BITA grafting can be safely offered to obese patients with significant long-term advantages without substantial additional risk of operative complications including deep sternal wound infection.

INTRODUCTION There is accumulating evidence that extracellular adenosine triphosphate (eATP) promotes many of the underlying mechanisms that exacerbate acute lung injury. However, much of this data is from inbred rodent models indicating the need for further investigation in higher vertebrates to better establish clinical relevance. To this end we evaluated a human recombinant apyrase therapy in a canine warm pulmonary ischemia-reperfusion injury (IRI) model and measured eATP levels in human lung recipients with or without primary lung allograft dysfunction (PGD). METHODS Warm ischemia was induced for 90 minutes in the left lung of 14 mongrel dogs. Seven minutes after reperfusion, the apyrase APT102 (1 mg/kg, N=7) or saline vehicle (N=7) was injected into the pulmonary artery. Arterial blood gases were obtained every 30 minutes up to 180 minutes after reperfusion. Bronchioalveolar lavage fluid (BALF) was analyzed for eATP concentration, cellularity and inflammatory mediator accumulation. Thirty bilateral human lung transplant recipients were graded for immediate early PGD and assessed for BALF eATP levels. RESULTS APT102-treated dogs had progressively better lung function and less pulmonary edema over the 3-hour reperfusion period when compared to vehicle-treated controls. Protection from IRI was observed with lower BALF eATP levels, fewer airway leukocytes and blunted inflammatory mediator expression. Additionally, human lung recipients with moderate to severe PGD had significantly higher eATP levels when compared to recipients without this injury. CONCLUSIONS Extracellular ATP accumulates in acutely injured canine and human lungs. Strategies that target eATP reduction may help protect lung recipients from IRI.

Objectives This study aimed at identifying the ideal right-to-left shunt-fraction to improve cardiac output (CO) and systemic perfusion in pulmonary arterial hypertension (PHT). Background Atrial septostomy has been a high-risk therapeutical option for symptomatic drug-refractory patients with PHT. Results have been unpredictable due to limited knowledge of the optimal shunt-quantity. Methods In 9 dogs, an 8-mm shunt-prosthesis was inserted between the superior vena cava (SVC) and the left atrium. With pulmonary artery banding, mean (±SEM) systolic right ventricular pressure increased from 37±1 mmHg at baseline to 44±1 mmHg (moderate PHT, P=0.005) and 50±2 mmHg (severe PHT, P<0.001). Shunt-flow was adjusted by total (forcing all flow through the shunt) or partial occlusion of the SVC and partial or total clamping of the shunt. Caval-, shunt- and aortic-flow were measured by ultrasonic flow-probes. Blood gases were drawn from the aortic root and pulmonary artery. Results At severe PHT, a shunt-flow of 11±1% of CO (253±90 mL/min) increased CO significantly by 25% (1.8±0.1 to 2.4±0.2 L/min, P=0.005) causing an increase of systemic oxygen delivery index (DO2I) by 23% (309±23 to 399±32 mL/min/M2, P=0.035). Arterial O2-saturation did not change significantly until a shunt-flow of 18±2% was exceeded, causing a drop from 96±1% to 84±4% (P=0.013). At moderate PHT, CO or DO2I did not improve significantly at any shunt-flow. Conclusions In severe PHT, a shunt-flow of 11% of CO represented the ideal shunt-fraction. Augmentation of CO compensated for declined O2-saturation due to right-to-left shunting and improved DO2I. In moderate PHT, atrial septostomy is less promising.

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