The efficacy of the hemostatic agent Ankaferd blood stopper on end-to-end unilateral sleeve fish-mouth anastomosis.

OBJECTIVE: The aim of this study was to examine if the application of Ankaferd Blood Stopper (ABS) reduces the number of sutures and therefore reduces anastomosis completion time in a unilateral end-to-end sleeve fish-mouth anastomosis model. METHODS: Femoral artery end-to-end unilateral fish-mouth anastomosis models were created from the right and left femoral arteries of 14 male Wistar albino rats (weight: 250 to 300 grams) and divided into 2 equal groups. Rats in Group A received ABS and Group B was the control group. Rats were further divided into equal 2 subgroups, and anastomoses of rats in Group 1A and 1B were explored on the 7th day and on the 14th day in Group 2A and 2B. The groups were compared for anastomosis completion time, macroscopic and microscopic patency, existence of microaneurysm and inflammatory response. RESULTS: In the ABS group (1A and 2A), mean anastomosis completion time was 13:00±1.50 minutes, and 18:56±2.5 minutes in the control groups (1B and 2B). This difference was statistically significant (p=0.001). CONCLUSION: Ankaferd Blood Stopper may be used to reduce the number of sutures and shorten the completion time of artery-to-artery anastomosis of arteries with small diameter and low blood flow rate.

Comparison of perivascular and intramuscular applied botulinum toxin a pretreatment on muscle flap ischemia-reperfusion injury and chemical delay.

BACKGROUND AND PURPOSE: Muscle flaps are known to be prone to local ischemia more than other flaps. The local and systemic injury that ensues after reperfusion of ischemic skeletal muscle is an important clinical problem in flap surgery. Flap delay may be applied chemically or sympathetically. Early use of botulinum toxin A (Btx-A) in muscle flap surgery relied on chemical denervation; however, in our study, we tried to emphasize a possible chemical delay mechanism of Btx-A, through the release of substance P and calcitonin gene-related peptide (CGRP) and vascular endothelial growth factor (VEGF). METHODS: Pretreatment with perivascular or intramuscular Btx-A was applied 1 week before the flap elevation, 3.5 units in 2 experimental groups each containing 8 Sprague-Dawley rats. The control groups (2 groups, each containing 8 rats) received 0.07 mL saline perivascularly and intramuscularly. The right gastrocnemius muscle flap was used as the experimental model. Ischemia-reperfusion cycle was applied to all groups. On the seventh day, the gastrocnemius flap was elevated, and perivascular tissues were observed macroscopically. Comparisons between perivascular Btx-A and intramuscular Btx-A groups were made, and the animals were killed. Muscle biopsies were taken. Damaged myocytes were counted using McCormack technique, and chemical delay was shown as angiogenesis, lymphocyte counts, and edema formation with VEGF3-R, CGRP, and substance P markers as immunohistochemical staining. RESULTS: The amount of muscle necrosis was the highest in intramuscular Btx-A admitted groups. The intramuscular and perivascular Btx-A groups showed significant angiogenesis scored blindly by the senior pathologist. CONCLUSIONS: Potential role of Btx-A in ischemic preconditioning of muscle flaps achieved through the release of substance P, CGRP, and VEGF was investigated. Chemical delay was shown objectively by Btx-applied groups.

Sequential limb ischemia demonstrates remote postconditioning protection of murine skeletal muscle.

BACKGROUND: Ischemic postconditioning, the process of exposing tissues to brief cycles of ischemia-reperfusion after critical ischemia, can mitigate local ischemia-reperfusion injury. Remote protection of skeletal muscle has never been demonstrated in postconditioning models of ischemia-reperfusion injury. METHODS: Mice were subjected to 2 hours of ipsilateral hind limb ischemia followed by reperfusion. Contralateral limb ischemia was subsequently induced for 2 hours after either 0 (n = 6), 20 (n = 6), or 120 (n = 5) minutes of ipsilateral limb reperfusion. These groups were compared with animals subjected to bilateral simultaneous injury (n = 8) and sham animals that did not undergo ischemia (n = 6). The gastrocnemius muscles were harvested for histologic evaluation, and injury was recorded as the percentage of injured fibers. RESULTS: The first limbs undergoing injury in the 20-minute interval group had a 59 percent injury reduction compared with contralateral limbs (16.0 +/- 2.4 percent versus 39.5 +/- 6.5 percent) after 24 hours of reperfusion and 62 percent reduction after 48 hours (24.4 +/- 3.0 percent versus 63.6 +/- 5.5 percent). In animals with no interval or a 120-minute interval between the onset of limb ischemia, there was no significant difference in injury between hind limbs. The injury in these groups was similar to that in hind limbs subjected to simultaneous bilateral ischemia. CONCLUSIONS: A 20-minute reperfusion interval between hind limb ischemia significantly protects against injury in the initially ischemic limb, while similar injury is observed with simultaneous ischemia or an interval of 120 minutes. This study demonstrates remote postconditioning of skeletal muscle and may lead to the development of post hoc therapies.

Ischemic preconditioning of skeletal muscle mitigates remote injury and mortality.

BACKGROUND: Ischemic preconditioning (IPC) mitigates ischemia-reperfusion (I/R) injury in experimental models. However, the clinical significance of this protection has been unclear and a mortality reduction has not been previously reported in noncardiac models. This study examined the local and remote protection afforded by skeletal muscle IPC and sought to determine the significance of this protection on mortality. METHODS: Mice subjected to 2 h hindlimb ischemia/24 h reperfusion (standard I/R injury) were compared with those undergoing a regimen of two 20-min cycles of IPC followed by standard I/R injury. Local injury was assessed via gastrocnemius histology, and remote injury was evaluated via intestinal histology and pulmonary neutrophil infiltration (n = 7). Mortality was compared in parallel groups for 1 week (n = 6). Groups were analyzed using an unpaired Student's t-test for gastrocnemius and pulmonary injury, and a Mann-Whitney rank sum test for intestinal injury. Mortality differences were interpreted through a hazard ratio. RESULTS: Significant protection was observed in preconditioned animals. There was a 35% local injury reduction in skeletal muscle (71.2% versus 46.0%, P < 0.01), a 50% reduction in remote intestinal injury (2.3 versus 1.1, P < 0.01), and a 43% reduction in remote pulmonary injury (14.9 versus 8.5, P < 0.01) compared with standard injury controls. Preconditioned animals were also significantly protected from mortality, demonstrating a 66.7% survival at 1 wk compared with 0% survival after standard injury alone (hazard ratio 0.20, 95% CI: 0.02-0.59). CONCLUSIONS: We have developed a murine model of IPC that demonstrates local and remote protection against I/R injury, and exhibits significant mortality reduction. This model demonstrates the powerful effect of IPC on local and remote tissues and will facilitate further study of potential mechanisms and therapies.