Clinical Department of Anesthesiology and Intensive Therapy, Wroclaw Medical University, Wroclaw, Poland.
Department of Anesthesia and Intensive Care, Karolinska Institutet at Danderyd Hospital, Stockholm, Sweden.
Arch Immunol Ther Exp (Warsz). 2024 Jun 7;72(1). doi: 10.2478/aite-2024-0011. eCollection 2024 Jan 1.
This is an animal model study to investigate changes in hemostasis during endotoxemic shock and to determine whether the combination of inhaled nitric oxide (iNO) + intravenous hydrocortisone had an effect on clot formation and fibrinolysis. iNO selectively decreases pulmonary artery pressure, without affecting cardiac index or systemic vascular resistance; however, the results of studies on the possible consequences of iNO administration on coagulation are inconsistent and require further research. Thirty-four piglets were included. Administering endotoxin caused severe hypodynamic shock. Half of the animals received iNO (30 ppm) + hydrocortisone, starting 3 h after endotoxin infusion and continuing to the end of the study. All animals developed coagulation disorders, manifested by a tendency to hypocoagulation; at the same time, fibrinolysis was impaired. Coagulation and fibrinolysis disorders persisted after endotoxin infusion was discontinued, with worse severity in the animals that died before the study was terminated. Administering iNO + hydrocortisone did not cause further changes in coagulation and fibrinolysis parameters, either during or after the endotoxin challenge, suggesting that potential therapeutic interventions with iNO to lower pulmonary arterial pressure will not affect hemostasis.
这是一项动物模型研究,旨在探讨内毒素性休克期间止血功能的变化,并确定吸入一氧化氮(iNO)+静脉注射氢化可的松的联合用药对内凝块形成和纤维蛋白溶解的影响。iNO 选择性降低肺动脉压,而不影响心指数或全身血管阻力;然而,关于 iNO 给药对凝血可能产生的后果的研究结果不一致,需要进一步研究。34 头小猪被纳入研究。给予内毒素可导致严重的低动力性休克。一半的动物接受 iNO(30ppm)+氢化可的松治疗,从内毒素输注后 3 小时开始,持续到研究结束。所有动物均出现凝血障碍,表现为低凝倾向;同时,纤维蛋白溶解受到损害。在停止内毒素输注后,凝血和纤维蛋白溶解障碍仍然存在,在研究结束前死亡的动物的严重程度更差。在接受内毒素挑战期间和之后,给予 iNO+氢化可的松并未导致凝血和纤维蛋白溶解参数进一步变化,这表明潜在的用 iNO 降低肺动脉压的治疗干预措施不会影响止血功能。