Cortical Blood Flow and Cerebral Perfusion Pressure in a New Noncraniotomy Model of Subarachnoid Hemorrhage in the Rat

TLDR

Acute cerebral ischemia after SAH is a major morbidity cause, but its exact etiology remains unclear. The study aimed to investigate how cerebral perfusion pressure relates to cortical blood flow during SAH in a novel rat model. SAH was induced by a suture perforating the internal carotid artery, and CPP, cortical laser‑Doppler flow, and EEG were continuously recorded in 16 ventilated rats. In this model, 50 % of rats died within 24 h, CPP fell rapidly to a nadir 59 s after SAH while cortical blood flow fell similarly but later, and subsequent reductions in flow were not correlated with CPP changes, suggesting secondary mechanisms such as vasoconstriction; the model offers advantages over existing SAH models.

Abstract

Acute cerebral ischemia after subarachnoid hemorrhage (SAH) is a major cause of morbidity whose precise etiology is unclear. The purpose of this study was to examine the relationships between cerebral perfusion pressure (CPP) and cortical blood flow during SAH using a new experimental model in the rat.CPP (mean arterial pressure minus intracranial pressure), cortical laser-Doppler flowmetry (LDF), and electroencephalogram were continuously recorded during and after SAH in 16 ventilated rats. SAH was produced by advancing an intraluminal suture from the external carotid artery through the internal carotid artery to perforate the vessel near its intracranial bifurcation.Eight rats (50%) died within 24 hours of SAH. In all rats, blood was widely distributed throughout the basal, convexity, and interhemispheric subarachnoid spaces and throughout the ventricular system. CPP decreased after SAH at an initial rate of 1.1 +/- 0.2 mm Hg/s, reaching its nadir 59 +/- 9 seconds after the onset of SAH. During the same period, LDF fell at a rate of 1.4 +/- 0.3%/s (P = NS vs CPP). After reaching its nadir, CPP rose at a rate of 0.4 +/- 0.01 mm Hg/s, but LDF continued to fall at 0.2 +/- 0.03%/s (P < .05 vs CPP) reaching a nadir of 21.7 +/- 2.5% significantly later than CPP (189.5 +/- 39 s after SAH, P < .05). No correlation was found between peak changes in CPP and LDF. Electroencephalogram activity followed the changes in LDF, reaching nadir values 289 +/- 55 seconds after SAH.These findings demonstrate that although reduced CPP causes the initial decrease in cortical blood flow after SAH, secondary reductions occurring after CPP has reached its nadir are caused by other factors such as acute vasoconstriction. This noncraniotomy model of SAH in the rat has several advantages over existing models.