Baxter G M
Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Ft Collins, USA.
Vet Surg. 1995 Mar-Apr;24(2):87-96. doi: 10.1111/j.1532-950x.1995.tb01301.x.
Low doses of endotoxin cause vasoconstriction and hypoperfusion of the digit, small intestine, and cecum in horses. To determine the potential cause of these vascular alterations, in vitro vascular responses of palmar digital arteries and veins were determined in 8 horses after intravenous (IV) infusion of 1 L 0.9% NaCl (control) and 0.1 microgram/kg Escherichia coli 055:B5 endotoxin in 1 L of 0.9% NaCl (endotoxin-treated). Vessels were surgically removed under general anesthesia, cut into 4-mm vascular rings, suspended in tissue baths, and attached to force displacement transducers for measurement of vascular tension. Cumulative concentration response curves to acetylcholine, bradykinin, nitroprusside, norepinephrine, 5-hydroxytryptamine (serotonin), and endothelin were determined. Maximal relaxation or contraction and the concentrations needed to produce 50% maximal relaxation or contraction were determined. Palmar digital arteries from endotoxin-treated horses relaxed significantly less in response to acetylcholine and bradykinin (endothelium-dependent), but not to nitroprusside (endothelium-independent) when compared with arteries from control horses. Digital arteries from endotoxin-treated horses also contracted significantly more with norepinephrine but less with serotonin. Digital veins responded less than digital arteries. In another study, vascular reactivity experiments documented that acetylcholine and bradykinin were endothelium-dependent vasodilators (endothelium-denuded vessels relaxed less than control vessels) in palmar digital vessels. Additionally, maximal relaxations for both vasodilators were significantly inhibited by N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide antagonist, suggesting that acetylcholine and bradykinin cause relaxation through the nitric oxide pathway. The data from these studies indicate that low dose endotoxin impairs endothelium-dependent relaxation and augments adrenergic contraction of palmar digital arteries in horses.
低剂量内毒素可导致马的指部、小肠和盲肠血管收缩及灌注不足。为确定这些血管改变的潜在原因，对8匹马进行静脉注射（IV）1升0.9%氯化钠（对照）和1升含0.1微克/千克大肠杆菌055:B5内毒素的0.9%氯化钠（内毒素处理组）后，测定了掌指动脉和静脉的体外血管反应。在全身麻醉下手术取出血管，切成4毫米的血管环，悬挂于组织浴中，并连接到力位移换能器以测量血管张力。测定了对乙酰胆碱、缓激肽、硝普钠、去甲肾上腺素、5-羟色胺（血清素）和内皮素的累积浓度反应曲线。确定了最大舒张或收缩以及产生50%最大舒张或收缩所需的浓度。与对照马的动脉相比，内毒素处理组马的掌指动脉对乙酰胆碱和缓激肽（内皮依赖性）的舒张反应明显减弱，但对硝普钠（非内皮依赖性）的反应无明显差异。内毒素处理组马的指动脉对去甲肾上腺素的收缩反应明显增强，但对血清素的反应减弱。指静脉的反应小于指动脉。在另一项研究中，血管反应性实验证明，乙酰胆碱和缓激肽是掌指血管中内皮依赖性血管舒张剂（内皮剥脱的血管舒张程度小于对照血管）。此外，一氧化氮拮抗剂N-硝基-L-精氨酸甲酯（L-NAME）显著抑制了两种血管舒张剂的最大舒张，表明乙酰胆碱和缓激肽通过一氧化氮途径引起舒张。这些研究的数据表明，低剂量内毒素损害了马掌指动脉的内皮依赖性舒张，并增强了肾上腺素能收缩。
