ISSN:0738-1085    

DOI:10.1002/micr.1920151002

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

ISSN:0738-1085    

DOI:10.1002/micr.1920151003

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

摘要:

AbstractNo single drug has yet been found which can overcome the inflammatory and microvascular changes which occur in a skin flap after ischemia‐reperfusion. Nevertheless, the continued failure of approximately 7% of all free flap transfers clinically suggests that there may be a place for pharmacological intervention at the time of threatened flap failure. To date, plastic and reconstructive microsurgeons have been reluctant to use drugs because of the mass of conflicting evidence emanating from the plastic surgery literature. However, scientists and surgeons now have a clearer understanding of the problems arising in ischemia‐reperfusion. Multi‐acting drugs which can inhibit most of the important inflammatory changes would be the ideal. This review considers some of the historical developments in the pharmacological treatment of ischemic flaps in the past decade and looks to the future when pharmacological infusions may be part of the routine for salvaging failing skin flaps. © 1994 Wiley‐L

ISSN:0738-1085    

DOI:10.1002/micr.1920151004

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

摘要:

AbstractThe chief aim of this study was to maximize flap survival by counteracting the pathophysiological changes occurring during ischemia‐reperfusion. Rabbit epigastric skin flaps given 21 hours of ischemia were infused intra‐arterially with selected drugs at the start of reperfusion. Compared with control infused ischemic flaps, which had a 33% survival rate on day 7 post‐ischemia, significant improvement was found with vasodilators nitrendipine (61%) and prostacyclin (65%) and the thrombolytic agent urokinase (65%); marginal improvement with the free radical scavenger desferrioxamine (53%); but no change with streptokinase (44%), heparin (21%), and ATP‐MgCl2(35%). A drug mixture comprising all of these agents except streptokinase and urokinase produced 87% survival, suggesting an additive effect. Biochemical assays on skin homogenates and blood implicated oxygen free radicals, neutrophil infiltration, and thromboxane in flap failure. These results imply that multiple factors are responsible for ischemic flap failure and that a mixture of drugs needs to be infused to counteract all of the detrimental changes. © 1994 Wiley

ISSN:0738-1085    

DOI:10.1002/micr.1920151005

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

摘要:

AbstractNitric oxide (NO), identified as the biochemical messenger of endothelial‐dependent relaxation, is of obvious chemical simplicity, but the range and complexity of its biological actions are only now emerging. NO is an important determinant of vascular resistance, it reduces thrombogenicity of the vascular endothelium, contributes to non‐specific, host‐defence mechanisms, and is a neurotransmitter in the peripheral and central nervous systems. In addition to these physiological roles, there is now convincing evidence that excessive, prolonged production of NO contributes to tissue damage in septicemia, ischemia/reperfusion injury, and other inflammatory conditions. © 1994 Wiley‐L

ISSN:0738-1085    

DOI:10.1002/micr.1920151006

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

摘要:

AbstractNitric oxide (NO), originally identified as the mediator of endothelial‐dependent relaxation of vascular smooth muscle, is now known to also have cytotoxic effects under certain conditions. Thus, we have investigated the effects of inhibition of NO synthesis on ischemia/reperfusion injury in the rabbit rectus femoris muscle. Three and a half hours of ischemia and 24 hours of reperfusion resulted in a 56% loss of viability. In muscles receiving an infusion of the nitric oxide synthase inhibitor, L‐NIO (30 μM), the loss of viability was reduced to 15%. Post‐ischemic blood flow was increased in muscles receiving a saline infusion, whereas there was a marked decrease in blood flow for at least the first 60 minutes of reperfusion in muscles treated with L‐NIO (30 μM). The increase in myeloperoxidase levels (indicative of neutrophil accumulation) following 24 hours of reperfusion was attenuated with L‐NIO infusion by approximately 50% and the reperfusion‐induced edema was also attenuated in L‐NIO treated muscle. These findings suggest that endogenous NO production during ischemia/reperfusion injury may be deleterious to muscle survival. © 1994

ISSN:0738-1085    

DOI:10.1002/micr.1920151007

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

摘要:

AbstractThe ability of nitric oxide (NO) synthase inhibitors to reduce ischemia‐induced skin flap necrosis was assessed using a modified McFarlane flap in the rat. Flap survival was significantly improved in L‐NIO treated (86 ± 2%), L‐NAME‐treated (84 ± 2%), and aminoguanidine‐treated (76 ± 2%) animals compared to the saline‐treated group (54 ± 2%),P<0.005. Inhibition of NO synthase significantly decreased the hyperemia and edema within the flaps at 24 hours post‐elevation. These findings suggest that endogenous NO production contributes to ischemic necrosis and that inhibition of NO synthase may prove useful in extending survival of tissues subjected to ischemia. © 19

ISSN:0738-1085    

DOI:10.1002/micr.1920151008

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

摘要:

AbstractCold stored femoral arteries or veins have been reinserted successfully as autografts into rabbits. The present study examines whether grafting with cold stored vascular allografts is equally successful. Rabbit femoral arteries and veins were stored at 4°C for 4 weeks before insertion as allografts into unrelated animals. Three weeks after insertion into the femoral artery all venous allografts and 80% of arterial allografts were patent, but patency of both graft types declined over the next few weeks. A small number of cold stored venous allografts when inserted into the femoral vein occluded within 3 weeks.No histological evidence of rejection was apparent. The findings suggest that cold stored vascular allografts could be used successfully as an arterial “prosthesis” to support free flaps where relatively short term patency is required until the flap can establish sufficient peripheral inset to survive in its own right. This technique could be applied when autologous veins are not available or not justified. © 1994 Wiley‐Li

ISSN:0738-1085    

DOI:10.1002/micr.1920151009

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

摘要:

AbstractPedicles created from a long vein graft increase the scope and applications of prefabricated skin flaps. This study reports the survival and pattern of neovascularization of lower abdominal skin flaps in rabbits based on a pedicle formed by interposition of a long vein graft between the divided ipsilateral femoral artery and vein. Flaps were elevated 2–5 weeks after pedicle implantation and the surviving area quantitated and vascular patterns examined 1 week later. Only 8 out of 35 flaps were greater than 50% alive, the most frequent cause of flap failure being pedicle non‐patency. If the pedicle remained patent, complete flap survival was possible as early as 2 weeks after implantation. In non‐patent pedicles, recanalization or formation of a new vascular network may, given at least 4 weeks, be sufficient to ensure partial flap survival. The findings indicate that implantation of a long, skeletonized vein graft is an unreliable method of prefabrication of abdominal skin flaps in this model. © 1994 Wiley‐L

ISSN:0738-1085    

DOI:10.1002/micr.1920151010

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY

摘要:

AbstractThe effect on distal blood flow in a 2 vessel limb of clamping one of the vessels or resecting it over a length is not known. Commonly this situation occurs clinically, for example, following lacerations to the radial or ulnar artery or as a result of removing a radial or ulnar artery flap. In a dog model established to mimic these clinical circumstances, a 2 vessel limb was created in which one vessel carried two‐thirds of the total flow and the other one‐third. Electromagnetic flow recordings were taken to measure the changes in flow in one vessel when the other was clamped or resected. Contrary to expectation, when one vessel was occluded the flow in the opposite vessel both immediately and for the following 30 minutes increased but remained well below the combined flow of 2 unclamped vessels. No increased flow was recorded in the dominant vessel when the smaller vessel was clamped, while an approximately 25% increase in flow was recorded in the smaller vessel when the larger one was clamped. This represents a reduction in total distal blood flow of one‐half of the preclamping levels. Clamping of the vessel or its resection over a length resulted in the same degree of alteration in flow in the opposite vessel. The sacrifice of a dominant vessel in a 2 vessel limb whether by simple ligation or by radical stripping as for free tissue transfer significantly decreases distal flow in that limb at least in the immediate and short term. End‐to‐side anastomosis or reconstitution of the vessel would be recommended. On the other hand, use of the non‐dominant vessel would appear to be safe. © 1994 Wil

ISSN:0738-1085    

DOI:10.1002/micr.1920151011

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1994

数据来源: WILEY