Changes in Skin Perfusion Pressure After Hyperbaric Oxygen Therapy Following Revascularization in Patients With Critical Limb Ischemia: A Preliminary Study.

Hyperbaric oxygen (HBO) therapy promotes wound healing in patients with ischemic disease; however, HBO-induced changes in skin peripheral circulation have not been evaluated in clinical practice. Here, we investigated these changes in patients with critical limb ischemia (CLI), with a focus on the angiosome of crural blood vessels with blood flow improved by endovascular therapy (EVT). Six patients with CLI and ulcers who were treated with HBO after EVT (7 limbs; 1 patient had ulcers in the bilateral limbs) and 3 healthy subjects (6 limbs) were enrolled. HBO therapy was performed at 2 atm under 100% oxygen for 90 min per session. Skin perfusion pressure (SPP) was measured in the dorsum and sole of the foot 1 hour before (pre-SPP) and after (post-SPP) HBO therapy. ΔSPP was calculated as post-SPP minus pre-SPP. SPP measurement regions were divided into those that did (direct region) and did not (indirect region) correspond to the vascular angiosome in which angiography findings of the crus were improved after EVT; i.e., when the anterior tibial artery was effectively treated with EVT, the dorsum was the direct region and the sole was the indirect region, and vice versa when the posterior tibial artery was treated. In the direct, indirect, and healthy subject groups, the ΔSPPs were 20.5±8.7 (p=0.002), -6.4±10.9, and -15.1±18.1 (p=0.014), respectively; that of the direct group was significantly greater than that of the other groups. These results suggest that short-term improvement of the peripheral circulation by HBO therapy was significant in patients with successful revascularization.

Zinc deficiency exacerbates pressure ulcers by increasing oxidative stress and ATP in the skin.

BACKGROUND: Zinc deficiency is believed to be a predisposing factor for the development and intractable healing of pressure ulcers (PUs); however, the mechanisms of this association have not been elucidated. OBJECTIVE: Objective was to elucidate the mechanisms of the formation of severe and prolonged PUs under the zinc deficiency condition. METHODS: We assessed PUs formation after cutaneous ischemia-reperfusion (I/R) injury in mice fed with a zinc-adequate (ZA) or a zinc-deficient (ZD) diet from 2 weeks before I/R injury. Wound size, vascular damage, apoptotic cells, adenosine triphosphate (ATP) amount, and the number of Langerhans cells (LCs) in I/R area were analyzed. We evaluated the extent of oxidative stress in I/R area in OKD48 mice through bioluminescence detection. RESULTS: We found that dietary zinc deficiency caused the formation of severe and prolonged PUs in mice. Zinc deficiency increased the vascular disorder, oxidative stress, and apoptosis induced by cutaneous I/R injury. I/R injury-induced oxidative stress signals were significantly higher in ZD OKD48 mice than in ZA OKD48 mice. Additionally, zinc deficiency reduced the number of LCs and increased the amount of ATP in cutaneous I/R-injured skin. Oral supplementation of zinc improved zinc deficiency-associated PUs. CONCLUSION: Zinc deficiency might increase cutaneous I/R injury-induced vascular damages, oxidative stress, and apoptosis, as well as ATP amount in I/R area due to the loss of LCs. These mechanisms might partly account for zinc deficiency-induced formation of severe and prolonged PUs. Oral supplementation of zinc might be a reasonable therapeutic choice for patients with PUs and zinc deficiency.