Fibrin glue coating of e-PTFE prostheses enhances seeding of human endothelial cells.

A laboratory study was undertaken to improve the initial count of endothelial cells (EC) adhering to the wall of e-PTFE prostheses when seeding of human EC is attempted. In our experiments pretreatment of the prosthetic wall with commercially available fibrin glue (Tissucol) improved the reliability of the seeding procedure. The number and the distribution of EC seeded onto fibrin glue presealed e-PTFE prostheses was compared to the number and distribution of EC adhering to blood preclotted grafts 24 hours following the initial seeding procedure. Fibrin glue presealed grafts showed a higher number of initially adhering EC and a more equal distribution over the graft surface when compared to blood pretreated grafts. Our results suggest that the use of fibrin glue enhances the seeding of human EC on e-PTFE grafts.

Effect of experimental cardiopulmonary bypass on systemic and transcardiac thromboxane B2 levels.

Systemic and cardiac metabolism of thromboxane was studied in a canine model (n = 13) of standard cardiopulmonary bypass and surgical cardioplegia. Sterile techniques were applied and no donor blood was used. Systemic samples (thoracic aorta) and transcardiac gradients (coronary sinus - aortic root) were obtained (1) 5 minutes after cannulation, (2) 20 minutes after the onset of partial bypass, (3) 5 seconds after the first administration of cardioplegic solution (CP-1), and (4) 5 seconds after the second administration of cardioplegic solution (CP-2). Cardioplegic doses were administered 30 minutes apart and consisted of 500 ml of hypothermic (8 degrees C), hyperkalemic (25 mEq potassium chloride) solution infused into the aortic root at 60 to 70 mm Hg. Thromboxane B2 was determined by a double-antibody radioimmunoassay (picograms per milliliter +/- standard error of the mean). Onset of partial bypass was followed by a significant rise in systemic arterial thromboxane B2 levels: after cannulation, 115 +/- 21 pg/ml; after the onset of partial bypass, 596 +/- 141 pg/ml; p less than 0.01). Significant transcardiac thromboxane B2 gradients were found during the first and second cardioplegic washouts (CP-1: aortic root 73 +/- 12 pg/ml, coronary sinus 306 +/- 86 pg/ml, p less than 0.01; CP-2: aortic root 65 +/- 11 pg/ml, coronary sinus 355 +/- 98 pg/ml, p less than 0.01). Transcardiac gradients of 6-keto-prostaglandin F1 alpha and thromboxane B2 were obtained at CP-1 and CP-2. Gradients of 6-keto-prostaglandin F1 alpha were not different from thromboxane B2 gradients during CP-1 but were significantly higher than thromboxane B2 gradients during CP-2. In a subgroup of five dogs, transcardiac thromboxane B2, lactate, and platelet gradients were measured simultaneously. Cardiac thromboxane B2 generation was found only in the presence of cardiac lactate production. Transcardiac platelet gradients were significantly higher at CP-1 (13,900 +/- 3,000/mm3) than at CP-2 (4,000 +/- 1,230/mm3) (p less than 0.05), whereas thromboxane B2 gradients were similar at CP-1 and CP-2. Our study demonstrates that thromboxane B2 is released into the coronary circulation during surgical cardioplegic arrest with anaerobiosis.

Influence of coronary artery obstruction on cardiac prostaglandin metabolism during experimental cardioplegic arrest.

In order to test the influence of coronary artery obstruction on cardiac prostaglandin metabolism during surgically induced cardioplegia (CP), we have measured transcardiac veno-arterial gradients of prostacyclin and thromboxane A2 (TXA A2) during experimental canine cardiopulmonary bypass. Cardiac arrest was induced by infusion of 500 ml of hypothermic (8 degrees C), hyperkalemic (25 meq) crystalloid CP solution into the aortic root with (group I) and without (group II) occlusion of the left anterior descending artery (LAD). After 30 minutes of cardioplegic arrest the LAD occlusion in group I was released and a second set of CP infusion was applied in both groups. Transcardiac gradients were obtained 5 seconds after onset of the first and second CP washouts. Significant prostacyclin and TXA A2 gradients were observed at both times. Prostacyclin gradients did not differ between group I and group II. In contrast, TXA A2 gradients were significantly higher during the second CP washout in group I as compared to the unoccluded group (group I 918 +/- 221, group II 244 +/- 144 pg/ml, p less than 0.05). The results of our study suggest that cardiac TXA A2 metabolism during cardioplegic arrest is increased distal to a coronary artery obstruction. Cardiac TXA A2 production might contribute to the increased ischemic myocardial injury observed in this setting.

Cardiac prostacyclin kinetics during cardiopulmonary bypass.

We have investigated the response of systemic and myocardial prostacyclin metabolism to cardiopulmonary bypass and 30 minutes of hypothermic (22 degrees C), hyperkalemic (25 mEq K+) surgical cardioplegia. Thirteen adult mongrel dogs of either sex (range 21 to 36 kg) underwent sterile cardiopulmonary bypass without donor blood. Prostacyclin levels were obtained after cannulation, 20 minutes after onset of partial bypass, and 5 seconds after the onset of cardioplegia 1 (CP-1) and cardioplegia 2 (CP-2, 30 minutes later). Samples were drawn from the thoracic aorta, the aortic root below cross-clamping, and the coronary sinus. The stable metabolite of prostacyclin, 6-keto-PGF1 alpha was measured by double-antibody radioimmunoassay (pg/ml; values +/- standard error of the mean). We found that the onset of partial bypass is associated with significant increase in the systemic production of 6-keto-PGF1 alpha (122 +/- 33 versus 518 +/- 187; p less than 0.05), which persists throughout the experiment. A small but significant positive cardiac gradient of 6-keto-PGF1 alpha is found after cannulation (aortic root 122 +/- 33, coronary sinus 202 +/- 57, p less than 0.05). This gradient is more pronounced during partial bypass (aortic root 518 +/- 187, coronary sinus 686 +/- 186 p less than 0.05), when significant cardiac lactate extraction (p less than 0.005) is observed. After cross-clamping, a significantly increased gradient of 6-keto-PGF1 alpha is found during CP-1 (aortic root 74 +/- 10, coronary sinus 264 +/- 46, p less than 0.05 versus cannulation) in the presence of significant cardiac lactate production (p less than 0.005). A further significant increase in 6-keto-PGF1 alpha production is noted during the CP-2 infusion (aortic root 73 +/- 10, coronary sinus 483 +/- 83; p less than 0.01 versus CP-1), which is inversely related to cardiac oxygen uptake and endocardial/epicardial flow ratio. Our data demonstrate significant production of prostacyclin in the systemic and cardiac circulations during cardiopulmonary bypass and surgical cardioplegia. They further indicate that both ischemic and nonischemic stimuli regulate prostacyclin metabolism during cardiopulmonary bypass.

Angioplasty in stenosis of the innominate artery.

We describe a successful percutaneous transluminal dilatation (PTD) of an innominate artery stenosis in a 40-year-old patient with aortic arch syndrome. Five years earlier both a left central carotid artery occlusion and an innominate and left subclavian artery stenosis were treated by grafting from the aorta to the distal vessels. At recurrence of the neurological symptoms, reocclusion of the graft to the innominate artery and subtotal stenosis of the left carotid anastomosis were noted. To prevent the hazards of a reoperation, the innominate artery stenosis was dilated by means of PTD via the right brachial artery. Success of the procedure was demonstrated by Doppler sonography and angiography. It appears that PTD serves as an excellent method of treating stenoses of the aortic arch branches in aortic arch syndrome.

Chronic vascular disease of the upper extremity: radiologic and clinical features.

The major chronic vascular diseases of the upper extremity are (1) subclavian artery occlusions, (2) thoracic outlet syndrome, and (3) angiospastic disease of the hand. Central subclavian artery lesions ease of the hand. Central subclavian artery lesions can have either hemodynamic consequences (subclavian steal syndrome) or, by peripheral embolization, can provoke ischemic symptoms of the hand. Costoclavicular narrowing can cause functional or fixed stenosis of the subclavian artery and can also involve the vein or brachial plexus. Symptoms due to pressure on the brachial plexus are most frequent, but embolization to the peripheral vessels may also occur. Angiospastic disease, the most frequent lesion of upper extremity vessels, comprises three types: Raynaud's disease, in which there are intermittent attacks of coldness and discoloration without evidence of occlusion on the angiogram; asphyxia manus et digitorum in which the attacks are also intermittent but there is morphologic evidence of occlusion; and digitus moriens or mortuus, in which there is a painful, permanent discoloration. All investigations of chronic vascular disease of the upper extremity should begin with arch aortography and then proceed to a selective catheterization of the vessels that are presumed to be involved.