Contractile function and myoplasmic free Ca2+ (Cam) in coronary and mesenteric arteries of endotoxemic guinea pigs.
Contractile function and myoplasmic free Ca2+ (Cam) in coronary and mesenteric arteries of endotoxemic guinea pigs.
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内毒素血症豚鼠冠状动脉和肠系膜动脉的收缩功能和肌质游离 Ca2 (Cam)。
DOI：
10.1097/00024382-199901000-00010
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Parker,JL
中科院分区：
文献类型：
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作者：
Jones,JJ;Rapps,JA;Sturek,M;Mattox,ML;Adams,HR;Parker,JL
内毒素引起的血管反应低下可能涉及血管平滑肌（VSM）肌浆游离钙（Cam）动员机制的改变。使用腹膜内（ip）注射盐水（对照；CON）或大肠杆菌内毒素脂多糖（LPS；4mg/kg）16小时后从豚鼠分离的冠状动脉（COR）和肠系膜（MES）动脉制剂（内径100-250μm）体外评估收缩功能和Cam（fura-2显微荧光法）调节。从 LPS 处理的动物中分离出的 COR 和 MES 动脉中，K+（5-100 mM）的浓度-反应关系显着增强。相反，LPS处理动物的COR和MES动脉对前列腺素F2α（PGF2α；1-100μM）的收缩反应明显受损，而内皮素-1（ET；1-100nM）介导的这些动脉的收缩反应在最大剂量（100nM）下增强。在COR动脉中，PGF2α(1-100μM)和ET(1-100nM)在CON和LPS组中产生Cam的双相增加。各组之间的初始瞬时峰值或继发持续 Cam 反应均未观察到显着差异，表明 LPS 对 COR 动脉中细胞内 Ca2+ 释放或 Ca2+ 流入机制缺乏影响。 MES动脉暴露于PGF2α和ET中，两组中Cam均产生浓度依赖性增加。然而，MES 动脉的 Cam 反应缺乏初始峰值反应，表明 COR 和 MES 动脉之间的 Cam 动员存在潜在差异。两组 MES 动脉中 Cam 对 K+(80 mM) 和 PGF2α(1-100 μM) 的反应相似；然而，与 CON MES 动脉相比，LPS 动脉中 ET 介导的 Cam 增加显着减弱。因此，内毒素血症对 COR 和 MES 动脉中的去极化（K+）和受体（PGF2α，ET）介导的收缩反应产生不同的影响。 VSM Cam 动员的减少似乎不太可能是 LPS 诱导的 COR 和 MES 动脉收缩功能受损的机制； LPS 对 COR 和 MES 动脉 VSM 功能的影响可能涉及其他机制（即收缩蛋白的 Ca2+ 敏感性降低）。
Endotoxin-induced vascular hyporesponsiveness could potentially involve alterations of vascular smooth muscle (VSM) myoplasmic free calcium (Cam) mobilization mechanisms. Contractile function and Cam (fura-2 microfluorometry) regulation were evaluated in vitro using coronary (COR) and mesenteric (MES) artery preparations (100-250 [mu] m inner diameter) isolated from guinea pigs 16 h after intraperitoneal (ip) injection of either saline (control; CON) or Escherichia coli endotoxin lipopolysaccharide (LPS; 4 mg/kg). Concentration-response relationships to K+(5-100 mM) were significantly enhanced in both COR and MES arteries isolated from LPS-treated animals. In contrast, contractile responses to prostaglandin F2 [alpha](PGF2 [alpha]; 1-100 [mu] M) were markedly impaired in COR and MES arteries from LPS-treated animals, while endothelin-1 (ET; 1-100 nM)-mediated contractile responses of these arteries were enhanced at the maximal dose (100 nM). In COR arteries, PGF2 [alpha](1-100 [mu] M) and ET (1-100 nM) produced biphasic increases in Cam in both CON and LPS groups. No significant differences were observed in either the initial transient peak or secondary sustained Cam responses between groups, suggesting a lack of effect of LPS upon intracellular Ca2+ release or Ca2+ influx mechanisms in COR arteries. Exposure of MES arteries to PGF2 [alpha] and ET produced concentration-dependent increases in Cam in both groups. However, Cam responses of MES arteries lacked initial peak responses, suggesting potential differences in Cam mobilization between COR and MES arteries. Cam responses to K+(80 mM) and PGF2 [alpha](1-100 [mu] M) were similar in MES arteries from both groups; however, ET-mediated increases in Cam were significantly blunted in LPS compared with CON MES arteries. Thus, endotoxemia produced differential effects upon depolarization (K+) and receptor (PGF2 [alpha], ET)-mediated contractile responses in both COR and MES arteries. Reductions in VSM Cam mobilization appear unlikely as a mechanism for LPS-induced impairment of contractile function of COR and MES arteries; other mechanisms (ie, decreased Ca2+ sensitivity of contractile proteins) may be involved in. effects of LPS upon VSM function of COR and MES arteries.