Abstract 288: Impaired Ischemic Myocutaneous Wound Revascularization And Transdermal H2S Emissions In Diabetic Rats

Abstract 288: Impaired Ischemic Myocutaneous Wound Revascularization And Transdermal H2S Emissions In Diabetic Rats

IntroductionHydrogen sulfide (H2S) has been recognized as an important signaling molecule in cellular O2 sensing, wound healing and angiogenesis. Studies have shown abnormal H2S levels in diabetic patients with cardiovascular disease. Diminished H2S signaling may play a causative role in diabetic fo...

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Veröffentlicht in:Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2022-05, Vol.42 (Suppl_1), p.A288-A288
Hauptverfasser: Giacolone, Joseph, Matheson, Benjamin, Shekarriz, Reza, Kanagy, Nancy, Clark, Ross
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container_end_page A288
container_issue Suppl_1
container_start_page A288
container_title Arteriosclerosis, thrombosis, and vascular biology
container_volume 42
creator Giacolone, Joseph
Matheson, Benjamin
Shekarriz, Reza
Kanagy, Nancy
Clark, Ross
description IntroductionHydrogen sulfide (H2S) has been recognized as an important signaling molecule in cellular O2 sensing, wound healing and angiogenesis. Studies have shown abnormal H2S levels in diabetic patients with cardiovascular disease. Diminished H2S signaling may play a causative role in diabetic foot wounds. The Transdermal Arterial Gasotransmitter Sensor (TAGS) device measures real-time H2S emissions through the skin. In this work, we utilize the novel TAGS device to characterize transdermal H2S emissions during diabetic and non-diabetic wound healing for the first time. MethodsDorsal peninsular-shaped myocutaneous ischemic flap wounds were created under anesthesia. Sprague Dawley (SD) and Zucker Diabetic Fatty (ZDF) rats (n=10 each) were compared. Transdermal H2S emissions, laser speckle contrast images (LSCI) and planimetric photos were serially taken from the wound flap area over 14 days. After animal sacrifice, healed flap tissue was collected for histologic (H&E) analysis of panniculus carnosus (skin muscle) viability as a proxy for degree of ischemic insult. ResultsZDF rats were significantly hyperglycemic (mean 516 mg/dL vs. 201 mg/dL for SD, P=0.002). Similar mean baseline (preoperative) H2S emissions were observed in SD (16 ppb) and ZDF (12 ppb) rats (P=0.25). During revascularization and healing, ZDF wounds emitted significantly less H2S (10 ppb at day 14) as compared to SD (28 ppb at day 14, P
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Studies have shown abnormal H2S levels in diabetic patients with cardiovascular disease. Diminished H2S signaling may play a causative role in diabetic foot wounds. The Transdermal Arterial Gasotransmitter Sensor (TAGS) device measures real-time H2S emissions through the skin. In this work, we utilize the novel TAGS device to characterize transdermal H2S emissions during diabetic and non-diabetic wound healing for the first time. MethodsDorsal peninsular-shaped myocutaneous ischemic flap wounds were created under anesthesia. Sprague Dawley (SD) and Zucker Diabetic Fatty (ZDF) rats (n=10 each) were compared. Transdermal H2S emissions, laser speckle contrast images (LSCI) and planimetric photos were serially taken from the wound flap area over 14 days. After animal sacrifice, healed flap tissue was collected for histologic (H&amp;E) analysis of panniculus carnosus (skin muscle) viability as a proxy for degree of ischemic insult. ResultsZDF rats were significantly hyperglycemic (mean 516 mg/dL vs. 201 mg/dL for SD, P=0.002). Similar mean baseline (preoperative) H2S emissions were observed in SD (16 ppb) and ZDF (12 ppb) rats (P=0.25). During revascularization and healing, ZDF wounds emitted significantly less H2S (10 ppb at day 14) as compared to SD (28 ppb at day 14, P&lt;0.01). ZDF wounds demonstrated impaired flap engraftment and revascularization by LSCI (mean 65.6 Perfusion Units (PU) for ZDF vs. 188.0 PU for SD at day 14, p&lt;0.01) and planimetric analysis (mean 16.6% necrosis for ZDF vs. 5.3% necrosis for SD at day 14, p=0.01). Panniculus carnosus mean myofibril count, myofibril diameter, and layer thickness were significantly decreased (p&lt;0.01) in the ZDF cohort, suggesting greater tissue ischemic insult and muscle loss. ConclusionDiabetic rats have impaired wound H2S production and poor revascularization. These physiologic alterations are accompanied by greater wound necrosis and histologic ischemic insult. This suggests H2S abnormalities in diabetes may play a role in the pathogenesis of impaired wound healing and could represent a potential future therapeutic target for these difficult wounds.</description><identifier>ISSN: 1079-5642</identifier><identifier>DOI: 10.1161/atvb.42.suppl_1.288</identifier><language>eng</language><publisher>Lippincott Williams &amp; Wilkins</publisher><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2022-05, Vol.42 (Suppl_1), p.A288-A288</ispartof><rights>Lippincott Williams &amp; Wilkins</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids></links><search><creatorcontrib>Giacolone, Joseph</creatorcontrib><creatorcontrib>Matheson, Benjamin</creatorcontrib><creatorcontrib>Shekarriz, Reza</creatorcontrib><creatorcontrib>Kanagy, Nancy</creatorcontrib><creatorcontrib>Clark, Ross</creatorcontrib><title>Abstract 288: Impaired Ischemic Myocutaneous Wound Revascularization And Transdermal H2S Emissions In Diabetic Rats</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><description>IntroductionHydrogen sulfide (H2S) has been recognized as an important signaling molecule in cellular O2 sensing, wound healing and angiogenesis. Studies have shown abnormal H2S levels in diabetic patients with cardiovascular disease. Diminished H2S signaling may play a causative role in diabetic foot wounds. The Transdermal Arterial Gasotransmitter Sensor (TAGS) device measures real-time H2S emissions through the skin. In this work, we utilize the novel TAGS device to characterize transdermal H2S emissions during diabetic and non-diabetic wound healing for the first time. MethodsDorsal peninsular-shaped myocutaneous ischemic flap wounds were created under anesthesia. Sprague Dawley (SD) and Zucker Diabetic Fatty (ZDF) rats (n=10 each) were compared. Transdermal H2S emissions, laser speckle contrast images (LSCI) and planimetric photos were serially taken from the wound flap area over 14 days. After animal sacrifice, healed flap tissue was collected for histologic (H&amp;E) analysis of panniculus carnosus (skin muscle) viability as a proxy for degree of ischemic insult. ResultsZDF rats were significantly hyperglycemic (mean 516 mg/dL vs. 201 mg/dL for SD, P=0.002). Similar mean baseline (preoperative) H2S emissions were observed in SD (16 ppb) and ZDF (12 ppb) rats (P=0.25). During revascularization and healing, ZDF wounds emitted significantly less H2S (10 ppb at day 14) as compared to SD (28 ppb at day 14, P&lt;0.01). ZDF wounds demonstrated impaired flap engraftment and revascularization by LSCI (mean 65.6 Perfusion Units (PU) for ZDF vs. 188.0 PU for SD at day 14, p&lt;0.01) and planimetric analysis (mean 16.6% necrosis for ZDF vs. 5.3% necrosis for SD at day 14, p=0.01). Panniculus carnosus mean myofibril count, myofibril diameter, and layer thickness were significantly decreased (p&lt;0.01) in the ZDF cohort, suggesting greater tissue ischemic insult and muscle loss. ConclusionDiabetic rats have impaired wound H2S production and poor revascularization. These physiologic alterations are accompanied by greater wound necrosis and histologic ischemic insult. This suggests H2S abnormalities in diabetes may play a role in the pathogenesis of impaired wound healing and could represent a potential future therapeutic target for these difficult wounds.</description><issn>1079-5642</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNqdTktOwzAU9AIkCvQEbN4FEmw3CYFdBUXNgk2p1GX04hjF4DiRn90KTo-RegIWo5Hmp2HsTvBciErcYzh2eSFzivNsW5HLur5gC8EfHrOyKuQVuyb65JwXUvIFo3VHwaMKkHJP0IwzGq97aEgNejQK3r4nFQM6PUWCwxRdDzt9RFLRojc_GMzkYJ3UvUdHvfYjWtjKd9iMhiiZBI2DF4OdDmluh4Fu2eUHWtLLM9-w4nWzf95mp8kG7enLxpP27aDRhqH9u7qqeJlJnh6XnIssQdSrf9Z-AWPcWa8</recordid><startdate>20220501</startdate><enddate>20220501</enddate><creator>Giacolone, Joseph</creator><creator>Matheson, Benjamin</creator><creator>Shekarriz, Reza</creator><creator>Kanagy, Nancy</creator><creator>Clark, Ross</creator><general>Lippincott Williams &amp; Wilkins</general><scope/></search><sort><creationdate>20220501</creationdate><title>Abstract 288: Impaired Ischemic Myocutaneous Wound Revascularization And Transdermal H2S Emissions In Diabetic Rats</title><author>Giacolone, Joseph ; Matheson, Benjamin ; Shekarriz, Reza ; Kanagy, Nancy ; Clark, Ross</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-wolterskluwer_health_00043605-202205001-001183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Giacolone, Joseph</creatorcontrib><creatorcontrib>Matheson, Benjamin</creatorcontrib><creatorcontrib>Shekarriz, Reza</creatorcontrib><creatorcontrib>Kanagy, Nancy</creatorcontrib><creatorcontrib>Clark, Ross</creatorcontrib><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Giacolone, Joseph</au><au>Matheson, Benjamin</au><au>Shekarriz, Reza</au><au>Kanagy, Nancy</au><au>Clark, Ross</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abstract 288: Impaired Ischemic Myocutaneous Wound Revascularization And Transdermal H2S Emissions In Diabetic Rats</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><date>2022-05-01</date><risdate>2022</risdate><volume>42</volume><issue>Suppl_1</issue><spage>A288</spage><epage>A288</epage><pages>A288-A288</pages><issn>1079-5642</issn><abstract>IntroductionHydrogen sulfide (H2S) has been recognized as an important signaling molecule in cellular O2 sensing, wound healing and angiogenesis. Studies have shown abnormal H2S levels in diabetic patients with cardiovascular disease. Diminished H2S signaling may play a causative role in diabetic foot wounds. The Transdermal Arterial Gasotransmitter Sensor (TAGS) device measures real-time H2S emissions through the skin. In this work, we utilize the novel TAGS device to characterize transdermal H2S emissions during diabetic and non-diabetic wound healing for the first time. MethodsDorsal peninsular-shaped myocutaneous ischemic flap wounds were created under anesthesia. Sprague Dawley (SD) and Zucker Diabetic Fatty (ZDF) rats (n=10 each) were compared. Transdermal H2S emissions, laser speckle contrast images (LSCI) and planimetric photos were serially taken from the wound flap area over 14 days. After animal sacrifice, healed flap tissue was collected for histologic (H&amp;E) analysis of panniculus carnosus (skin muscle) viability as a proxy for degree of ischemic insult. ResultsZDF rats were significantly hyperglycemic (mean 516 mg/dL vs. 201 mg/dL for SD, P=0.002). Similar mean baseline (preoperative) H2S emissions were observed in SD (16 ppb) and ZDF (12 ppb) rats (P=0.25). During revascularization and healing, ZDF wounds emitted significantly less H2S (10 ppb at day 14) as compared to SD (28 ppb at day 14, P&lt;0.01). ZDF wounds demonstrated impaired flap engraftment and revascularization by LSCI (mean 65.6 Perfusion Units (PU) for ZDF vs. 188.0 PU for SD at day 14, p&lt;0.01) and planimetric analysis (mean 16.6% necrosis for ZDF vs. 5.3% necrosis for SD at day 14, p=0.01). Panniculus carnosus mean myofibril count, myofibril diameter, and layer thickness were significantly decreased (p&lt;0.01) in the ZDF cohort, suggesting greater tissue ischemic insult and muscle loss. ConclusionDiabetic rats have impaired wound H2S production and poor revascularization. These physiologic alterations are accompanied by greater wound necrosis and histologic ischemic insult. This suggests H2S abnormalities in diabetes may play a role in the pathogenesis of impaired wound healing and could represent a potential future therapeutic target for these difficult wounds.</abstract><pub>Lippincott Williams &amp; Wilkins</pub><doi>10.1161/atvb.42.suppl_1.288</doi></addata></record>
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