Effect of Isoflurane on Skin-Pressure-Induced Vasodilation

Abstract

Since general anesthesia has been shown to attenuate endothelium-dependent vasodilation, it was of interest to verify whether general anesthesia would modify skin vasodilation in response to local pressure application, which is endothelium dependent. To study the effect of general anesthesia on pressure-induced vasodilation development, we examined the effects of low- and high-dose isoflurane. Skin blood flow was measured by laser Doppler flowmetry during 11.1 Pa s^–1 increases in locally applied pressure in anesthetized rats treated with low or high doses of isoflurane. Following the administration of low doses of isoflurane, skin blood flow increased from baseline, with increasing local pressure application (+37 ± 10% at 2.0 kPa). The increase in skin blood flow was absent in rats treated with high doses (–20 ± 5% at 2.0 kPa), even when the anesthesia-induced hypotension was corrected by gelofusine infusion (–20 ± 10% at 2.0 kPa). Whereas sodium-nitroprusside-induced vasodilation developed following low and high doses of isoflurane, acetylcholine-induced vasodilation was impaired with high doses compared to low doses. These data show that pressure-induced vasodilation is abolished with high doses of anesthetics. It is not the anesthesia-induced hypotension, but the depth of anesthesia, which can lead to the disappearance of pressure-induced vasodilation by an alteration in endothelial function.

[11C]Acetate rest–stress protocol to assess myocardial perfusion and oxygen consumption reserve in a model of congestive heart failure in rats

“…It has been reported that anesthesia led to a decrease in the systemic blood pressure compared to the values obtained with in conscious cats [36]. We believe that this effect is brought about by the use of isoflurane 1.5% while the animal is under spontaneous breathing conditions [37]. This unavoidable effect of anesthesia, which may affect the baseline values of MBF and MVO 2 , did not mask the effects of the drugs used in this study with the observation of a significant impact of pharmacological action on MBF and MVO 2 values determined with [ 11 C]acetate.…”

Evidence for the involvement of VPAC1 and VPAC2 receptors in pressure‐induced vasodilatation in rodents

“…PIV is related to the integrity of vascular and endothelial vasodilator capacities (Fromy et al 2000 b ; Fizanne et al 2003). On the one hand, sodium nitroprusside causes vasodilatation by directly relaxing vascular smooth muscle cells.…”

Neuroendocrine pathway involvement in the loss of the cutaneous pressure‐induced vasodilatation during acute pain in rats

“…Accordingly, interruption of the interaction between nervous and vascular systems would disrupt PIV, which relies on both systems. This would induce an inability of the cutaneous microcirculation to adapt to the applied pressure, as observed in deep anaesthesia (Fizanne et al 2003) and diabetes (Fromy et al 2002; Koitka et al 2004; Sigaudo‐Roussel et al 2004; Demiot et al 2006 a ). As usually described by clinicians, we showed using PIV assessment that long‐term diabetes with a severe neuropathy as well as vascular dysfunction aggravated the inability of the cutaneous microcirculation to adapt to pressure (Demiot et al 2006 b ), a mechanism which is very likely to be involved in diabetic foot lesions.…”