Browsing by Subject "Microvasculature"

Now showing 1 - 3 of 3
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    Cutaneous microvascular vasodilatory consequences of acute consumption of a caffeinated soft drink sweetened with high‐fructose corn syrup
    (Wiley, 2021) Greenshields, Joel T.; Keeler, Jason M.; Freemas, Jessica A.; Baker, Tyler B.; Johnson, Blair D.; Carter, Stephen J.; Schlader, Zachary J.; Medicine, School of Medicine
    This study tested the hypotheses that compared to drinking water, consumption of a caffeinated soft drink sweetened with high-fructose corn syrup (HFCS) attenuates the cutaneous vasodilatory response to local skin heating without (Protocol 1) and following ischemia-reperfusion injury (Protocol 2). In a randomized, counterbalanced crossover design, 14 healthy adults (25 ± 3 year, 6 women) consumed 500 ml of water (water) or a caffeinated soft drink sweetened with HFCS (Mtn. Dew, DEW). Thirty minutes following beverage consumption local skin heating commenced on the right forearm (Protocol 1), while on the left forearm ischemia-reperfusion commenced with 20 min of ischemia followed by 20 min of reperfusion and then local skin heating (Protocol 2). Local skin heating involved 40 min of heating to 39℃ followed by 20 min of heating to 44℃. Skin blood flow (SkBf, laser Doppler) data were normalized to mean arterial pressure and are presented as a cutaneous vascular conductance (CVC) and as percentage of the CVC response during heating to 44℃ (%CVCmax ). Protocol 1: During local heating at 39℃, no differences were observed in CVC (water: 2.0 ± 0.6 PU/mmHg; DEW: 2.0 ± 0.8 PU/mmHg, p = 0.83) or %CVCmax (water: 59 ± 14%; DEW 60 ± 15%, p = 0.84) between trials. Protocol 2: During local skin heating at 39℃, no differences were observed in CVC (water: 1.7 ± 0.5 PU/mmHg; DEW: 1.5 ± 0.5 PU/mmHg, p = 0.33) or %CVCmax (water: 64 ± 15%; DEW 61 ± 15% p = 0.62) between trials. The cutaneous microvascular vasodilator response to local heating with or without prior ischemia-reperfusion injury is not affected by acute consumption of a caffeinated soft drink sweetened with HFCS.
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    Intravital multiphoton microscopy as a tool for studying renal physiology and pathophysiology
    (Elsevier, 2017-09-01) Sandoval, Ruben M.; Molitoris, Bruce A.; Medicine, School of Medicine
    The kidney is a complex and dynamic organ with over 40 cell types, and tremendous structural and functional diversity. Intravital multi-photon microscopy, development of fluorescent probes and innovative software, have rapidly advanced the study of intracellular and intercellular processes within the kidney. Researchers can quantify the distribution, behavior, and dynamic interactions of up to four labeled chemical probes and proteins simultaneously and repeatedly in four dimensions (time), with subcellular resolution in near real time. Thus, multi-photon microscopy has greatly extended our ability to investigate cell biology intravitally, at cellular and subcellular resolutions. Therefore, the purpose of the chapter is to demonstrate how the use in intravital multi-photon microscopy has advanced the understanding of both the physiology and pathophysiology of the kidney.
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    Role of coagulation in persistent renal ischemia following reperfusion in an animal model
    (American Physiological Society, 2022) Dominguez, Jesus H.; Xie, Danhui; Dominguez, James M., II; Kelly, K. J.; Medicine, School of Medicine
    Ischemic acute kidney injury is common, deadly, and accelerates the progression of chronic kidney disease, yet has no specific therapy. After ischemia, reperfusion is patchy with early and persistent impairment in regional renal blood flow and cellular injury. We tested the hypothesis that intrarenal coagulation results in sustained renal ischemia following reperfusion, using a well-characterized model. Markedly decreased, but heterogeneous, microvascular plasma flow with microthrombi was found postischemia by intravital microscopy. Widespread tissue factor expression and fibrin deposition were also apparent. Clotting was accompanied by complement activation and inflammation. Treatment with exosomes derived from renal tubular cells or with the fibrinolytic urokinase, given 24 h postischemia when renal failure was established, significantly improved microvascular flow, coagulation, serum creatinine, and histological evidence of injury. These data support the hypothesis that intrarenal clotting occurs early and the resultant sustained ischemia is a critical determinant of renal failure following ischemia; they demonstrate that the coagulation abnormalities are amenable to therapy and that therapy results in improvement in both function and postischemic inflammation. NEW & NOTEWORTHY: Ischemic renal injury carries very high morbidity and mortality, yet has no specific therapy. We found markedly decreased, heterogeneous microvascular plasma flow, tissue factor induction, fibrin deposition, and microthrombi after renal ischemia-reperfusion using a well-characterized model. Renal exosomes or the fibrinolytic urokinase, administered after renal failure was established, improved microvascular flow, coagulation, renal function, and histology. Data demonstrate that intrarenal clotting results in sustained ischemia amenable to therapy that improves both function and postischemic inflammation.