Three methods for prevention of perioperative spasm of the internal mammary artery were compared in 78 patients undergoing coronary artery bypass grafting. In group 1, internal mammary artery pedicles were divided distally, clamped, and placed under the upper sternum submerged in papaverine solution (1.5 mg/ml). In group 2, as in group 1 but before clamping, 2 ml of heparinized blood with 1.5 mg/ml papaverine added was injected into the vessel lumen. In group 3 treatment was as in group 2, but heparinized blood with papaverine was injected a second time just before extracorporeal bypass was begun. In a univariate analysis free flow from dilated internal mammary arteries was not significantly different among the groups (group 1, 58 ml/min; group 2, 82 ml/min; group 3, 68 ml/min; p < 0.1). When free flow from dilated internal mammary arteries was the dependent variable in a regression analysis, the use of intraluminal papaverine, high blood pressure during flow measurement, and high initial blood flow were predictors of high flow (all p < 0.01). Morphometric measurements on the resected distal portion of the dilated internal mammary arteries disclosed less folding of the internal elastic lamina and a larger luminal area in groups 2 and 3 compared with respective findings in group 1 (1.21 mm2 and 1.42 mm2 versus 0.77 mm2; p < 0.02). Mechanical vessel wall injury occurred in 8 of 52 internal mammary arteries treated with intraluminal papaverine. Intraluminal papaverine solution injected once or twice in addition to external papaverine exposure therefore provides a better blood flow rate and distal dilation than mere submersion in papaverine solution, but at a considerable risk of mechanical wall injury.
Valve thrombosis and its prevention was studied in 33 Labrador retriever dogs who received Hall-Haster mitral disc valves during extracorporeal circulation with extreme hemodilution. Three antithrombotic regimes were used. (1) 12 dogs received 1 g heparin preoperatively, and Warfarin tablets from the first postoperative day. Anticoagulation was controlled with thrombotest (TT), aiming at 20–25% of normal coagulation activity. (2) 9 dogs received 10 mg of heparin intravenously hourly for 10 h, and intravenous injections of Warfarin daily, aiming at TT values of 15–20%. (3) The last 12 dogs had continuous heparin infusion for 24 h, and Warfarin injections before as well as after the operation in doses sufficient to reduce the TT to 10–15% of normal. Stable anticoagulation was very difficult to maintain. Only 15 dogs survived the first postoperative day, 7 were alive after 4 weeks. 7 early and 5 late deaths were due to valve thrombosis. All three antithrombotic regimes were equally ineffective in preventing thrombosis, and more intensive antithrombotic prophylaxis is needed to make the canine model suitable for experimental open-heart surgery.
Functional beta-adrenoceptor populations in the human heart were studied in vitro in electrically-paced strips of the right auricular and ventricular myocardium. The relative potency of selected agonists in producing inotropic responses (Tmax, T'max) in the presence of blockers for neuronal and extraneuronal uptakes was found to be as follows: isoprenaline greater than noradrenaline = adrenaline = salbutamol greater than dobutamine. Prenalterol had a negative inotropic effect in these preparations. The selective beta 1-(practolol) and beta 2-(H 35/25) blockers reduced inotropic responses to adrenaline (Tmax, T'max) and noradrenaline (T'max) in the auricular strips. These results indicate the participation of beta 2-adrenoceptors in inotropic responses in the human auricular and ventricular myocardium. For comparison, inotropic responses of electrically-paced rat myocardium to beta-adrenergic agonists in the presence of blockers for neuronal and extraneuronal uptakes were likewise studied. The relative potencies for Tmax were: noradrenaline = adrenaline greater than prenalterol greater than dobutamine = salbutamol. Given the high relative potency of salbutamol in the human myocardial strips (analogous to that previous shown in the beta 2-dominated atria of the frog and trout) and the low relative potency of salbutamol in the rat tissue, these findings indicate a greater population of functionally active beta 2-adrenoceptors in the human than in the rat myocardium.
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