Sudden Death in a Rat Subarachnoid Hemorrhage Model

Abstract

The pathogenesis of sudden death during subarachnoid hemorrhage (SAH) still remains to be eluci dated. A new rat common carotid artery-prechiasmal extracorporeal shunt model was designed to study the effect of different severities of SAH on intracranial pressure (ICP), regional cerebral blood flow (rCBF), and mortality. Different severities of SAH were induced by controlling the bleeding period (from 30 to 90 sec) and number of bleedings (one or three times). SAH caused a dramatic increase in ICP and immediate depression of rCBF, which recovered slowly to a certain extent. ICP increased sharply within the first 30 seconds and reached a plateau concomitant with nearly zero rCBF, which suggested the occurrence of cerebral circulation arrest. Bleeding of more than 60 seconds and increased ICP over 80 mmHg were directly correlated with the mortality. Respiratory arrest was the first sign of death, immediately followed by cardiac depression resulting in sudden death. This model combines arterial bleeding with systemic blood pressure and controlled bleeding time to simulate the acute period of SAH.

Differentiating between comatose patients resuscitated from acute coronary syndrome-associated and subarachnoid hemorrhage-associated out-of-hospital cardiac arrest

“…These observations suggest that SAH should be considered when PEA/asystole is the initial cardiac rhythm in OHCA patients. Experimental studies have shown that the mechanism of cardiac arrest secondary to SAH has been attributed to a sudden increase in intracranial pressure caused by SAH, which results in brainstem herniation leading to respiratory arrest [30]. Asphyxia-induced hypoxia causes asystole rather than VF [31].…”

Subarachnoid Hemorrhage Causing Cardiopulmonary Arrest: Resuscitation Profiles and Outcomes

“…After massive bleeding into the subarachnoid space, sharp ICP rise results in substantial decrease or even transient arrest of the cerebral blood flow (CBF). 21) In SAH-CPA patients, the narrower therapeutic window may be attributed to the combined detrimental effect of SAH-induced CBF reduction and cessation of systemic blood flow.…”

Experimental Subarachnoid Hemorrhage: Subarachnoid Blood Volume, Mortality Rate, Neuronal Death, Cerebral Blood Flow, and Perfusion Pressure in Three Different Rat Models

“…After experimental SAH in rats, CBF has been observed to decrease for at least 1 hour (2,3,20,37,43,47). The mechanism underlying CBF reduction is not clearly understood.…”