Microvascular research
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Microvascular research · Sep 2015
Laser speckle contrast imaging for assessing microcirculatory changes in multiple splanchnic organs and the gracilis muscle during hemorrhagic shock and fluid resuscitation.
Hemorrhagic shock induces both macrocirculatory and microcirculatory impairment. Persistent microcirculatory dysfunction is associated with the dysfunction of multiple organs, especially in the splanchnic organs. However, few studies have simultaneously investigated microcirculation in multiple organs. In the present study, we used laser speckle contrast imaging to simultaneously investigate microcirculatory changes secondary to hemorrhagic shock and after fluid resuscitation among multiple splanchnic organs and the gracilis muscle. ⋯ Hemorrhagic shock induced the largest reduction in microcirculatory blood flow intensity in the intestinal mucosa. By comparison, the reduction of tissue oxygen saturation was not significantly different among the various splanchnic organs. Although fluid resuscitation restored the MAP, the intestinal microcirculation remained damaged.
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Microvascular research · Sep 2015
Combined peri-ischemic administration of Bβ15-42 in treating ischemia reperfusion injury of the mouse kidney.
The disruption of endothelial integrity is a crucial step for the development of vascular leakage and consequently ischemia-reperfusion injury (IRI). Regarding the molecular cell-cell interaction, the fibrinopeptide Bβ15-42 prevents vascular leakage by stabilizing the inter-endothelial junctions via association with the vascular endothelial-cadherin. In a previous study we showed that a renoprotective effect in early IRI may be achieved by intravenous administration of Bβ15-42 at the time of reperfusion. ⋯ Overall, we detected significantly reduced endothelial activation, lower tissue infiltration of neutrophils as well as lower tissue levels of neutrophil gelatinase-associated lipocalin (NGAL) in all mice treated with Bβ15-42 compared to mice treated with NaCl. Our data confirm the renoprotective effect of Bβ15-42 in the early therapeutic treatment of acute kidney injury due to ischemia and reperfusion. However, a combined pre-and post-ischemic administration of Bβ15-42 appears to provide no additional benefit compared with a sole administration at reperfusion.
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Microvascular research · Jul 2015
Soluble Jagged-1 inhibits restenosis of vein graft by attenuating Notch signaling.
The excessive proliferation of vascular smooth muscle cells was key factor in the restenosis of vein graft. And the Notch signaling was demonstrated to regulate vSMC proliferation and differentiation. Soluble Jagged-1 (sJag1) can inhibit Notch signaling in vitro and in vivo; however, its capacity to suppress restenosis of vein graft remains unknown. ⋯ Notch1-Hey2 signaling is critical for the development of intima thickening by controlling vSMC-fate determination. By blocking Notch signaling, Ad-Jag1 can significantly inhibit intima thickening. These studies identify that Ad-Jag1 can restore the vSMC phenotype and inhibit the vSMC proliferation by suppression of Notch1 signaling, and thus open a new avenue for the treatment of restenosis in vein graft.
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Microvascular research · May 2015
New insights into systemic sclerosis related microcirculatory dysfunction by assessment of sublingual micr\ocirculation and vascular glycocalyx layer. Results from a preliminary study.
Initial morphological and functional markers of systemic sclerosis (SSc) are evidenced in microvascular structural damage. However, nailfold videocapillaroscopy (NVC) explores only morphological abnormalities. Sidestream Dark Field (SDF) imaging of sublingual microcirculation enables assessment of both morphological and functional capillary impairment and allows measurement of the glycocalyx layer, which is an indicator of endothelial dysfunction. ⋯ Our results suggest for the first time in SSc, that sublingual microcirculation and glycocalyx are impaired and that SDF imaging findings correlate with those of NVC. Nevertheless, further studies are required for the validation of our preliminary results.
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Microvascular research · May 2015
The beneficial effects of acute hypercapnia on microcirculatory oxygenation in an animal model of sepsis are independent of K(+)ATP channels.
Acute hypercapnia maintains the microcirculatory oxygenation of the splanchnic region during sepsis. The first aim of this study was to characterize the role of K(+)ATP channels on the microcirculatory flow and oxygenation during acute moderate hypercapnia. The second aim was to investigate whether a short period of hypercapnia induces detrimental effects in an otherwise undamaged rodent lung. ⋯ The observed beneficial effect of hypercapnia on microvascular oxygenation of the colon in sepsis does not seem to be mediated via K(+)ATP channels.