Related Experiment Video
Updated: Aug 29, 2026

Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
Published on: June 3, 2021
[Mechanical stress and cerebrovascular response--resemblance to cerebral vasospasm after subarachnoid hemorrhage]
Koichi Nakayama1, Kazuo Obara, Yoshiyuki Tanabe
1Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526.
The autoregulatory mechanism, including myogenic response, so-called "Bayliss effect", is well developed in the brain circulatory area, where also, cerebral vasospasm is often encountered after subarachnoid hemorrhage. In the cerebral artery smooth muscle, protein kinases, such as Rho-associated kinase, tyrosine kinase, and protein kinase C, are activated in response to mechanical stresses, including stretch, pressure and flow. All of these kinases are also activated in due course of time after development of the vasospasm. Myogenic response is a kind of reception and subsequent reaction to mechanical stress, whereas cerebral vasospasm is primarily caused by oxyhemoglobin, i.e., oxidative stress. Thus both myogenic and vasospastic episodes imply a common stress-responding mechanism. It seems possible that various kinases activated by mechanical stress act as not only a physiological signaling but also a proatherogenic/remodeling one. The stiffness of vasospastic artery was enormously increased in particular in the late phase of vasospasm, indicating the augmented process of pathologic remodeling. Therefore, "Bayliss effect" in modern sense and cerebral vasospasm can be argued in terms of a stress-reaction of cerebral artery.
The autoregulatory mechanism, including myogenic response, so-called "Bayliss effect", is well developed in the brain circulatory area, where also, cerebral vasospasm is often encountered after subarachnoid hemorrhage. In the cerebral artery smooth muscle, protein kinases, such as Rho-associated kinase, tyrosine kinase, and protein kinase C, are activated in response to mechanical stresses, including stretch, pressure and flow. All of these kinases are also activated in due course of time after development of the vasospasm. Myogenic response is a kind of reception and subsequent reaction to mechanical stress, whereas cerebral vasospasm is primarily caused by oxyhemoglobin, i.e., oxidative stress. Thus both myogenic and vasospastic episodes imply a common stress-responding mechanism. It seems possible that various kinases activated by mechanical stress act as not only a physiological signaling but also a proatherogenic/remodeling one. The stiffness of vasospastic artery was enormously increased in particular in the late phase of vasospasm, indicating the augmented process of pathologic remodeling. Therefore, "Bayliss effect" in modern sense and cerebral vasospasm can be argued in terms of a stress-reaction of cerebral artery.
Related Concept Videos
Hemorrhagic Stroke ll: Pathophysiology
Cerebral Edema ll: Pathophysiology
Hemorrhagic Stroke l: Introduction
Vascular Spasm
Ischemic Stroke ll: Pathophysiology
Increased Intracranial Pressure ll: Pathophysiology
