Rahmiati Dwi Utari, Gunanti Gunanti, Noviana Deni, Soehartono Raden Harry, Harlina Eva
Postgraduate student of Veterinary Biomedical Sciences Study Program, School of Veterinary Medicine and Biomedical Sciences, IPB University, Dramaga, Indonesia.
Division of Surgery and Radiology, School of Veterinary Medicine and Biomedical Sciences, IPB University, Dramaga, Indonesia.
Open Vet J. 2025 Mar;15(3):1253-1263. doi: 10.5455/OVJ.2025.v15.i3.17. Epub 2025 Mar 31.
Hemorrhagic shock is a life-threatening condition resulting from acute blood loss, leading to compromised tissue perfusion and organ dysfunction. Currently, the guidelines for categorizing and managing hemorrhagic shock in pets are based on protocols developed for humans.
This study employed New Zealand White rabbits as an animal model to systematically evaluate the physiological and biochemical responses to fixed-volume hemorrhage, aiming to establish its role in inducing shock and significant physiological alterations.
A total of 21 New Zealand White rabbits, weighing 2-3 kg, were subjected to controlled hemorrhage by withdrawing 30%-35% of their total blood volume via the auricular artery using a 24-G IV catheter over 15 minutes. Parameters were assessed at baseline and 45 minutes post-induction.
Hemorrhage induced significant increases in heart rate and respiratory rate, reflecting compensatory mechanisms to maintain perfusion during shock. The mean arterial pressure and blood pressure significantly declined, consistent with hemorrhagic shock. Oxygen saturation initially decreased but partially recovered over time. All hematological variables decreased. Coagulopathy was indicated by prolonged prothrombin time and activated partial thromboplastin time. Elevated lactate levels indicate a shift to anaerobic metabolism due to hypoxia. The increased levels of interleukin-10 and tumor necrosis factor-alpha suggested an adaptive anti-inflammatory response to mitigate excessive inflammation.
Fixed-volume hemorrhage in New Zealand White rabbits induces the physiological changes characteristic of hemorrhagic shock, providing valuable insights into the pathophysiological response to acute blood loss.
失血性休克是一种由急性失血导致的危及生命的状况，会导致组织灌注受损和器官功能障碍。目前，宠物失血性休克的分类和管理指南是基于为人类制定的方案。
本研究以新西兰白兔作为动物模型，系统评估对固定容量出血的生理和生化反应，旨在确定其在诱导休克和显著生理改变中的作用。
总共21只体重2 - 3千克的新西兰白兔，通过使用24G静脉导管在15分钟内从耳动脉抽取其总血量的30% - 35%进行控制性出血。在基线和诱导后45分钟评估各项参数。
出血导致心率和呼吸频率显著增加，反映出在休克期间维持灌注的代偿机制。平均动脉压和血压显著下降，符合失血性休克表现。氧饱和度最初下降，但随时间部分恢复。所有血液学指标均下降。凝血酶原时间和活化部分凝血活酶时间延长表明存在凝血功能障碍。乳酸水平升高表明由于缺氧转向无氧代谢。白细胞介素 - 10和肿瘤坏死因子 - α水平升高表明存在适应性抗炎反应以减轻过度炎症。
新西兰白兔的固定容量出血诱导了失血性休克的特征性生理变化，为急性失血的病理生理反应提供了有价值的见解。
