title: The arterial circle of Willis of the mouse helps to decipher secrets of cerebral vascular accidents in the human.
abstract: The human brain represents an elaborate product of hominizing evolution. Likewise, its supporting vasculature may also embody evolutionary consequences. Thus, it is conceivable that the human tendency to develop cerebral vascular accidents (CVAs) might represent a disease of hominization. In a search for hominizing changes on the arterial circle of Willis (hWAC), we attempted an anatomical comparison of the hWAC with that of the mouse (mWAC) by injecting aliquots of resin into the vasculature of the mouse and then creating vascular endocasts of the mWAC. The internal carotid artery of the mouse (mICA) unites with the mWAC midway between the middle cerebral artery (mMCA) and posterior cerebral artery (mPCA). The mWAC does not complete a circle: the mWAC nourishes the anterior portion of the circle which branches out to the olfactory artery (OlfA) and mPCA, along with the mMCA, and the basilar artery (mBA) does not connect to the mPCA. The OlfA is thicker than the mMCA. The relative brain weight of the mouse was 74 g on average for a 60 kg male and 86 g for a 60 kg female, respectively, as compared with 1424 g for a 60 kg man. These findings are consistent with the mouse being a nocturnal carnivore that lives on olfactory information in contrast to the human that lives diurnally and depends on visual and auditory information. In man, the human ICA (hICA) unites with the hWAC at a point where the human middle cerebral artery (hMCA) branches out, and thus, blood from the hICA does not flow through the hWAC but drains into the hMCA directly. The hMCA is thicker than the anterior cerebral artery. The hPCA receives blood from the hBA rather than from the hICA, and thus, the entire hWAC forms a closed circuit. Since the hICA drains directly into the hMCA without flowing a distance through the hWAC, the capacitor and equalizer functions of the WAC will be mitigated so much that the resultant hemodynamic changes would render the hMCA more likely to contribute to CVAs. Thus, anatomical findings and possibly functions of the arterial circle of Willi may vary from one species to another, depending on one's specific cerebral evolution.
authors.affiliation: Evolution of Diseases Laboratory, Kamo 4-4-5, Izumi, Sendai 981-3122, Japan. shinichiokuyama@evolution-of-diseases-lab.org
authors.forename: Shinichi
authors.initials: S
authors.lastname: Okuyama
authors.forename: Jun
authors.initials: J
authors.lastname: Okuyama
authors.forename: Junko
authors.initials: J
authors.lastname: Okuyama
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Tamatsu
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Shimada
authors.forename: Hajime
authors.initials: H
authors.lastname: Hoshi
authors.forename: Junichi
authors.initials: J
authors.lastname: Iwai
mesh_terms: D000818:Animals; D005075:Biological Evolution; D001921:Brain / Q000098:blood supply* / Q000473:pathology* / Q000503:physiopathology; D002561:Cerebrovascular Disorders / Q000473:pathology* / Q000503:physiopathology*; D002941:Circle of Willis / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D051379:Mice; D008805:Mice, Inbred A; D008955:Models, Cardiovascular; D008957:Models, Genetic; D009929:Organ Size; D013045:Species Specificity