Study objectives/design: Impaired function of striated and arterial smooth muscle is known to occur in humans and animals with various forms of cardiac diseases, but limited information is available on the mechanical behavior of airway smooth muscle. We tested the hypothesis that the baseline mechanical properties of tracheal smooth muscle (TSM) were impaired at an early stage of cardiac overload.
Animals: We used a model of cardiac hypertrophy induced by surgical abdominal aortic stenosis (AS) in adult rabbits. Twelve animals with AS and 8 sham-operated control rabbits were studied 12 weeks after surgery. In rabbits with AS, the heart weight/body weight ratio was higher than in control rabbits (2.36 ± 0.43 g/kg vs 1.98 ± 0.20 g/kg, p < 0.05) [mean ± SD], attesting to moderate cardiac hypertrophy. No clinical signs of congestive heart failure were observed.
Measurements: Isolated TSM strips were electrically stimulated at 37°C, 2.5 mM [Ca2+]0, against 8 to 10 load levels, from zero load to full isometry. Force-velocity relationship was elicited using the conventional afterloaded isotonic method.
Results: Peak isometric tension was lower in rabbits with AS than in control rabbits (25 ± 11 mN/mm2 vs 34 ± 14 mN/mm2, p < 0.05), whereas maximum unloaded shortening velocity, maximum extent of muscle shortening, and relaxation parameters did not differ between groups. The curvature of the force-velocity relationship (which reflects the myothermal economy of force generation) and peak mechanical efficiency were lower in rabbits with AS than in control rabbits.
Conclusions: These results indicate that the contraction of isolated rabbit TSM was less powerful and less economical in cardiac hypertrophy, attesting to early impairment of the mechanical properties of TSM during cardiac overload.