Microcirculatory Effects of Botulinum Toxin A in the Rat

Abstract

Pretreatment with BTX may induce the arteriolar resting diameter to be closer to their maximum potential diameter. Additionally, BTX does not display a synergistic effect with topical vasodilators on vasodilation.

Non-invasive intra-uterine administration of Botulinum Toxin A enhances endometrial angiogenesis and improves the rates of embryo implantation

“…The effect of BoTA on the microvascular remodeling and its activation has been studied to a lesser extent. Consistent with the previous reports demonstrating a signi cant increase in resting diameter of arterioles and venules with the topical application of BoTA to the rat cremaster muscle [25,48], in the present study we have demonstrated that non-invasive intrauterine BoTA administration increases the numbers of microvessel formation in the lining of the endometrium, which has been shown with the assessment of CD31 and CD34 immunoreactivity in the longitudinally-sectioned tissues (Fig. 4), and more abundant and thicker uterine arteries were observed surrounding the sites of embryo implantation in the BoTA-applied mouse uterus compared to controls (Fig.…”

“…In addition to these usages, BoTA is commonly used in medical applications to treat chronic myofascial pain, headache, urinary incontinence, and hyperhidrosis [21][22][23][24]. Lately, there have been reports demonstrating the effect of BoTA on ap survival, which was suggested to occur by increased vasodilation and angiogenesis via elevated hypoxia-inducible factor (HIF)1α and vascular endothelial growth factor (VEGF) [25,26]. Moreover, BoTA is reported to enhance re-epithelialization of human keratinocytes and angiogenesis of endothelial cells [27].…”

Non-invasive Intrauterine Administration of Botulinum Toxin A Enhances Endometrial Angiogenesis and Improves the Rates of Embryo Implantation

“…In addition to these usages, BoTA is commonly used in medical applications to treat chronic myofascial pain, headache, urinary incontinence, and hyperhidrosis [20][21][22][23]. Lately, there have been reports demonstrating the effect of BoTA on flap survival, which was suggested to occur by increased vasodilation and angiogenesis via elevated hypoxia-inducible factor (HIF)1α and vascular endothelial growth factor (VEGF) [24,25]. Moreover, BoTA is reported to enhance reepithelialization of human keratinocytes and angiogenesis of endothelial cells [26].…”

Role of botulinum neurotoxin–A in cerebral revascularization graft vasospasm prevention: current state of knowledge

“…1,6-8, 10, 22, 32, 36, 39, 40, 49, 50, 54, 57,62 In these studies, a rat model was most commonly used (n = 14/15) and there was significant variability in BTX dose (0.1-20 IU), application method (subdermal, intradermal, subcutaneous, intramuscular or perivascular injection, direct application to the vessels, or tissue bath), treated flaps (random cutaneous, abdominal or dorsal cutaneous, transverse rectus abdominis myocutaneous, cremaster, spinotrapezius, or gastrocnemius muscular), and evaluation time points (5 minutes to 21 days). Better flap survival rates, 10,22,32,36,39,50,54,57 increased angiogenesis and angiogenic marker expression, 36,39,40,49,50,54 improved blood flow, 54,57 vasodilation, 8,39,50,62 and reduced inflammation and inflammatory marker expression 1,6 were observed in the BTX treatment groups as compared to controls. Interestingly, BTX-A also improved random cutaneous flap survival in rats after short-and long-term tobacco exposure, demonstrating its potential efficacy for the prevention of reconstructive and revascularization surgery complications in smokers.…”

“…49,57 In these and numerous other animal studies, improved flap survival, increased tissue perfusion, vasodilation, and angiogenesis after BTX-A pretreatment has been demonstrated. 6,8,39,49,57,66 Hence, the reported upregulation of Rho kinase expression in response to BTX-A seems to be contradictory to its well-reported vasodilatory effects in animal models and Raynaud's phenomenon treatments in humans. 20,46,64 Accordingly, Schweizer et al hypothesized that increased RhoA immunoexpression after BTX-A administration could result from a compensatory overexpression in response to functional inhibition, 57 however, no targeted investigations of BTX A-specific effects on RhoA downstream effectors in the ROCK pathway have been reported.…”