Our objective was to test the hypothesis that acute exposure of human skin vasculature to nicotine may have deleterious effects on endothelial function. Vasoconstriction and vasorelaxation in isolated perfused human skin flaps (approximately 8 x 18 cm) derived from dermolipectomy specimens were assessed by studying changes in skin perfusion pressure measured by a pressure transducer, and skin perfusion was assessed by a dermofluorometry technique (n = 4 or 5). It was observed that nicotine (10(-7) M) amplified (P < 0.05) the norepinephrine (NE)-induced concentration-dependent (10(-7)-10(-5) M) increase in skin vasoconstriction compared with the control. This amplification effect of nicotine in NE-induced skin vasoconstriction was not blocked by the nicotine-receptor antagonist hexamethonium (10(-6) M) or the cyclooxygenase inhibitor indomethacin (10(-5) M). It was also observed that ACh and nitroglycerin (NTG) elicited a concentration-dependent (10(-8)-10(-5) M) vasorelaxation in skin flaps preconstricted with 8 x 10(-7) M of NE. The vasorelaxation induced by ACh was attenuated (P < 0.05) in the presence of nicotine (10(-7) M) compared with the control. However, skin vasorelaxation induced by NTG was not affected by nicotine (10(-7) M). ACh and NTG are known to induce endothelium-dependent and -independent vasorelaxation, respectively. The present findings were interpreted to indicate that acute exposure of human skin vasculature to nicotine was associated with 1) amplification of NE-induced skin vasoconstriction and 2) impairment of endothelium-dependent skin vasorelaxation. Cyclooxygenase products and nicotine receptors blocked by hexamethonium were not involved in the amplification of NE-induced skin vasoconstriction by nicotine. These findings may provide further insight into the pathogenesis of skin vasospasm in skin flap surgery and skin ischemic disease associated with cigarette smoking or use of smokeless tobacco.
The study validates theoretical relationships among concepts in the developmental model of health and nursing and contributes to better understanding health promotion in families led by adolescent mothers.
Pang. Pharmacological characterization of vasomotor activity of human musculocutaneous perforator artery and vein. J Appl Physiol 89: 2268-2275, 2000.-Vasospasm is one of the main causes of skin ischemic necrosis in cutaneous and musculocutaneous flap surgery, but the pathogenic mechanism is unclear. We planned to test the hypothesis derived from clinical impression that veins are more susceptible to vasospasm than arteries in flap surgery and, once established, that venous vasospasm is difficult to resolve and more detrimental than arterial vasospasm. To this end, we investigated the differences in sensitivity to vasoconstrictors and vasodilators between the human musculocutaneous perforator (MCP) artery and vein by measuring the isometric tension of arterial and venous rings suspended in organ chambers. Vascular contraction was expressed as a percentage of the tension induced by 50 mM KCl. Relaxation was expressed as a percentage of contraction induced by a submaximal concentration (3 ϫ 10 Ϫ9 M) of endothelin-1 (ET-1). We observed that the vasoconstrictor potency of norepinephrine was significantly higher in the MCP vein than in the MCP artery. The vasoconstrictor potency of ET-1 and the thromboxane A 2 mimetic U-46619 were similar in the MCP vein and artery, but the maximal contraction induced by ET-1 and U-46619 was significantly higher in the MCP vein than in the MCP artery. On the other hand, the MCP vein was less sensitive than the MCP artery to the relaxation effect of nitroglycerin, nifedipine, and lidocaine. These differences between the human MCP artery and vein in response to vasoactive agents lend support to the clinical impression in flap surgery that veins appear to be more susceptible to vasospasm than arteries and venous vasospasm seems to be more difficult to resolve than arterial vasospasm in cutaneous and musculocutaneous flap surgery.
Vasospasm in the vascular pedicle is a major cause of ischemic necrosis in autogenous skin transplantation (i.e., skin free flap surgery), and the pathophysiology is unclear. The clinical impression is that veins are more susceptible to vasospasm than arteries in the vascular pedicle of skin free flaps. The purpose of this study was to compare the vasoconstrictor response of the human radial artery (RA) and radial vein (RV) to endothelin (ET)-1 and to investigate the mechanism mediating ET-1-induced vasoconstriction. The isometric tension of RA and RV rings (4 mm) obtained from the vascular pedicle of human radial forearm skin free flaps were studied in organ chambers containing Krebs bicarbonate buffer. It was observed that ET-1 elicited concentration-dependent (5 x 10 (-11)to 2 x 10 (-8) ) contractions in RA and RV rings with similar contractile potency. However, the concentration-dependent contractile response to ET-1 was significantly (P < 0.05) higher in RV rings than in RA rings, with the maximum contractile response twice as high in RV rings than in RA rings. The contractile response to ET-1 in RA and RV rings was blocked by the ET receptor antagonist BQ 123 (10 (-5M)), but not by the ET receptor antagonist BQ 788 (5 x 10 (-6)). The ET(B) receptor agonist BQ 3020 (10 (-10) to 2 x 10(-8) ) had no significant contractile effect in RA and RV rings. Furthermore, the L-type Ca channel antagonist nifedipine (5 x 10 (-6)), the protein kinase C (PKC) inhibitor chelerythrine (10(-5M)), and the intracellular Ca chelator BAPTA-AM (10(-5M)) significantly reduced the contractile potency of ET-1 in RA rings and the maximum contractile response to ET-1 in RA and RV rings. It was concluded that the human RV is more responsive than RA to the contractile effect of ET-1. The contractile response to ET-1 in RA and RV is predominantly mediated by ET(A) receptors and the postreceptor mechanism involves L-type Ca (2+) channels, PKC, and intracellular Ca(2+).
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