» Articles » PMID: 12493115

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

Overview
Journal Neurosurgery
Specialty Neurosurgery
Date 2002 Dec 21
PMID 12493115
Citations 78
Authors
Affiliations
Soon will be listed here.
Abstract

Objective: To investigate which of three subarachnoid hemorrhage (SAH) models is the most suitable for studies of pathological and pathophysiological processes after SAH.

Methods: 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.

Results: 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.

Conclusion: 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.

Citing Articles

Inflammatory changes in the choroid plexus following subarachnoid hemorrhage: the role of innate immune receptors and inflammatory molecules.

Solar P, Brazda V, Bares M, Zamani A, EmamiAref P, Joukal A Front Cell Neurosci. 2025; 18():1525415.

PMID: 39839349 PMC: 11747387. DOI: 10.3389/fncel.2024.1525415.


Progressive histological and behavioral deterioration of a novel mouse model of secondary hydrocephalus after subarachnoid hemorrhage.

Deng X, Ding J, Liu C, Wang Z, Wang J, Duan Q Sci Rep. 2024; 14(1):31794.

PMID: 39738570 PMC: 11685592. DOI: 10.1038/s41598-024-82843-4.


Establishment of a novel protocol for assessing the severity of subarachnoid hemorrhage in circle Willis perforation mouse model.

Zhang R, Khan D, Muhammad S Sci Rep. 2024; 14(1):10147.

PMID: 38698100 PMC: 11066000. DOI: 10.1038/s41598-024-60237-w.


Secondary Ischemia Assessment in Murine and Rat Preclinical Subarachnoid Hemorrhage Models: A Systematic Review.

Furstenau E, Lindauer U, Koch H, Hollig A J Am Heart Assoc. 2024; 13(5):e032694.

PMID: 38420758 PMC: 10944078. DOI: 10.1161/JAHA.123.032694.


The Role of Serum Monocytes and Tissue Macrophages in Driving Left Ventricular Systolic Dysfunction and Cardiac Inflammation Following Subarachnoid Hemorrhage.

Geraghty J, Saini N, Deshpande A, Cheng T, Nazir N, Testai F Neurocrit Care. 2023; 40(3):1127-1139.

PMID: 38062302 DOI: 10.1007/s12028-023-01891-2.