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Plain-film coronary angiography of the cardiac explant on the operating table should be considered when conventional cardiac catheterization is desired but unavailable. We compared the effects of three contrast solutions on cold-preserved, isolated guinea pig hearts. Hearts were excised, perfused for 30 minutes, and arrested with Plegisol solution at 7o C. Twenty minutes after arrest, experimental hearts were perfused with one of three solutions: hyperosmolar Hexabrix solution ( n = 6), hyperosmolar Renografin-76 solution ( n = 6), or diluted, isosmotic Omnipaque solution ( n = 8). The hearts were flushed with cold Plegisol solution 5 minutes later. Control hearts received no contrast during arrest ( n = 9). The hearts were reperfused after 1 hour of arrest, and coronary blood flow (in millimeters per minute), left ventricular developed pressure (in millimeters of mercury), and rate of developed pressure (in millimeters of mercury per second) were measured. Endothelium-dependent smooth muscle relaxation to bradykinin administration and endothelium-independent relaxation to sodium nitroprusside administration were also assessed. No significant difference in myocardial or endothelial function was noted between control hearts and hearts perfused with Omnipaque solution. Hearts perfused with Renografin solution or Hexabrix solution, however, were found to have significantly impaired endothelial and myocardial function. We conclude that an isosmotic contrast solution should be used for ex vivo coronary angiography in cold-preserved hearts to avoid impairment of endothelial and myocardial function. (J Thorac Cardiovasc Surg 1996;112:306-9)

Single-lung transplantation has been abandoned for the treatment of pulmonary hypertension by many centers because of overperfusion of the graft following implantation. Euro-Collins solution is currently used for lung preservation despite the vasoconstrictive effect of this intracellular-type solution. We hypothesized that high-flow reperfusion, alone or in combination with Euro-Collins–induced vasoconstriction, may cause lung dysfunction. Twenty-eight New Zealand White rabbit lungs were harvested and studied in an isolated, blood-perfused model of lung function after 4 hours of cold ischemia. Control lungs were preserved with 50 ml/kg cold saline solution flush and reperfused at either normal flow (60 ml/min) or high flow (120 ml/min). Experimental lungs were preserved with 50 ml/kg cold Euro-Collins solution and reperfused at normal or high flow rates. The arteriovenous oxygen gradient at the end of the 30-minute reperfusion period was significantly lower in the high-flow versus the low-flow experimental group (31.1 ± 4.2 vs 130.6 ± 41.6 mm Hg, p < 0.05). The pulmonary vascular resistance was increased in the high-flow groups and the experimental groups, with a statistically significant difference between low-flow experimental and control groups (64374.4 ± 5722.6 vs 37041.5 ± 2110.9 dynes•sec•cm–5, p < 0.001). The percentage decrease in dynamic airway compliance in the high-flow experimental group was markedly different from that in the high-flow control group (–51% ± 13.3% vs –10.15% ± 3.4%, p < 0.05). Similarly, the wet/dry ratio of the lungs in the high-flow experimental group (13.92 ± 2.32) was significantly greater than that in the low-flow experimental group (6.27 ± 0.19, p < 0.01) and than that in the high-flow control group (5.88 ± 0.23, p < 0.001). These data demonstrate that high-flow reperfusion and preservation with Euro-Collins solution are deleterious to lung function, both individually and in combination, in an ex vivo rabbit lung model. Lung preservation with Euro-Collins solution may not be optimal when high-flow reperfusion is anticipated, as in the setting of unilateral lung transplantation for pulmonary hypertension. (J Thorac Cardiovasc Surg 1996;112:111-6)

Background Staged procedures for extensive aneurysmal disease of the thoracic aorta are associated with a substantial cumulative mortality (>20%) that includes hospital mortality for the 2 procedures and death (often from aortic rupture) in the interval between the 2 procedures. We have used a single-stage technique for operative repair of most or all of the thoracic aorta. Methods Forty-six patients with extensive disease of the thoracic aorta were managed with a single-stage procedure by using a bilateral anterior thoracotomy and transverse sternotomy, hypothermic circulatory arrest, and reperfusion of the aortic arch vessels first to minimize brain ischemia. Thirty-one patients with chronic, expanding type A aortic dissections had previous operations for acute type A dissection (n = 22), aortic valve repair or replacement (n = 4), coronary artery bypass grafting (n = 4), or no previous operation (n = 1). The remaining 15 patients had degenerative aneurysms (n = 12) or chronic type B dissections with proximal extension (n = 3). The ascending aorta and aortic arch were replaced in all patients combined with resection of various lengths of descending aorta (proximal one third [n = 19], proximal two thirds to three quarters [n = 22], or all [n = 5]). Coronary artery bypass grafting, valve replacement, or both were performed concomitantly in 19 patients. Results Hospital mortality was 6.5% (3 patients). Morbidity included reoperation for bleeding (17%), mechanical ventilation for more than 72 hours (42%), temporary tracheostomy (13%), and temporary renal dialysis (9%). No patient sustained a stroke. There have been 5 late deaths (3, 18, 34, 51, and 79 months postoperatively) unrelated to the aortic disease. Four patients have undergone successful reoperation on the aorta (false aneurysm [n = 1], endocarditis [n = 1], and progression of disease [n = 2]). Five-year survival was 75%. Conclusion The single-stage, arch-first technique is a safe and suitable alternative to the 2-stage procedure for repair of extensive thoracic aortic disease.

Background: Reperfusion injury remains a significant problem after lung transplantation and is thought to be in part mediated by neutrophils. Ulinastatin inhibits release of elastase and cathepsin G from neutrophil granules. We hypothesized that inhibition of these neutrophil endopeptidases (proteases) would attenuate pulmonary reperfusion injury. Methods: With an isolated, whole blood–perfused, ventilated rabbit lung model, we studied the effects of ulinastatin. All lungs were flushed with cold Euro-Collins solution, harvested en bloc, stored inflated at 4° C for 18 hours, and reperfused with whole blood. The 18-hour control lungs ( n = 8) were stored and reperfused. Low-dose ( n = 8) and high-dose ( n = 7) groups were treated with total doses of ulinastatin of 25,000 and 50,000 units, respectively, during flush and reperfusion. An additional control group of lungs ( n = 8) was harvested, flushed, and immediately reperfused. Results: The pulmonary artery pressure was significantly lower in the high-dose group than in the 18-hour control group (36.7 ± 1.8 vs 44.8 ± 2.9 mm Hg, p = 0.034). The percentage decrease in dynamic airway compliance was significantly less in the high-dose group than in the 18-hour control group (-13.8% ± 4.4% vs -25.1% ± 3.7%, p = 0.032). Both low-dose and high-dose ulinastatin treatments did not result in a significant improvement in oxygenation with respect to the 18-hour control group (72.2 ± 25.8 vs 32.5 ± 4.9 mm Hg, p = 0.21). Conclusions: Ulinastatin diminishes reperfusion injury after 18 hours of hypothermic pulmonary ischemia, with resultant improvements in pulmonary artery pressure and airway compliance. Improvement in pulmonary function after preservation and reperfusion with a neutrophil endopeptidase inhibitor confirms the role of endopeptidases in reperfusion injury and suggests an intervention to reduce their detrimental effects on early graft function. (J THORAC CARDIOVASC SURG 1996;112:607-13)

The binding of leukocytes to intercellular adhesion molecules expressed on endothelial surfaces during ischemia and subsequent reperfusion initiates leukocyte-mediated reperfusion injury. Interruption of this leukocyte-endothelium interaction may therefore prevent reperfusion injury. In an isolated, ventilated, blood-perfused rabbit lung preparation, we studied the effect of a monoclonal anti–intercellular adhesion molecule antibody on lung function during reperfusion. Lungs were harvested with 50 ml/kg cold Euro-Collins flush and 30 μg prostaglandin E 1 before storage for 18 hours at 4o C. Experimental groups received low-dose (100 μg) or high-dose (200 μg) anti–intercellular adhesion molecule antibody added to the pulmonary flush at harvest and to the initial reperfusate. Eighteen-hour control preparations were preserved for 18 hours and received saline solution vehicle. Immediate control preparations were harvested and immediately reperfused. The oxygen tension in the recirculated pulmonary venous effluent was measured after 30 minutes of reperfusion. Histologic specimens were graded by blinded observers for degree of leukocyte infiltration (0, normal, to 4, severe infiltration). The mean oxygen tensions (±standard error of the mean) were 138.29 ± 6.23, 58.86 ± 9.14, 86.87 ± 11.32, and 139.33 ± 16.15 mm Hg in immediate control preparations, 18-hour control preparations, low-dose antibody group, and high-dose antibody group, respectively ( p = 0.0001). The leukocyte grades (mean ± standard error of the mean) were 1.5 ± 0.723, 3.0 ± 0.955, 1.9 ± 0.899, and 1.2 ± 0.834, respectively ( p = 0.0002). We conclude that anti–intercellular adhesion molecule antibody added to the pulmonary flush and initial reperfusate results in a dose-dependent enhancement of the reperfused lung's ability to oxygenate blood, possibly as a result of decreased leukocyte sequestration. (J THORAC CARDIOVASC SURG 1996;111:941-7)