This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Coyle, P. Articles by Sing, C. F. Search for Related Content PubMed PubMed Citation Articles by Coyle, P. Articles by Sing, C. F.

Stroke, Vol 15, 711-716, Copyright © 1984 by American Heart Association

ARTICLES

Cerebral infarction after middle cerebral artery occlusion in progenies of spontaneously stroke-prone and normal rats

P Coyle, DJ Odenheimer and CF Sing

A differential outcome results from rapid middle cerebral artery (MCA) occlusion in young normotensive Wistar (NW) rats as compared to the spontaneously hypertensive stroke-prone (SHRSP) rat. The SHRSP invariably infarcts; the NW usually does not. To determine if segregation at a single autosomal locus explains the difference between strains, a NW male was crossed with several SHRSP females to produce F1 rats. The segregation of the strain difference was studied in the F2 and backcrosses to the NW and SHRSP parental strains. The relative frequency of infarcting and noninfarcting animals in the segregating progenies supported a single locus recessive model of inheritance for susceptibility to infarction after sudden occlusion of the MCA. Mean infarct size was largest for SHRSP and proportional to the SHRSP gene dosage in the segregating progenies. Variation in the size of the infarct within segregating classes may be attributable to the segregation of polygenes and/or environmental influences during the initial formation of the cerebral anastomoses.

This article has been cited by other articles:

				H. Yao, Z.-H. Cui, J. Masuda, and T. Nabika Congenic removal of a QTL for blood pressure attenuates infarct size produced by middle cerebral artery occlusion in hypertensive rats Physiol Genomics, June 19, 2007; 30(1): 69 - 73. [Abstract] [Full Text] [PDF]

				A. J. Catto Genetic aspects of the hemostatic system in cerebrovascular disease Neurology, September 1, 2001; 57(90002): S24 - 30. [Abstract] [Full Text]

				H. V. O. Carswell, N. H. Anderson, J. S. Clark, D. Graham, B. Jeffs, A. F. Dominiczak, and I. M. Macrae Genetic and Gender Influences on Sensitivity to Focal Cerebral Ischemia in the Stroke-Prone Spontaneously Hypertensive Rat Hypertension, February 1, 1999; 33(2): 681 - 685. [Abstract] [Full Text] [PDF]

				K.-A. Hossmann Experimental models for the investigation of brain ischemia Cardiovasc Res, July 1, 1998; 39(1): 106 - 120. [Full Text] [PDF]

				J. A. Gratton, A. Sauter, M. Rudin, K. R. Lees, J. McColl, J. L. Reid, A. F. Dominiczak, I. M. Macrae, and D. F. Bohr Susceptibility to Cerebral Infarction in the Stroke-Prone Spontaneously Hypertensive Rat Is Inherited as a Dominant Trait • Editorial Comment Stroke, March 1, 1998; 29(3): 690 - 694. [Abstract] [Full Text] [PDF]

				L. C. Wang, N. Futrell, D. Z. Wang, F.-J. Chen, Q.-h. Zhai, and L. R. Schultz A Reproducible Model of Middle Cerebral Infarcts, Compatible with Long-term Survival, in Aged Rats Stroke, November 1, 1995; 26(11): 2087 - 2090. [Abstract] [Full Text]