The effects of anesthetics on transmembrane potential, transmembrane currents and EDHF in resistance and capacitance blood vessels (microcirculation)

我们通过测量小肠系膜动脉和静脉血管平滑肌（VSM）跨膜电位的原位反应，间接评价了麻醉剂对SD大鼠血管平滑肌（VSM）张力的体内影响。在麻醉药或抑制剂输注血管之前、期间和之后进行测量。吸入麻醉剂可减弱交感神经和非神经对VSM跨膜电位和张力的调节。在人类高血压的神经源性SH大鼠模型中，异氟醚诱导的抵抗和容量调节血管中VSM极化升高的主要机制是中枢神经抑制兴奋性交感神经输入。异氟醚在SH和WKY大鼠vsm中的外周神经和非神经介导的超极化相似。在存在和不存在四种钾通道的选择性抑制剂的情况下进行了测量。异丙酚介导的VSM超极化可以部分归因于K_Ca和K_ATP的开放，而不是K_V和k_ir的开放。动脉超极化，静脉超极化。异丙酚可消除疼痛诱导的EDHF超极化。这些结果表明，异丙酚减弱了交感神经和非神经对VSM音调的调节。他们还认为异丙酚和乙酰胆碱可能在第二信使级联中相互竞争，调节系膜抵抗动脉中VSMK^+通道的活性。异丙酚介导的VSM超极化可部分归因于NO-cGMP途径，而非PGI_2-cAMP途径。

We indirectly assessed the in vivo effect of anesthetics on vascular smooth muscle (VSM) tone in SD rats by measurement of in situ responses of VSM transmembrane potential in small mesenteric arteries and veins. Measurements were made before, during, and after anesthetic or inhibitor infusions into vessels.1. Inhaled anesthetics attenuate both sympathetic neural and nonneural regulation of VSM transmembrane potentials and tone.2. In the neurogenic SH rat model of human hypertension, a primary mechanism underlying elevated isoflurane-induced VSM heperpolarization in both resistance- and capacitance-regulating blood vessels is a central neural inhibition of excitatory sympathetic input. Peripheral neural and nonneurally mediated hyperpolarization by isoflurane is similar in SH and WKY rat VSM.3. Measurements were taken in the presence and absence of selective inhibitors of eaeh of four types of potassium channels. Propofol-mediated hyperpolarization of VSM can be attributed in part to an opening of K_Ca and K_ATP but not K_V and K_IR.4. Ach hyperpolarized arterial, but not venous VSM. Ach-induced (EDHF) hyperpolarization was eliminated by propofol. These results suggest that propofol attenuates both sympathetic neural and nonneural regulation of VSM tone. They also suggest that propofol and Ach may act competitively in the second messenger cascade regulating VSMK^+ channel activity in mesenteric resistance arteries.5. Propofol-mediated hyperpolarization of VSM can be attributed in part to NO-cGMP pathway but not PGI_2-cAMP pathway.