Influence of topical heparin on stasis‐induced thrombosis of microvascular anastomoses

Abstract

An experiment was done to determine whether topical heparin and the association of anastomoses with dependent tissue (free flaps) exert any influences on stasis-induced microvascular thrombosis. Rat femoral vessel anastomoses with or without free flap construction were used in a total of 50 male Sprague-Dawley rats. Saline either with or without heparin was used for intralumenal irrigation during the anastomosis. Following anastomotic repair, the femoral vessels were reclamped, inducing stasis for either 2 or 4 hr. Our results showed that static blood had little adverse effect on thrombosis at the arterial anastomosis when reclamped for up to 4 hr in both standard and flap-associated anastomoses. Topical heparin significantly reduced the incidence of stasis-induced thrombosis of venous anastomoses. The venous patency rates in standard anastomoses were lower than those in flap-associated anastomoses after both 2 and 4 hr of stasis. From these results, we conclude the following. 1) Arteries may be reclamped for up to 4 hr without detriment despite static blood being in contact with the anastomotic site. 2) Topical heparin may be helpful in increasing the patency rate of venous anastomoses after a period of blood stasis. 3) Free flap construction may play a role in decreasing stasis-induced microvascular thrombosis.

Effect of clamp versus anastomotic-induced ischemia on critical ischemic time and survival of rat epigastric fasciocutaneous flap

“…[15][16][17] Heparin irrigation acts to remove local vessel thrombus. Heparin also acts to decrease new thrombus formation at the anastomotic site and decrease the number of downstream microvascular emboli from the anastomosis site.…”

Experimental prevention of free flap thrombosis. I: A model of free flap failure

“…Numerous models have been described to study thrombosis in free flaps or microvascular anastomoses. Arterial or venous ischemia techniques [5][6][7][8][9][10][11][12] consist of clamping the pedicle (or only one of the vessels) for a determined time and then re-establishing the blood flow, thus causing a reperfusion injury. These models probably give an insight into the effect of thrombosis occurring in the flap microcirculation, but they do not mimic the process of thrombosis at the microvascular anastomosis site leading to flap failure.…”

Effect of aging on cellular mechanotransduction

“…Boluyt and colleagues using captopril, demonstrated that fibronectin expression is increased in the senescent spontaneous hypertensive rat heart (Boluyt and Bing, 2000). Similarly, as the heart ages, collagen expression has also been shown to increase (Li et al, 1992; Orlandi et al, 2004; Lieber et al, 2008). It is thought that these changes in fibronectin and collagen may be associated with increased diastolic stiffness (Burgess et al, 2001; Merx et al, 2005).…”