TY - JOUR
T1 - Nitric oxide and prostacyclin-dependent pathways involvement on in vitro induced hypothermia
AU - Evora, Paulo R.B.
AU - Cable, David G.
AU - Chua, Yeow L.
AU - Rodrigues, Alfredo J.
AU - Pearson, Paul J.
AU - Schaff, Hartzell V.
N1 - Funding Information:
Supported in part by: The Mayo Foundation (USA) and the CNPq – Conselho de Desenvolvimento Cientı´fico e Tecnológico (Brazil).
PY - 2007/2
Y1 - 2007/2
N2 - Nitric oxide and prostacyclin are endogenous endothelium-derived vasodilators, but little information is available on their release during hypothermia. This study was carried out to test the hypothesis that endothelium may modulate vascular reactivity to decreased temperature changes. Segments of contracted (prostaglandin F2α, 2 × 10-6 M) canine coronary, femoral, and renal arteries, with and without endothelium, were in vitro ("organ chambers") exposed to progressive hypothermia (from 37 to 10 °C) in graded steps. The study is limited to physiological measurements of vascular tone, in the presence or absence of PGI2 and/or NOS inhibitors, which show correlation with the relaxation. Hypothermia induced vasodilatation of vessels with intact endothelium, which became endothelium-independent below 20 °C. This vasodilatation began at 35 °C and, in the presence of indomethacin (2 × 10-6 M), at 30 °C. Endothelium-dependent vasodilatation to hypothermia was blocked by l-NMMA or l-NOARG (10-5 M), two competitive inhibitors of nitric oxide synthase (n = 5 each, P < 0.05). Oxyhemoglobin (2 × 10-6 M) also inhibited vasodilatation induced by hypothermia (n = 6, P < 0.05). Pretreatment with either atropine or pirenzepine (10-6 M) inhibited hypothermia-mediated vasodilatation (n = 5 each, P < 0.05). The present in vitro study concluded that the endothelium is sensitive to temperature variations and indicated that PGI2 and NO-dependent pathways may be involved endothelium-dependent relaxation to hypothermia. The endothelium-dependent vasodilatation to hypothermia, in systemic and coronary arteries, is mediated by the M1 muscarinic receptor.
AB - Nitric oxide and prostacyclin are endogenous endothelium-derived vasodilators, but little information is available on their release during hypothermia. This study was carried out to test the hypothesis that endothelium may modulate vascular reactivity to decreased temperature changes. Segments of contracted (prostaglandin F2α, 2 × 10-6 M) canine coronary, femoral, and renal arteries, with and without endothelium, were in vitro ("organ chambers") exposed to progressive hypothermia (from 37 to 10 °C) in graded steps. The study is limited to physiological measurements of vascular tone, in the presence or absence of PGI2 and/or NOS inhibitors, which show correlation with the relaxation. Hypothermia induced vasodilatation of vessels with intact endothelium, which became endothelium-independent below 20 °C. This vasodilatation began at 35 °C and, in the presence of indomethacin (2 × 10-6 M), at 30 °C. Endothelium-dependent vasodilatation to hypothermia was blocked by l-NMMA or l-NOARG (10-5 M), two competitive inhibitors of nitric oxide synthase (n = 5 each, P < 0.05). Oxyhemoglobin (2 × 10-6 M) also inhibited vasodilatation induced by hypothermia (n = 6, P < 0.05). Pretreatment with either atropine or pirenzepine (10-6 M) inhibited hypothermia-mediated vasodilatation (n = 5 each, P < 0.05). The present in vitro study concluded that the endothelium is sensitive to temperature variations and indicated that PGI2 and NO-dependent pathways may be involved endothelium-dependent relaxation to hypothermia. The endothelium-dependent vasodilatation to hypothermia, in systemic and coronary arteries, is mediated by the M1 muscarinic receptor.
KW - Endothelium
KW - Hypothermia
KW - Nitric oxide
KW - Prostacyclin
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U2 - 10.1016/j.cryobiol.2006.12.002
DO - 10.1016/j.cryobiol.2006.12.002
M3 - Article
C2 - 17274973
AN - SCOPUS:33847144098
SN - 0011-2240
VL - 54
SP - 106
EP - 113
JO - Cryobiology
JF - Cryobiology
IS - 1
ER -