Experimental subarachnoid hemorrhage: subarachnoid blood volume, mortality rate, neuronal death, cerebral blood flow, and perfusion pressure in three different rat models

• Published in: Neurosurgery Vol. 52; no. 1; p. 165
• Main Authors: Prunell, Giselle Fabiana, Mathiesen, Tiit, Diemer, Nils Henrik, Svendgaard, Niels-Aage
• Format: Journal Article
• Language: English
• Published: United States 01.01.2003
• Subjects: Animals; Blood Flow Velocity - physiology; Blood Pressure - physiology; Blood Volume - physiology; Brain - blood supply; Brain - pathology; Brain Ischemia - mortality; Brain Ischemia - pathology; Brain Ischemia - physiopathology; Cell Death - physiology; Disease Models, Animal; Intracranial Pressure - physiology; Male; Neurons - pathology; Rats; Rats, Sprague-Dawley; Regional Blood Flow - physiology; Subarachnoid Hemorrhage - mortality; Subarachnoid Hemorrhage - pathology; Subarachnoid Hemorrhage - physiopathology; Survival Rate; Vasospasm, Intracranial - mortality; Vasospasm, Intracranial - pathology; Vasospasm, Intracranial - physiopathology
• ISSN: 0148-396X
• DOI: 10.1097/00006123-200301000-00022

To investigate which of three subarachnoid hemorrhage (SAH) models is the most suitable for studies of pathological and pathophysiological processes after SAH. SAH was induced in rats via intracranial endovascular perforation (perforation model), blood injection into the cisterna magna (300 microl), or blood injection into the prechiasmatic cistern (200 microl). The subarachnoid blood volume was quantitatively measured. Cerebral blood flow (CBF) (as assessed with laser Doppler flowmetry), intracranial pressure, and mean arterial blood pressure were recorded for 90 minutes after SAH. Mortality was recorded, and neuronal death was assessed in animals that survived 7 days after SAH. The subarachnoid blood volume was close to the injected amount after prechiasmatic SAH. In the other models, the volume varied between 40 and 480 microl. The mortality rates were 44% in the perforation SAH group, 25% in the prechiasmatic SAH group, and 0% in the cisterna magna SAH group; the corresponding values for neuronal death were 11, 44, and 28%. Cerebral perfusion pressure approached baseline values within 5 minutes after SAH in all three models. CBF decreased to approximately 35% of baseline values immediately after SAH in all groups; it gradually increased to normal values 15 minutes after SAH in the cisterna magna SAH group and to 60 and 89% of baseline values 90 minutes post-SAH in the perforation and prechiasmatic SAH groups. CBF was significantly correlated with the subarachnoid blood volume. The prechiasmatic SAH model seems to be the most suitable for study of the sequelae after SAH; it produces a significant decrease in CBF, an acceptable mortality rate, and substantial pathological lesions, with high reproducibility. The CBF reduction is predominantly dependent on the amount of subarachnoid blood.