Acute muscle damage in latissimus dorsi grafts mobilized for cardiac assist: is vasospasm an important factor?

Abstract

Muscle damage in latissimus dorsi grafts is known to occur following surgical mobilization for cardiomyoplasty. It is believed that ischemia may be a contributory factor. We tested the hypothesis that surgical manipulation of the muscle graft resulted in vasospasm of the intramuscular arteries that compromised muscle viability by examining the effects of vasodilators in the early ischemic period. Rat latissimus dorsi muscles were mobilized from all truncal attachments with preservation of the thoracodorsal neurovascular pedicle. Undisturbed contralateral muscles served as controls. After 24 hours, regional analysis of muscle viability was performed by enzyme macrohistochemistry and histologic assessment. The experimental interventions in four randomized groups (n = 5 each) included: group A, control; group B, topical papaverine (1%); group C, intravenous hydralazine (0.5 mg/kg); and group D, intravenous verapamil (75 microg/kg). All mobilized muscles showed loss of viability, as compared to controls, with damage most apparent in the distal part (mobilized vs control: viable area = 56.76% [51.26-62.26] vs 98.54% [97.87-99.21]; p < 0.001). All three vasodilators failed to prevent muscle necrosis whereas papaverine appeared to aggravate the damage (papaverine vs control: viable area = 53.60% [30.73-76.47] vs 76.60% [75.02-78.18] in the middle region; p < 0.05 and 44.27% [29.53-59.01] vs 56.76% [51.26-62.26] in the distal region; p < 0.05). The rodent model appears to be useful for studying latissimus dorsi muscle injury. The use of vasodilators at the time of surgical mobilization of the latissimus dorsi muscle does not appear to influence the degree of early muscle damage. Topical papaverine may be detrimental to the muscle in this regard.