title: Cerebral blood flow autoregulation following subarachnoid hemorrhage in rats: chronic vasospasm shifts the upper and lower limits of the autoregulatory range toward higher blood pressures.
abstract: We sought to determine whether chronic vasospasm following subarachnoid hemorrhage (SAH) would abolish the cerebral blood flow (CBF) autoregulation in anesthetized Sprague-Dawley rats. SAH was induced by intracisternal injection of autologous blood; in control animals saline was injected instead. CBF was measured 48 h after SAH, that is during chronic vasospasm, by laser-Doppler flowmetry over the frontal cortex under condition of hypertension (SAH, n = 6; control, n = 8) or hypotension (SAH, n = 6; control, n = 6). Hyper- and hypotension were induced by increasing mean arterial blood pressure (MABP) stepwise from 90 to 180 mmHg with phenylephrine (0.1-10 micrograms/min i.v.), or by decreasing it from 90 to 40 mmHg by controlled hemorrhage. An autoregulatory index (AI) expressed as delta CBF (%) per 10 mmHg increase or decrease in MABP was employed to analyze CBF response. CBF remained constant (-7 < AI < 7) at MABPs ranging from 60 to 130 mmHg in the control group and from 70 to 140 mmHg in the SAH group, showing CBF autoregulation. In the SAH group, that is, the upper and the lower limits of autoregulatory range were increased by 10 mmHg (p < 0.05). SAH did not increase intracranial pressure significantly (control 9.2 +/- 0.67 vs. SAH 10.0 +/- 1.05 mmHg, n = 5) 48 h after SAH was induced. These results indicate that, during chronic vasospasm, SAH does not abolish the autoregulation process but raises its lower and upper blood pressure limits. The capacity of spastic cerebral arteries to dilate in case of hypotension decreased, while their tolerance to hypertension increased.
authors.affiliation: Department of Neurosurgery, Hamamatsu University School of Medicine, Japan. seijiy@hama-med.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Yamamoto
authors.forename: S
authors.initials: S
authors.lastname: Nishizawa
authors.forename: H
authors.initials: H
authors.lastname: Tsukada
authors.forename: T
authors.initials: T
authors.lastname: Kakiuchi
authors.forename: T
authors.initials: T
authors.lastname: Yokoyama
authors.forename: H
authors.initials: H
authors.lastname: Ryu
authors.forename: K
authors.initials: K
authors.lastname: Uemura
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002908:Chronic Disease; D006706:Homeostasis / Q000502:physiology*; D007022:Hypotension / Q000503:physiopathology; D007427:Intracranial Pressure / Q000502:physiology; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*