Pulmonary artery counterpulsation with a skeletal muscle power source. We evaluated the feasibility of using skeletal muscle (SM) to provide pulmonary artery (PA) counterpulsation in an acute pulmonary hypertension (PHT) model. PA counterpulsation was achieved in six dogs with a dual chambered pump powered by the latissimus dorsi muscle. A rate-responsive stimulator was used to make the muscle contract in counterpulsation. Graded PHT was induced by infusing 150 microns glass beads into the PA, while RV and PA pressures were monitored. With PA pressures ranging from 19/10 to 115/62 mmHg, effective counterpulsation was observed. The degree of counterpulsation was influenced by the extent of PHT induced, with the amount of RV tension-time index (TTI) unloading correlated with the level of PA systole (r = 0.92). Therefore, results were divided into two groups (Group 1: PA systole less than or equal to 40 mmHg, and Group 2: PA systole greater than 40 mmHg). In Group 1, RV TTI decreased from 11.29 +/- 0.76 to 9.99 +/- 0.72 mmHg.sec, PA diastole increased from 20 +/- 2.3 to 31 +/- 3.0 mmHg, and PA mean increased from 24 +/- 2.2 to 2.9 +/- 2.2 mmHg (all p less than 0.05). In Group 2, RV TT1 decreased from 15.12 +/- 1.83 to 10.99 +/- 0.90 mmHg.sec, PA diastole increased from 41 +/- 3.5 to 64 +/- 6.2 mmHg, and PA mean increased from 49 +/- 4.8 to 55 +/- 5.7 mmHg (all p less than 0.05). 