PubMed · 8475606
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K Miller. 1993. [Urinary diversion: pathophysiological principles].. https://pubmed.ncbi.nlm.nih.gov/8475606/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
BACKGROUND: Microvascular anastomoses must be constructed perfectly in order to be successful. One of the subtle technical errors that can occur during construction is twisting of the anastomosis. In the present study, we examined the effect of twist on the immediate, 2-h postoperative angiographic dimensions and patency of microvascular anastomoses. MATERIALS AND METHODS: Sixty-four Sprague-Dawley rats were assigned randomly to four groups. The femoral arteries were dissected for a distance sufficient to permit the application of an 8.5-mm-long microanastomotic approximator clamp. Microarteriorrhaphies were performed with twists of 0 degrees, 90 degrees, 180 degrees, or 270 degrees. Patency was assessed 2 h after surgery using transabdominal aortic arteriography with run-off. Measurements were recorded for each anastomosis, as well as for the narrowest and widest diameters of the vessels within 10 mm of the anastomosis. RESULTS: Fifty-nine of the 64 rats had technically satisfactory angiograms which permitted measurement of vascular dimensions. The cross-sectional areas of the narrowest areas and the anastomoses were inversely related to the degree of twist, and were significantly reduced at 270 degrees (P < 0.05). Two-hour patency rates were 86% with 0 degrees twist, 82% with 90 degrees twist, 71% with 180 degrees twist, and 33% with 270 degrees twist. The reduction in patency with 270 degrees twist was statistically significant (P < 0.05). CONCLUSIONS: Twists of 0 degrees, 90 degrees, and 180 degrees did not impair patency at a statistically significant level, but twists of 270 degrees did significantly reduce patency of microvascular anastomoses (P < 0.05).
Arteries enlarge in response to increased blood flow, but the molecular signals controlling this enlargement are not well understood. Basic fibroblast growth factor (bFGF) is a potent mitogen for endothelial cells (EC) and smooth muscle cells (SMC) and promotes cellular proliferation and differentiation. In order to determine whether bFGF is expressed in response to increased blood flow in vivo, carotid-jugular arteriovenous fistulas (AVF) were created in Japanese white rabbits. The carotid artery proximal to the fistula was harvested after 1, 3, or 7 days and compared to nonoperated, control carotid arteries. Arterial blood flow increased five- to eightfold in all AVF animals and resulted in a significant increase in wall shear stress. The proximal carotid artery arterial diameter was no different from control after 1 and 3 days (2.3 +/- 0. 1 mm) but enlarged to 2.9 +/- 0.1 mm (P < 0.05) after 7 days. RT-PCR revealed early transcription of bFGF mRNA at 1 and 3 days with increased densitometric band ratio (bFGF/beta-actin) at 7 days. Immunohistochemical analysis revealed bFGF protein localization in EC of control arteries as well as AVF arteries at all time points. SMC and adventitia expression of bFGF was absent in controls, minimal at 1 day, and increased after 3 and 7 days in the experimental groups. Western blotting confirmed the presence of bFGF in samples and transmission immunoelectron microscopy confirmed its nuclear localization. Endothelial cells in vivo express bFGF under both normal and elevated flow conditions. Smooth muscle cells, however, do not express bFGF under normal flow conditions but begin to express bFGF after 1 day of high flow with increased expression after 3 and 7 days. Flow-induced arterial enlargement begins after SMC expression of bFGF. Therefore, bFGF may play a role in arterial enlargement and adaptive remodeling in response to increased flow.
In an attempt to reduce platelet deposition and inhibit neointimal hyperplasia, we evaluated the effect of coating expanded polytetrafluoroethylene (ePTFE) grafts with phosphorylcholine (PC), a lipid found in animal cell membranes, in a dog model of femoral arteriovenous (AV) grafts. Eight mongrel dogs underwent placement of a PC-coated femoral AV graft on one side and an untreated control graft on the contralateral side. Platelet deposition was measured by autologous 111Indium-labeling and scintillation camera imaging analysis. Platelet deposition on the PC-coated grafts at 30 and 90 min. was 9.32 +/- 4.35 x 10(9) and 10.00 +/- 4.38 x 10(9), respectively, as compared with 10.26 +/- 4.36 x 10(9) and 11.64 +/- 5.08 x 10(9) platelet deposition on control grafts (P < 0.05). All grafts were patent at 4 weeks. There was a significant reduction of neointimal area at both arterial (0.07 +/- 0.05 mm2) and venous (0. 18 +/- 0.09 mm2) anastomoses in the treated grafts as compared with arterial (0.15 +/- 0.05 mm2) and venous (0.43 +/- 0.22 mm2) anastomoses in the control grafts (P < 0.05). In addition, neointimal cell proliferation assayed by bromodeoxyuridine (BrdU) incorporation was reduced in both arterial (2.05 +/- 0.81%) and venous (3.25 +/- 0.17%) anastomoses of treated grafts compared with arterial (3.12 +/- 1.23%) and venous (5.36 +/- 1.18%) anastomoses of control grafts (P < 0.05). These data demonstrated that PC coating of ePTFE grafts significantly reduced platelet deposition, anastomotic neointimal hyperplasia, and neointimal cell proliferation in a dog model of AV grafts. This may represent a new strategy for prolonging hemodialysis graft patency.