Acute electrical stimulation increases extramyocardial collateral blood flow after a cardiomyoplasty.

We hypothesized that acute electrical stimulation of a latissimus dorsi cardiomyoplasty would augment the collateral blood flow delivered by the skeletal muscle to the heart. This hypothesis was tested in an animal model (13 goats) of coronary artery disease. Six weeks after a cardiomyoplasty was performed, myocardial collateral blood flow derived from the latissimus dorsi muscle was measured with colored microspheres when the muscle was at rest and during electrical stimulation of the thoracodorsal nerve at 1.25 Hz. The area at risk for ischemia averaged 13.37 +/- 2.08 g (mean +/- standard error), or 18.4% of left ventricular mass (n = 13). At rest, significant skeletal muscle-derived collaterals developed in 9 animals, and formed predominantly to chronic ischemic myocardium (mean +/- standard error, 0.07 +/- 0.02 mL.g-1 x min-1; n = 9), rather than infarct (0.03 +/- 0.02 mL.g-1 x min-1; n = 5), or normal myocardium (0.0005 +/- 0.0001 mL.g-1 x min-1; n = 9). Stimulation increased skeletal muscle-derived collateral blood flow to chronic ischemic areas to 0.38 +/- 0.09 mL.g-1 x min-1 (n = 9) (p < 0.05). During stimulation, the collateral flow was greater in the epicardium (0.46 +/- 0.11 mL.g-1 x min-1) than in endocardium (0.14 +/- 0.09 mL.g-1.min-1) (p < 0.05). This study demonstrates that electrical stimulation of a latissimus dorsi cardiomyoplasty increases extramyocardial collateral blood flow to chronic ischemic myocardium.

Chronic stimulation enhances extramyocardial collateral blood flow after a cardiomyoplasty.

We have previously demonstrated that collateral blood flow can be established between skeletal muscle and myocardium in animals that have undergone a latissimus dorsi cardiomyoplasty. We have also shown that 5 minutes after the thoracodorsal nerve is electrically stimulated at 1.25 Hz, there is a sixfold increase in the collateral blood flow between the latissimus dorsi and the heart. In this experiment, we hypothesized that chronic stimulation of a latissimus dorsi cardiomyoplasty would result in a sustained increase in the latissimus-derived collateral blood flow. In 24 adult male goats, an ameroid constrictor was placed around a branch of the circumflex coronary artery, and a latissimus dorsi cardiomyoplasty was performed. After a rest period of about 1 week, the latissimus dorsi cardiomyoplasties were stimulated continuously at a 2-Hz frequency for 6 weeks. Collateral blood flow between the muscle and the heart was then measured with colored microspheres. Sixteen animals survived to the final experiment, and collaterals developed in 10. In these 10 animals, the latissimus collaterals continuously delivered 0.17 +/- 0.03 mL.g-1 x min-1 (mean +/- the standard error) of blood to ischemic myocardium. This flow represents 24.0% +/- 3.9% of the flow measured to normal myocardium. These results demonstrate that in an animal model of coronary artery disease, chronic electrical stimulation of a latissimus dorsi cardiomyoplasty maintains an elevated level of latissimus-derived collateral blood flow to the myocardium.

Collateral blood flow from skeletal muscle to normal myocardium.

Collateral blood vessels from skeletal muscle to myocardium might supplement intramyocardial collaterals during periods of acute myocardial ischemia. This study was conducted to verify the existence of such collaterals and to measure their contribution to collateral flow. In 12 male goats, the innate coronary collateral system to a moderate size myocardial risk area was defined with colored microspheres, and a latissimus dorsi pedicle flap was then apposed to the heart. After 3 weeks, skeletal muscle to myocardial collaterals were characterized by (a) creation of vascular casts (three animals); (b) estimation of skeletal muscle to myocardial collateral blood flow (three animals); and, (c) measurement of total collateral blood flow to the risk area (innate plus skeletal muscle to myocardial collateral flow). Under a dissecting microscope the vascular casts revealed direct communications from the skeletal muscle which penetrated deeply into the myocardium. With the coronary artery to the risk area open, the estimated myocardial collateral blood flow derived from the muscle flap was 0.01, 0.02, and 0.04 ml/min. With the coronary artery to the risk area closed, there was no significant increase in total coronary collateral blood flow. Although the quantity of blood flow delivered by skeletal muscle collaterals was small, this study demonstrates that clearly identified collateral blood vessels form between skeletal muscle and myocardium in a cardiomyoplasty model. This raises the possibility that, under conditions more favorable to their development, extramyocardial collaterals from skeletal muscle might be exploited to augment the intramyocardial collateral system.

After a cardiomyoplasty, collaterals from skeletal muscle form to chronic ischemic myocardium.

We measured the collateral formation between skeletal muscle and the heart after a latissimus dorsi cardiomyoplasty in an animal model that contained normal, chronic ischemic, and infarcted myocardium. The area at risk for ischemia was 27.0 +/- 3.2% of the left ventricular mass (n = 10, mean +/- SE). In five animals the risk area developed predominantly into chronic ischemic myocardium; in five others the risk area became an infarct. The collateral blood flow from the skeletal muscle to chronic ischemic myocardium (6.05 +/- 1.36 ml/100 g/min, n = 5) was higher than flow to the infarct (0.46 +/- 0.31 ml/100 g/min, n = 5). The collateral blood flow to normal myocardium was minimal (0.04 +/- 0.01 ml/100 g/min). The collateral blood flow appeared to be concentrated in the outer half of the left ventricular wall, with the epicardium having a higher skeletal muscle derived collateral blood flow than endocardium (p < 0.05). We conclude that after a cardiomyoplasty a collateral blood flow, which approaches clinical significance, is preferentially established between skeletal muscle and chronic ischemic myocardium. Enhancement of this collateral blood flow might provide a means to revascularize patients with presently inoperable coronary disease.

The coronary collateral circulation in normal goats.

This study was undertaken to evaluate the coronary collateral circulation of the goat. Year old, castrated male goats were anesthetized with sodium pentobarbital. A branch of the left circumflex coronary artery was dissected and a snare placed around it. Regional myocardial blood flow was measured by injecting colored microspheres into the left atrium before and during 3 hr of occlusion of this coronary artery. The Area At Risk for infarction, as defined by a left atrial injection of Brilliant Green dye, was divided into a central Ischemic zone and a peripheral Ischemic Border zone. The degree of overlap in the blood flow distributions between the risk and the nonrisk areas was quantitatively assessed by injecting microspheres directly into the artery to the Area At Risk. Baseline blood flow to the normally perfused goat myocardium was 1.13 +/- 0.18 ml/min/g (mean +/- SE). Following occlusion, the flow to the Ischemic zone was 0.07 +/- 0.03 ml/min/g and to the Ischemic Border zone was 0.31 +/- 0.18 ml/min/g. Flow to either zone did not increase during the 3-hr observation period. Overlap at the perimeter of the risk and nonrisk areas was approximately 22%. We conclude that flow to the Ischemic zone is low because the goat has few native collateral blood vessels, and that flow to the Ischemic Border zone is significantly affected by overlap with normal myocardium.

Vertical deceleration trauma. Principles of management.

A highly complex interaction of several physical and biomechanical factors determines the patterns of injury and probability of survival in free falls. Falls from extreme heights result in massive visceral and vascular injuries, which are usually lethal. Urban falls tend to result in severe lower extremity, spinal, and pelvic fractures. Retroperitoneal hemorrhage is a significant cause of death and is best managed by emergency angiography and embolization. Early fixation of fractures reduces morbidity.

Some effects of Bunnell suture on otherwise uninjured tendons in subhuman primates.

An experimental study was performed in rhesus monkeys (M. mulatta) to examine the contribution of Bunnell tendon suture to the production of postoperative tendon adhesions. It was found that Bunnell suture used with atraumatic technique caused a significant depression of in vitro tendon surface plasminogen activator activity, allowing the in vivo persistence and fibrous organization of fibrinous postoperative adhesions to sutured areas. Bunnell suture also produced coagulation necrosis of the sutured area of tendon. Collagen, which replaced the destroyed areas, was oriented randomly and frequently was continuous with surface tendon adhesions to surrounding connective tissues. Bunnell suture appears to be a cause of tendon adhesions in subhuman primates. The importance of fibrin and depressed local fibrinolysis in the relationship of tendon ischemia and adhesion formation is discussed.

A physiologic basis for the adhesion-free healing of deperitonealized surfaces.

PIP: Male albino rats were used in this experimental study designed to determine the physiological basis for the formation of peritoneal adhesions postoperatively, and hence to discover a physiological basis for adhesion-free healing after abdominal surgery. Recent evidence had shown that failure of the peritoneal fibrinolytic system may be the important etiological factor in postoperative adhesion formation; hence, the working hypothesis was that adhesion formation could be explained by alterations of intrinsic peritoneal fibrinolytic mechanisms. All rats underwent repeated biopsy to obtain control determinations of plasminogen activator activity (PAA), and then 70 animals had 2 by 2 cm areas of parietal peritonium resected to a thin layer of adherent underlying muscle on the abdominal wall on both sides of the original midline incision. On 1 side, the perioneal patch was immediately sutured back in place as an avascular, free graft. On the other, the raw peritoneal defect was left unrepaired. In 40 of these 70 rats, polyethylene patches were used to cover the peritoneal graft and defect. Animals were sacrificed in groups of 10 at various intervals postoperation to determine PAA and adhesion formation. 24 hours postoperatively, mean graft PAA had decreased to one-sixth the control value (P .001). Similar wide discrepancies were seen through 96 hours postoperation (all statistically significant at P .001). PAA was unchanged in controls. 96 hours postoperation, adhesions to the parietal defects had completely disappeared in 8 of 10 animals, yet all of the grafts remained covered by dense adhesions. By 2 weeks, all deperitonealized wounds showed complete absence of adhesions, compared with dense adhesions on the graft wound.^ieng