Tissue response to biomaterials used for staple-line reinforcement in lung resection: a comparison between expanded polytetrafluoroethylene and bovine pericardium.

OBJECTIVE: A study in a canine model of lung-reduction surgery evaluated the tissue response to polytetrafluoroethylene (ePTFE) and bovine pericardium (BP) used for staple-line reinforcement. METHODS: In each of ten dogs, BP was placed in one lung and ePTFE in the other. The implants were retrieved at 30, 95, or 167 days after implantation and studied histologically. The connective tissue covering the implants was measured and analysis of variance was used to compare results with the two materials. RESULTS: At 30 days, the BP specimens showed focal chronic inflammation and thin tissue coverage, whereas the ePTFE specimens had no focal inflammation and thick tissue coverage. At 95 and 167 days, the inflammation in the BP specimens had resolved, but tissue coverage remained minimal, and there was no resorption of the BP. In the ePTFE specimens, tissue coverage had increased. Analysis of variance comparing representative tissue specimens showed that the tissue encapsulating the ePTFE was significantly thicker than that surrounding the BP (P < 0.0001). No air leaks, staple-line disruptions, or infections occurred in the study. CONCLUSIONS: Neither ePTFE nor BP is resorbable. Both materials have been used successfully, without resultant infections, for clinical staple-line reinforcement. The more favorable tissue response to ePTFE observed in this study may have clinical ramifications. Comparative clinical studies of the two materials are needed.

Fistula formation after implanting an ePTFE membrane. A case report.

BACKGROUND: Expanded polytetrafluoroethylene (ePTFE) membranes have been used successfully as permanent implants to prevent adhesions after gynecologic surgery. Fistulization involving such an implant has not been reported previously. CASE: A 27-year-old woman had micturition problems and pain four years after a myomectomy and implantation of an ePTFE membrane. Laparotomy revealed that the membrane was partly inserted into a hole in the anterior bladder wall, close to the vesicouterine pouch. The membrane was removed and the fistula repaired. Pathologic studies of the specimen showed multispecies bacterial contamination. CONCLUSION: The fistula may have originated with ischemia at the vesicouterine fold caused by the suture in the corner of the ePTFE membrane. This led to intussusception of the prosthesis. The hole that was created expanded, and pelvic inflammatory disease probably produced the local sepsis. In patients with posterior or fundal uterine incisions for myomectomy, the ePTFE membrane is a useful permanent adhesion barrier in an area at substantial risk of adhesion formation. In cases using anterior incisions, however, in which the membrane may be fixed close to the vesicouterine fold, surgeons should consider removing the prosthesis after peritoneal healing has occurred.

Perioperative myocardial ischemia. Its relation to anatomic pattern of coronary artery stenosis.

BACKGROUND: Recently, the frequency of intraoperative myocardial ischemic episodes in patients with steal-prone coronary anatomy, compared with other groups of patients undergoing coronary artery surgery (CABG), has been characterized. Because the relationship between anatomic distribution of coronary stenosis and myocardial ischemic episodes over the entire perioperative period has not been well defined, the authors sought to examine this relationship in 100 adult patients undergoing CABG surgery. METHODS: Continuous electrocardiographic (ECG) monitoring was performed in the pre-, intra-, and postoperative periods, quantifying the frequency (episodes/hour of monitoring [epis/h]) and duration (minutes/hour of monitoring [min/h]) of ECG ischemic episodes defined as a reversible ST segment shift > or = 1 mm at J + 60 ms of > or = 1 min duration. Based on preoperative coronary angiography, patients were categorized into the following groups: group 1 (n = 40), steal-prone coronary anatomy (occluded major coronary artery and > or = 50% stenosis of left main coronary artery or > or = 70% proximal stenosis 2 (n = 17), left main or equivalent coronary stenosis (> or = 50% stenosis of left main coronary artery or > or = 70% proximal stenosis of the left anterior descending and circumflex coronary arteries); and group 3 (n = 43), coronary artery stenosis > or = 70% not fitting the preceding categories. RESULTS: Compared with group 3, patients in group 1 had more frequent and longer ECG ischemic events preoperatively, and were nearly two times more likely (relative risk 1.82, 95% confidence interval 1.07-3.10) to develop an ischemic event during this period. There were no differences in the relative risk, frequency, or duration of an ischemic episode between groups 1 and 3 during the intraoperative and postoperative periods, or between groups 1 and 2 or groups 2 and 3 during any perioperative period. In group 2 patients, the frequency of ischemic epis/h was less intra- compared with preoperatively, while, in group 3, the ischemic epis/h decreased postoperatively compared with the intraoperative period. The duration of ischemic episodes (min/h) in group 3, however, increased postoperatively compared with the pre- and intraoperative periods, while, in group 2, the duration of ischemic episodes (min/h) was less intraoperatively compared with the preoperative period. Ninety-seven percent of preoperative ECG ischemic episodes occurred without symptoms. Postoperative myocardial infarction occurred in three patients in group 3, two in group 2, and one in group 1. There were no perioperative deaths. CONCLUSION: These data indicate that, compared with patients with non-left main or equivalent coronary stenosis, those with steal-prone coronary anatomy have more frequent and longer ECG ischemic episodes preoperatively. The data also indicate that there are no other differences in the risk, frequency, or duration of ischemic episodes between groups perioperatively. Thus, different distributions of coronary artery stenosis may be associated with changes in the perioperative characteristics of ECG ischemic episodes.

Herpes simplex virus inhibits endothelial cell attachment and migration to extracellular matrix proteins.

Herpes simplex virus (HSV) infection may be involved in various endothelial-injury syndromes, including vasculitis and atherosclerosis. In a previous study, it was reported that HSV-infected human umbilical endothelial cells are more vulnerable to detachment mediated by granulocyte-secreted proteases. To elucidate the molecular basis of this observation, the authors examined the interaction of infected endothelial cells with the purified basement membrane proteins, fibronectin, laminin, and type IV collagen. HSV-infected endothelial cells exhibited defects in their ability to adhere, spread, and migrate on all three matrix components. This defective adhesion could be partially overcome by increasing concentrations of fibronectin; in contrast, no abrogation of deficient binding occurs with increased levels of laminin or collagen type IV. This suggests that endothelial cells may use different surface constituents for binding to the three proteins and use multiple "receptors" for adhesion to the fibronectin molecule--"receptors" that are variably affected by HSV infection. The authors investigated this supposition by assaying adhesion of normal and infected endothelial cells to two non-overlapping cell-adhesion promoting fragments of fibronectin: 1) a 75 kd motility-promoting fragment which contains the arginyl-glycyl-aspartylserine (RGDS) adhesion sequence, and 2) a 33 kd carboxyl-terminal heparin binding fragment, which promotes cell adhesion by an RGDS-independent mechanism. Normal endothelial cells adhered and spread on both purified fragments. In contrast, while infected endothelial cells could adhere, albeit rather poorly, to high coating concentrations of the 75 kd fragment, these cells did not bind to the 33 kd heparin binding fragment of fibronectin at all. These results support the concept that endothelial cells adhere to multiple domains of fibronectin, and that HSV infection preferentially abrogates binding to the heparin-binding domain, while leaving relatively intact receptors for the RGDS-containing domain. In support, soluble RGDS significantly blocked fibronectin adhesion of infected, but not control, endothelial cells. It is concluded that HSV infection inhibits the interaction of endothelial cells with basement membrane proteins and weakens their tethering to substratum. This tethering is inadequate for proper cell spreading or movement to occur and may result in both excessive endothelial lift-off and impaired vascular repair in HSV infections.

Differential effects of laminin, intact type IV collagen, and specific domains of type IV collagen on endothelial cell adhesion and migration.

Laminin and type IV collagen were compared for the ability to promote aortic endothelial cell adhesion and directed migration in vitro. Substratum-adsorbed IV promoted aortic endothelial cell adhesion in a concentration dependent fashion attaining a maximum level 141-fold greater than controls within 30 min. Aortic endothelial cell adhesion to type IV collagen was not inhibited by high levels (10(-3) M) of arginyl-glycyl-aspartyl-serine. In contrast, adhesion of aortic endothelial cells on laminin was slower, attaining only 53% of the adhesion observed on type IV collagen by 90 min. Type IV collagen when added to the lower well of a Boyden chamber stimulated the directional migration of aortic endothelial cells in a concentration dependent manner with a maximal response 6.9-fold over control levels, whereas aortic endothelial cells did not migrate in response to laminin at any concentration (.01-2.0 X 10(-7) M). Triple helix-rich fragments of type IV collagen were nearly as active as intact type IV collagen in stimulating both adhesion and migration whereas the carboxy terminal globular domain was less active at promoting adhesion (36% of the adhesion promoted by intact type IV collagen) or migration. Importantly, aortic endothelial cells also migrate to substratum adsorbed gradients of type IV collagen suggesting that the mechanism of migration is haptotactic in nature. These results demonstrate that the aortic endothelial cell adhesion and migration is preferentially promoted by type IV collagen compared with laminin, and has a complex molecular basis which may be important in angiogenesis and large vessel repair.

beta-Adrenergic regulation of adenosine 3',5'-monophosphate concentration in brain microvessels.

Norepinephrine increases the concentration of adenosine 3',5'-monophosphate (cyclic AMP) in an incubated suspension of brain microvessels. This response can be matched by other drugs that stimulate the beta receptors, but the alpha-adrenergic agonist phenylephrine is without effect; beta-adrenergic blockade abolishes the response while alpha-adrenergic blockade produces no change. The data support the contention that cerebral capillary function is subject to adrenergic neural control.