Effects of Graded Hyperventilation on Cerebral Blood Flow Autoregulation in Experimental Subarachnoid Hemorrhage

Abstract

An impaired CBF autoregulation can be restored by hyperventilation at a PaCO2 level of about 2.9 to 4.1 kPa (22 to 31 mm Hg). However, it is uncertain whether the restoring effect can take place at lesser degrees of hypocapnia. In the current study, CBF autoregulation was studied at four PaCO2 levels: 5.33 kPa (40 mm Hg, normoventilation), 4.67 kPa (35 mm Hg, slight hyperventilation), 4.00 kPa (30 mm Hg, moderate hyperventilation), and 3.33 kPa (25 mm Hg, profound hyperventilation). At each PaCO2 level, eight rats 2 days after experimental subarachnoid hemorrhage (SAH) and eight sham-operated controls were studied. The CBF was measured by the intracarotid 133Xe method. The CBF autoregulation was found to be intact in all controls but completely disturbed in the normoventilated SAH rats. However, by slight hyperventilation, CBF autoregulation was restored in seven of eight SAH rats with a decline in CBF of 10%. The CBF autoregulation was found intact in all of the moderately or profoundly hyperventilated SAH rats, whereas the decline in CBF was 21% and 28%, respectively. In conclusion, hyperventilation to a PaCO2 level between 4.00 and 4.67 kPa (30 to 35 mm Hg) appears to be sufficient for reestablishing an impaired autoregulation after SAH.

Effect of Graded Hyperventilation on Cerebral Metabolism in a Cisterna Magna Blood Injection Model of Subarachnoid Hemorrhage in Rats

“…In the same model of SAH, we have demonstrated that hyperventilation at P a CO 2 between 4.00 and 4.67 kPa normalizes a defective CBF autoregulation. 7,8 Taking into account that hyperventilation at a P a CO 2 of 3.33-4.30 kPa (25-32 mm Hg) in most cases exerts an effective control of ICP, 34 it appears that hyperventilation at a P a CO 2 lower than 3.33 kPa may be neither beneficial nor necessary. The present methods used in determining CBF and CMR reflect only global changes.…”

“…7,8,25,26,35,36 Prunell et al 37 recently compared three different models of SAH in SpragueDawley rats: SAH was induced either by injection of 0.3 mL of autologous blood into the cisterna magna, by endovascular perforation of the internal carotid artery or by injection of 0.2 mL of autologous blood into the prechiasmatic cistern. No mortality was found in the cisterna magna SAH group in contrast to mortality rates of 44% and 25% in the perforation SAH group and prechiasmatic SAH group, respectively.…”

“…At this time, after experimental SAH, a significant cerebrovascular instability is known to be present. 8,[25][26][27] On the day of the experiment, the animal was again anesthetized with a mixture of 2% halothane in 70% N 2 O and 30% O 2 . After tracheotomy, the animal was connected to a respirator, and for the rest of the experiment the concentration of halothane was reduced to 0.06%.…”

“…[1][2][3][4] Furthermore, hyperventilation seems to normalize an impaired cerebral autoregulation. [5][6][7][8] Because of the cerebral CO 2 reactivity, hyperventilation leads to constriction of the cerebral resistance vessels. Hyperventilation reduces not only the intracranial pressure (ICP) through a reduction of the cerebral blood volume, but it also effectively reduces cerebral blood flow (CBF).…”

“…This model is well established for the study of cerebrovascular dysfunction in the late SAH phase. 7,8 The hypothesis to be tested is that the reduction in plasma CO 2 induced by hyperventilation does not substantially lower cerebral oxidative metabolism in either normal rats or at 48 hours after SAH in this rat model.…”