctions and the appearance of muscle fibers in the MG muscle were indistinguishable from those of symptom-free animals. In contrast, in more proximal muscles, many neuromuscular junctions were disassembled, with some postsynaptic specializations only partially occupied by motor nerve terminals, and muscle fiber atrophy and degeneration were also apparent. These observations suggest that the motor unit tetanic failure observed in the MG muscle in homozygous animals is not due to synaptic degeneration or to pathological processes that affect muscle fibers directly. Together with previous physiological analyses, our results suggest that motor unit failure is due to failure of neuromuscular synaptic transmission that precedes nerve or muscle degeneration.

Animals↗
PubMed2001

Effects of diaspirin cross-linked hemoglobin on motor function of the duodenum and biliary system in the Australian brush-tailed possum in vivo.

Chemically altered hemoglobin-based oxygen carriers have been developed as prototype blood substitutes. Such molecules may affect numerous biological processes, since free hemoglobin scavenges nitric oxide (NO). Diaspirin cross-linked hemoglobin (DCLHb) is a chemically cross-linked molecule, which has a pressor effect on blood pressure, mainly mediated by NO scavenging. However, the effects of DCLHb on the gastrointestinal and biliary motility have not been reported. This study was conducted to investigate the effects of DCLHb on the duodenal and biliary motility and determine if the underlying mechanism involves a NO pathway. Blood pressure, duodenal, sphincter of Oddi and gallbladder motility and trans-sphincteric flow were recorded in anesthetized Australian Brush-tailed possums. The effects of intravenously administered DCLHb (10% solution) or oncotically matched human serum albumin (HSA) solution on these parameters were investigated. To determine the involvement of a NO-mediated pathway in these effects, animals were pretreated with N(omega)-nitro-L-arginine methyl ester (L-NAME) before DCLHb or HSA was given. DCLHb increased blood pressure and duodenal contraction frequency and slowed trans-sphincteric flow compared with the HSA control. The effects of DCLHb on blood pressure and trans-sphincteric flow were immediate and transient, whereas the effect on duodenal contraction frequency was delayed and long-lived. Pretreatment with L-NAME alone increased blood pressure and duodenal contraction frequency and slowed trans-sphincteric flow. DCLHb-induced changes were not evident in the presence of L-NAME. These findings suggest that DCLHb affects duodenal and trans-sphincteric flow predominantly by NO scavenging.

Animals↗