scholarly journals Application of a Novel Microfluidic Device for Studying Microvascular Blood Flow Regulation In Vivo

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Gaylene M Russell McEvoy ◽  
Hamza Shogan ◽  
Graham M Fraser
2021 ◽  
Vol 12 ◽  
Author(s):  
Céline Boudart ◽  
Fuhong Su ◽  
Lorenzo Pitisci ◽  
Arnaud Dhoine ◽  
Olivier Duranteau ◽  
...  

Background: Sepsis is a common condition known to impair blood flow regulation and microcirculation, which can ultimately lead to organ dysfunction but such contribution of the coronary circulation remains to be clarified. We investigated coronary blood flow regulatory mechanisms, including autoregulation, metabolic regulation, and endothelial vasodilatory response, in an experimental porcine model of early hyperdynamic sepsis.Methods: Fourteen pigs were randomized to sham (n = 7) or fecal peritonitis-induced sepsis (n = 7) procedures. At baseline, 6 and 12 h after peritonitis induction, the animals underwent general and coronary hemodynamic evaluation, including determination of autoregulatory breakpoint pressure and adenosine-induced maximal coronary vasodilation for coronary flow reserve and hyperemic microvascular resistance calculation. Endothelial-derived vasodilatory response was assessed both in vivo and ex vivo using bradykinin. Coronary arteries were sampled for pathobiological evaluation.Results: Sepsis resulted in a right shift of the autoregulatory breakpoint pressure, decreased coronary blood flow reserve and increased hyperemic microvascular resistance from the 6th h after peritonitis induction. In vivo and ex vivo endothelial vasomotor function was preserved. Sepsis increased coronary arteries expressions of nitric oxide synthases, prostaglandin I2 receptor, and prostaglandin F2α receptor.Conclusion: Autoregulation and metabolic blood flow regulation were both impaired in the coronary circulation during experimental hyperdynamic sepsis, although endothelial vasodilatory response was preserved.


Endocrinology ◽  
2004 ◽  
Vol 145 (10) ◽  
pp. 4507-4512 ◽  
Author(s):  
Yasuhiro Shibata ◽  
Bunzo Kashiwagi ◽  
Seiji Arai ◽  
Yoshitatsu Fukabori ◽  
Kazuhiro Suzuki ◽  
...  

Abstract Previous studies on prostate blood flow regulation have indicated that androgen regulates prostate blood flow. However, the mechanism responsible for this regulation is unknown. In the present study, we focused on the effects of vascular endothelial growth factor (VEGF), a key factor responsible for angiogenesis and androgenic blood flow regulation. We examined in vivo the effect of VEGF on prostate blood flow and its participation in the androgenic regulation of this blood flow using a castrated rat model following subcapsular intraprostatic injection method. We found that VEGF is involved in blood flow regulation with an activity equal to that of dihydrotestosterone (DHT). The effect of VEGF on prostate blood flow was already seen at 30 min after the administration. The elevating effect of DHT on castrated rat prostate blood flow was abolished by coadministration of DHT with neutralizing anti-VEGF antibody. The change in VEGF-A mRNA expression in response to androgen stimulation was examined by double-fluorescent probe quantitative PCR (Taqman PCR). The results showed that androgenic regulation of VEGF gene expression occurred shortly after androgen stimulation. VEGF gene up-regulation was abolished or down-regulated by coadministration of neutralizing anti-VEGF antibody. This is the first report on the importance of VEGF in the androgenic regulation signaling pathway that affects prostate blood flow. Alternative treatment targeted toward anti-VEGF activity as a substitute for ordinary antiandrogenic therapy may be effective against prostate diseases, especially those with androgen-independent and hyperhemorrhagic status.


2009 ◽  
Vol 6 (3) ◽  
pp. 159-167 ◽  
Author(s):  
Thomas Forst ◽  
Thomas Hach ◽  
Thomas Kunt ◽  
Matthias M. Weber ◽  
Andreas Pfützner

2018 ◽  
Author(s):  
◽  
Charmain Angela Fernando

Skeletal muscle has a remarkable capacity to regenerate following injury, and although muscle regeneration has been studied extensively, little is known about the recovery of the skeletal muscle microcirculation during regeneration. To determine the restoration of blood flow regulation during skeletal muscle regeneration, this dissertation explored the recovery of vasomotor responses to physiological agonists and of functional vasodilation in response to muscle contraction. A novel injury model in the mouse gluteus maximus muscle was developed to study the microcirculation in vivo using intravital microscopy at welldefined time points (5, 10, 21 and 35 days) post injury compared to uninjured Control muscles. Studies encompassed feed arteries and the principal branches (1st, 2nd and 3rd order) of arteriolar networks comprising the resistance vasculature. Vasomotor responses to agonists and active force developed by muscle fibers recovered by 21d, however functional vasodilation required [about]35d to recover. This research provides novel insight into when and to what extent blood flow regulation is restored during skeletal muscle regeneration and provides novel perspective towards developing therapeutic strategies for restoring skeletal muscle function during recovery from injury.


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