Skin grafting impairs postsynaptic cutaneous vasodilator and sweating responses

Scott L. Davis, Manabu Shibasaki, David A. Low, Jian Cui, David M. Keller, Gary F. Purdue, John L. Hunt, Brett D. Arnoldo, Karen J. Kowalske, Craig G. Crandall

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

This study tested the hypothesis that postsynaptic cutaneous vascular responses to endothelial-dependent and -independent vasodilators as well as sweat gland function, are impaired in split-thickness grafted skin 5 to 9 months after surgery. Intradermal microdialysis membranes were placed in grafted and adjacent control skin, thereby allowing local delivery of the endothelial-dependent vasodilator, acetylcholine (ACh; 1 × 1017 to 1 × 10-1 M at 10-fold increments) and the endothelial-independent nitric oxide donor, sodium nitroprusside (SNP; 5 × 10-8 to 5 × 10-2 M at 10-fold increments). Skin blood flow and sweat rate were simultaneously assessed over the semipermeable portion of the membrane. Cutaneous vascular conductance (CVC) was calculated from the ratio of laser Doppler-derived skin blood flow to mean arterial blood pressure. ΔCVC responses from baseline to these drugs were modeled via nonlinear regression curve fitting to identify the dose of ACh and SNP causing 50% of the maximal vasodilator response (EC50). A rightward shift in the CVC dose response curve for ACh was observed in grafted (EC50 = -2.61 ± 0.44 log M) compared to adjacent control skin (EC50 = -3.34 ± 0.46 log M; P = .003), whereas the mean EC50 for SNP was similar between grafted (EC50 = -4.21 ± 0.94 log M) and adjacent control skin (EC50 = -3.87 ± 0.65 log M; P = 0.332). Only minimal sweating to exogenous ACh was observed in grafted skin whereas normal sweating was observed in control skin. Increased EC50 and decreased maximal CVC responses to the exogenous administration of ACh suggest impairment of endothelial-dependent cutaneous vasodilator responses in grafted skin 5 to 9 months after surgery. Greatly attenuated sweating responses to ACh suggests either abnormal or an absence of functional sweat glands in the grafted skin.

Original languageEnglish (US)
Pages (from-to)435-441
Number of pages7
JournalJournal of Burn Care and Research
Volume28
Issue number3
DOIs
StatePublished - May 1 2007

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Skin Transplantation
Sweating
Vasodilator Agents
Skin
Blood Vessels
Single Nucleotide Polymorphism
Sweat Glands
Arterial Pressure
Membranes
Nitric Oxide Donors
Sweat
Microdialysis
Nitroprusside

All Science Journal Classification (ASJC) codes

  • Surgery
  • Emergency Medicine
  • Rehabilitation

Cite this

Davis, S. L., Shibasaki, M., Low, D. A., Cui, J., Keller, D. M., Purdue, G. F., ... Crandall, C. G. (2007). Skin grafting impairs postsynaptic cutaneous vasodilator and sweating responses. Journal of Burn Care and Research, 28(3), 435-441. https://doi.org/10.1097/BCR.0B013E318053d32E
Davis, Scott L. ; Shibasaki, Manabu ; Low, David A. ; Cui, Jian ; Keller, David M. ; Purdue, Gary F. ; Hunt, John L. ; Arnoldo, Brett D. ; Kowalske, Karen J. ; Crandall, Craig G. / Skin grafting impairs postsynaptic cutaneous vasodilator and sweating responses. In: Journal of Burn Care and Research. 2007 ; Vol. 28, No. 3. pp. 435-441.
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abstract = "This study tested the hypothesis that postsynaptic cutaneous vascular responses to endothelial-dependent and -independent vasodilators as well as sweat gland function, are impaired in split-thickness grafted skin 5 to 9 months after surgery. Intradermal microdialysis membranes were placed in grafted and adjacent control skin, thereby allowing local delivery of the endothelial-dependent vasodilator, acetylcholine (ACh; 1 × 1017 to 1 × 10-1 M at 10-fold increments) and the endothelial-independent nitric oxide donor, sodium nitroprusside (SNP; 5 × 10-8 to 5 × 10-2 M at 10-fold increments). Skin blood flow and sweat rate were simultaneously assessed over the semipermeable portion of the membrane. Cutaneous vascular conductance (CVC) was calculated from the ratio of laser Doppler-derived skin blood flow to mean arterial blood pressure. ΔCVC responses from baseline to these drugs were modeled via nonlinear regression curve fitting to identify the dose of ACh and SNP causing 50{\%} of the maximal vasodilator response (EC50). A rightward shift in the CVC dose response curve for ACh was observed in grafted (EC50 = -2.61 ± 0.44 log M) compared to adjacent control skin (EC50 = -3.34 ± 0.46 log M; P = .003), whereas the mean EC50 for SNP was similar between grafted (EC50 = -4.21 ± 0.94 log M) and adjacent control skin (EC50 = -3.87 ± 0.65 log M; P = 0.332). Only minimal sweating to exogenous ACh was observed in grafted skin whereas normal sweating was observed in control skin. Increased EC50 and decreased maximal CVC responses to the exogenous administration of ACh suggest impairment of endothelial-dependent cutaneous vasodilator responses in grafted skin 5 to 9 months after surgery. Greatly attenuated sweating responses to ACh suggests either abnormal or an absence of functional sweat glands in the grafted skin.",
author = "Davis, {Scott L.} and Manabu Shibasaki and Low, {David A.} and Jian Cui and Keller, {David M.} and Purdue, {Gary F.} and Hunt, {John L.} and Arnoldo, {Brett D.} and Kowalske, {Karen J.} and Crandall, {Craig G.}",
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Davis, SL, Shibasaki, M, Low, DA, Cui, J, Keller, DM, Purdue, GF, Hunt, JL, Arnoldo, BD, Kowalske, KJ & Crandall, CG 2007, 'Skin grafting impairs postsynaptic cutaneous vasodilator and sweating responses', Journal of Burn Care and Research, vol. 28, no. 3, pp. 435-441. https://doi.org/10.1097/BCR.0B013E318053d32E

Skin grafting impairs postsynaptic cutaneous vasodilator and sweating responses. / Davis, Scott L.; Shibasaki, Manabu; Low, David A.; Cui, Jian; Keller, David M.; Purdue, Gary F.; Hunt, John L.; Arnoldo, Brett D.; Kowalske, Karen J.; Crandall, Craig G.

In: Journal of Burn Care and Research, Vol. 28, No. 3, 01.05.2007, p. 435-441.

Research output: Contribution to journalArticle

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T1 - Skin grafting impairs postsynaptic cutaneous vasodilator and sweating responses

AU - Davis, Scott L.

AU - Shibasaki, Manabu

AU - Low, David A.

AU - Cui, Jian

AU - Keller, David M.

AU - Purdue, Gary F.

AU - Hunt, John L.

AU - Arnoldo, Brett D.

AU - Kowalske, Karen J.

AU - Crandall, Craig G.

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N2 - This study tested the hypothesis that postsynaptic cutaneous vascular responses to endothelial-dependent and -independent vasodilators as well as sweat gland function, are impaired in split-thickness grafted skin 5 to 9 months after surgery. Intradermal microdialysis membranes were placed in grafted and adjacent control skin, thereby allowing local delivery of the endothelial-dependent vasodilator, acetylcholine (ACh; 1 × 1017 to 1 × 10-1 M at 10-fold increments) and the endothelial-independent nitric oxide donor, sodium nitroprusside (SNP; 5 × 10-8 to 5 × 10-2 M at 10-fold increments). Skin blood flow and sweat rate were simultaneously assessed over the semipermeable portion of the membrane. Cutaneous vascular conductance (CVC) was calculated from the ratio of laser Doppler-derived skin blood flow to mean arterial blood pressure. ΔCVC responses from baseline to these drugs were modeled via nonlinear regression curve fitting to identify the dose of ACh and SNP causing 50% of the maximal vasodilator response (EC50). A rightward shift in the CVC dose response curve for ACh was observed in grafted (EC50 = -2.61 ± 0.44 log M) compared to adjacent control skin (EC50 = -3.34 ± 0.46 log M; P = .003), whereas the mean EC50 for SNP was similar between grafted (EC50 = -4.21 ± 0.94 log M) and adjacent control skin (EC50 = -3.87 ± 0.65 log M; P = 0.332). Only minimal sweating to exogenous ACh was observed in grafted skin whereas normal sweating was observed in control skin. Increased EC50 and decreased maximal CVC responses to the exogenous administration of ACh suggest impairment of endothelial-dependent cutaneous vasodilator responses in grafted skin 5 to 9 months after surgery. Greatly attenuated sweating responses to ACh suggests either abnormal or an absence of functional sweat glands in the grafted skin.

AB - This study tested the hypothesis that postsynaptic cutaneous vascular responses to endothelial-dependent and -independent vasodilators as well as sweat gland function, are impaired in split-thickness grafted skin 5 to 9 months after surgery. Intradermal microdialysis membranes were placed in grafted and adjacent control skin, thereby allowing local delivery of the endothelial-dependent vasodilator, acetylcholine (ACh; 1 × 1017 to 1 × 10-1 M at 10-fold increments) and the endothelial-independent nitric oxide donor, sodium nitroprusside (SNP; 5 × 10-8 to 5 × 10-2 M at 10-fold increments). Skin blood flow and sweat rate were simultaneously assessed over the semipermeable portion of the membrane. Cutaneous vascular conductance (CVC) was calculated from the ratio of laser Doppler-derived skin blood flow to mean arterial blood pressure. ΔCVC responses from baseline to these drugs were modeled via nonlinear regression curve fitting to identify the dose of ACh and SNP causing 50% of the maximal vasodilator response (EC50). A rightward shift in the CVC dose response curve for ACh was observed in grafted (EC50 = -2.61 ± 0.44 log M) compared to adjacent control skin (EC50 = -3.34 ± 0.46 log M; P = .003), whereas the mean EC50 for SNP was similar between grafted (EC50 = -4.21 ± 0.94 log M) and adjacent control skin (EC50 = -3.87 ± 0.65 log M; P = 0.332). Only minimal sweating to exogenous ACh was observed in grafted skin whereas normal sweating was observed in control skin. Increased EC50 and decreased maximal CVC responses to the exogenous administration of ACh suggest impairment of endothelial-dependent cutaneous vasodilator responses in grafted skin 5 to 9 months after surgery. Greatly attenuated sweating responses to ACh suggests either abnormal or an absence of functional sweat glands in the grafted skin.

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