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Biomedical subjects

G S Supinski

Publications and source records attributed to G S Supinski.

41 records · Page 3Linked to original sources
PubMed1986

Comparative effects of theophylline and adenosine on respiratory skeletal and smooth muscle.

This study compared the effects of theophylline and adenosine on the contractile activity of respiratory smooth and skeletal muscles in vitro. Studies were performed on isolated strips of tracheal smooth and diaphragmatic skeletal muscle from 22 Hartley strain guinea pigs. The changes in diaphragm and tracheal smooth muscle tension in response to electrical stimulation and histamine-induced contraction, respectively, were assessed over a range of theophylline and adenosine concentrations (10(-7) to 10(-3) M for each). Theophylline increased diaphragmatic tension and reversed histamine-induced smooth muscle contractions in a dose-dependent fashion. Theophylline, however, decreased tracheal tension at concentrations an order of magnitude lower than those that increased diaphragmatic tension. Adenosine mimicked the effect of theophylline on tracheal muscle but had no effect on the force of diaphragm contraction. Moreover, adenosine failed to alter the theophylline dose-response curve for diaphragmatic tension. This study demonstrates that airway smooth muscle is more sensitive than is respiratory skeletal muscle to the effects of theophylline. Furthermore, these data suggest that the effects of theophylline on diaphragm skeletal muscle are not mediated by adenosine receptor blockade.

Adenosine↗
PubMed1984

The effects of caffeine and theophylline on diaphragm contractility.

The present study examined the effect of single, orally administered, doses of caffeine (600 mg) on diaphragmatic muscle contractility in 6 normal subjects and compared the magnitude of the effect with that of theophylline. The force-generating ability of the diaphragm was assessed from measurements of transdiaphragmatic pressure (Pdi) obtained via catheters in the esophagus and stomach, and the level of diaphragmatic excitation was assessed from the diaphragmatic electromyogram recorded with an esophageal electrode. Caffeine increased Pdi at all levels of diaphragmatic electromyographic activity in all 6 subjects. Increases in the ability of the diaphragm to generate pressure were caused by increases in muscle contractility rather than by changes in end-expiratory lung volume or thoracoabdominal configuration. Theophylline administered in a dose equal to that of caffeine increased Pdi in 5 of the 6 subjects. The magnitude of the increase in Pdi was greater with caffeine than with theophylline, however. The greater effect of caffeine than of theophylline on Pdi was not explained by differences in the blood concentrations of the 2 drugs. Neither drug produced consistent changes in blood pressure or heart rate. We conclude that caffeine, which, like theophylline, augments respiratory muscle contractility, may prove useful in the treatment of selected patients with respiratory muscle weakness.

Adult↗
PubMed1982

Effect of elastase-induced emphysema on the force-generating ability of the diaphragm.

The effect of emphysema on the ability of the diaphragm to generate force was examined in costal diaphragm muscle strips from 10 Golden hamsters killed 18 mo after intratracheal injection of pancreatic elastase in a dose producing hyperinflation (mean total lung capacity [TLC] = 163% of control) and generalized panacinar emphysema. 13 saline-injected normal animals served as controls. The time course of isometric tension and the effect of alterations in muscle fiber and sarcomere length on the isometric tension (T) generated in response to tetanizing electrical stimuli (length-tension [L-T] relationship) were examined. Elastase administration caused an increase in diaphragm muscle thickness and reduction in the length of costal diaphragm muscle fibers measured in situ. Emphysema significantly increased the maximum tetanic tension as a result of hypertrophy. Maximal tension corrected for increases in muscle cross-sectional area (T/cm(2)), however, was the same in emphysematous (E) and control (C) animals. Emphysema also shifted the muscle fiber L-T curve of the diaphragm but not of a control muscle, the soleus, toward shorter lengths. In contrast to the effects of E on the diaphragm muscle fiber L-T curve, the sarcomere L-T curve was the same in E and C. Since the length at which tension was maximal correlated closely with sarcomere number (r = 0.94; P < 0.001) reduction in the number of sarcomeres in series in muscles from emphysematous animals appeared to explain the shift in the muscle fiber L-T curve. We conclude that in elastase-induced emphysema adaptive changes both in diaphragm cross-sectional area and sarcomere number augment the force-generating ability of the diaphragm. We speculate that changes in sarcomere number compensate for alterations in muscle fiber length resulting from chronic hyperinflation of the thorax, while diaphragmatic muscle hypertrophy represents a response to changes in respiratory load and/or diaphragm configuration (LaPlace relationship).

Animals↗