Abstract
Background:
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.

Aim:
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.

Methods:
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 24G IV catheter over 15 minutes. Parameters were assessed at baseline and at 45 minutes post-induction.

Results:
Hemorrhage induced significant increases in heart rate (HR) and respiratory rate (RR), reflecting compensatory mechanisms to maintain perfusion during shock. Mean arterial pressure (MAP) and blood pressure significantly declined, consistent with hemorrhagic shock. Oxygen saturation (SpO2) initially decreased and showed a partial recovery over time. All hematological variables decreased. Coagulopathy was evidenced by prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT). Elevated lactate levels indicated a shift to anaerobic metabolism due to hypoxia. The increase in IL-10 and TNF-α suggested an adaptive anti-inflammatory response to mitigate excessive inflammation.

Conclusion:
Fixed-volume hemorrhage in New Zealand White rabbits induces physiological changes characteristic of hemorrhagic shock, providing valuable insights into the pathophysiological responses to acute blood loss.

Key words: Animal model, Coagulation, Fixed volume, Hemorrhage, Inflammation