Decreased nitric oxide production following extremity ischemia and reperfusion

John Blebea; Bradley Bacik; Gregory Strothman; Leslie Myatt

doi:10.1016/S0002-9610(96)00141-9

Decreased nitric oxide production following extremity ischemia and reperfusion

John Blebea, Bradley Bacik, Gregory Strothman, Leslie Myatt

Research output: Contribution to journal › Article › peer-review

26 Scopus citations

Abstract

BACKGROUND: Nitric oxide (NO), the endogenous vasodilator, is an important regulator of vascular tone. We investigated NO production following lower extremity ischemia. METHODS: Rabbits underwent 6 hours of bilateral leg ischemia followed by unrestricted reperfusion. Physiologic parameters were continuously measured and blood was assayed for NO₂ and NO₃. RESULTS: Acute ischemia of the lower extremities produced an immediate increase in mean arterial blood pressure while later reperfusion induced a significant decrease (P < 0.0005). There was a fall in femoral blood flow during reperfusion. NO₂/NO₃ concentrations decreased significantly to 89% of baseline values after ischemia and 77% after 1 hour of reperfusion (P < 0.005). A significantly higher mortality was found in association with decreased NO₂/NO₃ concentrations. CONCLUSIONS: Nitric oxide appears to be a regulator of regional blood flow during reperfusion following extremity ischemia. Decreased NO production may contribute to impaired regional blood flow and mortality.

Original language	English (US)
Pages (from-to)	158-162
Number of pages	5
Journal	American journal of surgery
Volume	172
Issue number	2
DOIs	https://doi.org/10.1016/S0002-9610(96)00141-9
State	Published - Aug 1996
Externally published	Yes

ASJC Scopus subject areas

Surgery

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10.1016/S0002-9610(96)00141-9

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@article{7d4cdf816378409fb2d4b73e26ab66ab,

title = "Decreased nitric oxide production following extremity ischemia and reperfusion",

abstract = "BACKGROUND: Nitric oxide (NO), the endogenous vasodilator, is an important regulator of vascular tone. We investigated NO production following lower extremity ischemia. METHODS: Rabbits underwent 6 hours of bilateral leg ischemia followed by unrestricted reperfusion. Physiologic parameters were continuously measured and blood was assayed for NO2 and NO3. RESULTS: Acute ischemia of the lower extremities produced an immediate increase in mean arterial blood pressure while later reperfusion induced a significant decrease (P < 0.0005). There was a fall in femoral blood flow during reperfusion. NO2/NO3 concentrations decreased significantly to 89% of baseline values after ischemia and 77% after 1 hour of reperfusion (P < 0.005). A significantly higher mortality was found in association with decreased NO2/NO3 concentrations. CONCLUSIONS: Nitric oxide appears to be a regulator of regional blood flow during reperfusion following extremity ischemia. Decreased NO production may contribute to impaired regional blood flow and mortality.",

author = "John Blebea and Bradley Bacik and Gregory Strothman and Leslie Myatt",

note = "Funding Information: This study was supported by research grant from the American Heart Association, Ohio Affiliate (JB).",

year = "1996",

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doi = "10.1016/S0002-9610(96)00141-9",

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volume = "172",

pages = "158--162",

journal = "American journal of surgery",

issn = "0002-9610",

publisher = "Elsevier Inc.",

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TY - JOUR

T1 - Decreased nitric oxide production following extremity ischemia and reperfusion

AU - Blebea, John

AU - Bacik, Bradley

AU - Strothman, Gregory

AU - Myatt, Leslie

N1 - Funding Information: This study was supported by research grant from the American Heart Association, Ohio Affiliate (JB).

PY - 1996/8

Y1 - 1996/8

N2 - BACKGROUND: Nitric oxide (NO), the endogenous vasodilator, is an important regulator of vascular tone. We investigated NO production following lower extremity ischemia. METHODS: Rabbits underwent 6 hours of bilateral leg ischemia followed by unrestricted reperfusion. Physiologic parameters were continuously measured and blood was assayed for NO2 and NO3. RESULTS: Acute ischemia of the lower extremities produced an immediate increase in mean arterial blood pressure while later reperfusion induced a significant decrease (P < 0.0005). There was a fall in femoral blood flow during reperfusion. NO2/NO3 concentrations decreased significantly to 89% of baseline values after ischemia and 77% after 1 hour of reperfusion (P < 0.005). A significantly higher mortality was found in association with decreased NO2/NO3 concentrations. CONCLUSIONS: Nitric oxide appears to be a regulator of regional blood flow during reperfusion following extremity ischemia. Decreased NO production may contribute to impaired regional blood flow and mortality.

AB - BACKGROUND: Nitric oxide (NO), the endogenous vasodilator, is an important regulator of vascular tone. We investigated NO production following lower extremity ischemia. METHODS: Rabbits underwent 6 hours of bilateral leg ischemia followed by unrestricted reperfusion. Physiologic parameters were continuously measured and blood was assayed for NO2 and NO3. RESULTS: Acute ischemia of the lower extremities produced an immediate increase in mean arterial blood pressure while later reperfusion induced a significant decrease (P < 0.0005). There was a fall in femoral blood flow during reperfusion. NO2/NO3 concentrations decreased significantly to 89% of baseline values after ischemia and 77% after 1 hour of reperfusion (P < 0.005). A significantly higher mortality was found in association with decreased NO2/NO3 concentrations. CONCLUSIONS: Nitric oxide appears to be a regulator of regional blood flow during reperfusion following extremity ischemia. Decreased NO production may contribute to impaired regional blood flow and mortality.

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JO - American journal of surgery

JF - American journal of surgery

IS - 2

ER -

Decreased nitric oxide production following extremity ischemia and reperfusion

Abstract

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