Suture-line reinforcement with glutaraldehyde-preserved bovine pericardium for nonanatomic resection of lung tissue.

In this study we assessed the usefulness of glutaraldehyde-preserved bovine pericardium (GPBP), preparated in our laboratory, in nonanatomic resection of lung tissue in dogs. A 30% resection of the right cranial lobe of the lung was performed in 18 mongrel dogs. The suture line was reinforced with GPBP strips. For group I (n = 6), the GPBP strips were fixed on the lung with nonabsorbable suture by thoracotomy. In Group II (n = 6), the resection and fixation of the GPBP strips were performed with an endoscopic linear stapler by thoracotomy. In Group III (n = 6), the resection and fixation of the GPBP strips were performed with a linear stapler by thoracoscopy. The animals were evaluated each day during the first week after surgery and every other day during the study time. At the end of the study all animals were euthanized with an overdose of pentobarbital. Macroscopic and microscopic examinations of the bioprosthesis and lung were evaluated. All animals survived the surgical procedure and study time (8 weeks). In the three groups, macroscopic examination of the bioprosthesis showed good adaptation to the lung tissue. Microscopically, all groups of animals presented good healing, with the presence of fibrotic tissue layer on the GPBP and its periphery as well as in the lung. However, in group I we observed the presence of giant cells in the suture line. GPBP proved to be a useful material for reinforcement of the nonanatomic resection suture line of lung tissue in dogs.

Effect of prostaglandin E2 on the tracheobronchial distribution of lung preservation perfusate.

Complete lung preservation requires the perfusate to reach the cell it intends to protect; this is directly related to the distribution of the preserving solution throughout the lung vasculature. Several prostanoids are clinically used to enhance lung preservation. We evaluated the effect of prostaglandin E2 (PGE2) on the distribution of lung perfusate throughout tracheobronchial tissue. Fourteen pulmonary blocks were procured from an equal number of dogs and divided according to whether or not they had previously received a PGE2 infusion. All lung blocks were perfused with a glucose-insulin-potassium solution, and distribution within the lung parenchyma and tracheobronchial tissue was measured using the flow reference technique and gadolinium-153-labeled microspheres. Once perfusion had taken place, samples of lung parenchyma, tracheobronchial tissue, and flow reference were measured for radioactivity, and flow was calculated per 100 g tissue. Animals receiving PGE2 had an expected 38% decrease in systemic arterial pressure; the duration of infusion of lung perfusate during procurement was shorter in those animals receiving PGE2 (5.75 +/- 0.3 min, vs. no PGE2 8.9 +/- 1.2 min; p < .05). Perfusate flow of bronchial mucosa and cartilage increased by two to three times with the infusion of PGE2 (p < .01). Perfusate flow to lobar bronchus or lung parenchyma was similar in both groups. Flow within the lung parenchyma did not differ statistically when compared to its lobar distribution. In conclusion, PGE2-treated animals had a two- to threefold increase in perfusate flow to mainstem bronchi (including mucosa); these findings to some extent support the rationale for utilizing prostanoids in order to enhance lung preservation in clinical lung transplantation.

Plasma thromboxane B2 concentrations and pulmonary vascular resistance during lung reperfusion.

The purpose of this study was to measure the behavior of plasmatic thromboxane B2 (pITxB2) after reperfusion of a glucose-insulin-potassium preserved lung. Seven adult mongrel dogs underwent a left lung allotransplantation. Hemodynamic changes including pulmonary artery pressure and cardiac output were measured. Pulmonary artery vascular resistance, systemic resistance, arterio-venous oxygen difference, and shunt were calculated. Immunoreactive arterial and venous plasma thromboxane B2 concentrations were measured at 0 (basal), 60, 120, and 180 min after reperfusion. Hemodynamic measurements were made after 5 min of occlusion of the right pulmonary artery and ventilation with 100% oxygen. Prepreservation, pre-reperfusion, and posttransplant lung weights were obtained. All animals survived the procedure. Ischemic time was 14.72 (+/-0.31) h. Cardiac output, systemic arterial pressure, and arterio-venous oxygen difference decreased while systemic vascular resistance, pulmonary vascular resistance, and shunt increased during the study. Mean pulmonary artery pressure correlated with pulmonary vascular resistance (p < .01). Oxygen tension diminished significantly at 180 min after reperfusion. Mean basal pulmonary arterial TxB2 was 3589 (+/-424) pg/ml; mean plasma pulmonary venous TxB2 was 6578 (+/-1571) pg/ml. Pulmonary arterial to venous TxB2 ratio (a/vTxB2) increased from 0.70 at basal measurement to 0.83 at 60 min, and 0.99 at 120 and 180 min after reperfusion (p < .05). Pulmonary arterial TxB2 had a positive correlation with mean pulmonary artery pressure (p < .05); also, a/v pITxB2 correlated with pulmonary vascular resistance (r = .616, p < .01). Mean post-reperfusion lung weight increase was 74.88% (45.37 g). In conclusion, pITxB2 a/v ratio ratio increases after reperfusion of a 14-h preserved lung; pulmonary vascular resistance significantly increases after 180 min of reperfusion and correlates with the increase in pITxB2 a/v ratio.