title: Role of substantia innominata in cerebral blood flow autoregulation.
abstract: Ascending projections from the substantia innominata (SI) may have an important role in the regulation of cerebral blood flow (CBF). However, several reports have suggested that unilateral lesion of the SI does not affect CBF autoregulation. On the other hand, it is also reported that several cortical and subcortical functions may be regulated not only by ipsilateral SI, but also by contralateral SI. Thus, the objective of this study is to test the hypothesis that bilateral lesions of the SI affect CBF autoregulation. Experiments were performed on anesthetized male Sprague-Dawley rats. Ibotenic acid or physiological saline was microinjected into bilateral SI. Rats were classified into four groups as follows: bilateral SI lesion rats (ibotenic acid was injected bilaterally), left or right SI lesion rats (ibotenic acid was injected into the unilateral SI and saline into the contralateral SI), and control rats (saline was injected bilaterally). Ten days after injection, CBF in the left frontal cortex was measured by laser-Doppler flowmetry during stepwise controlled hemorrhagic hypotension. In bilateral SI lesion rats, CBF was started to decrease significantly at 80 mm Hg (p<0.01). In the other three groups, CBF was well maintained until 50 mm Hg. Changes in CBF through stepwise hypotension in bilateral SI lesion rats were significantly different from the other groups (p<0.01). These results suggest that bilateral SI regulates cortical vasodilator mechanisms during hemorrhagic hypotension. Under unilateral SI lesion, some compensatory effects from the contralateral SI may maintain CBF autoregulation.
authors.affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan. kaota@mvd.biglobe.ne.jp
authors.forename: Kazuki
authors.initials: K
authors.lastname: Ota
authors.forename: Takanari
authors.initials: T
authors.lastname: Kitazono
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Ooboshi
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kamouchi
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Katafuchi
authors.forename: Shuji
authors.initials: S
authors.lastname: Aou
authors.forename: Yoshichika
authors.initials: Y
authors.lastname: Yamashita
authors.forename: Setsuro
authors.initials: S
authors.lastname: Ibayashi
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Iida
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001776:Blood Circulation Time; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D018690:Excitatory Amino Acid Agonists / Q000009:adverse effects; D007839:Functional Laterality; D018698:Glutamic Acid / Q000494:pharmacology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology*; D007051:Ibotenic Acid / Q000009:adverse effects; D066298:In Vitro Techniques; D017078:Laser-Doppler Flowmetry / Q000379:methods; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000187:drug effects; D013377:Substantia Innominata / Q000187:drug effects / Q000293:injuries / Q000502:physiology*
chemical_list: D018690:Excitatory Amino Acid Agonists; D007051:Ibotenic Acid; D018698:Glutamic Acid