Microinfarction as a result of hypertension in a primate model of cerebrovascular disease

Abstract

Ten adult cynomolgus monkeys were studied as a non-human primate model of hypertensive cerebrovascular disease. Seven were made hypertensive by surgical coarctation of the aorta and three served as unoperated controls. After survival periods of 8-30 months, the brains were serially sectioned and surveyed for neuropathological changes. The most conspicuous change was minute areas of microinfarction in the white and gray matter. The lesions were of irregular shape with an average maximum diameter of less than 0.5 mm. They were slightly larger in the gray than in the white matter and appeared to be of different ages. Their area of predilection was the white matter of the forebrain, with smaller numbers in the cerebral cortex and scattered lesions elsewhere in the forebrain, brain stem and cerebellum. These microinfarcts did not correspond to usually described lesions in the human brain in hypertension or in other animal models of hypertensive cerebrovascular disease. We suggest that they represent an early change in the natural history of hypertensive neuropathology.

Neuroimaging Predictors of Cognitive Impairment in Confluent White Matter Lesion: Volumetric Analyses of 99 Brain Regions

“…We postulate that other hypertensive related pathologies that are not visualized by MRI, e.g. microinfarcts [32] , may contribute to cGM atrophy.…”

Doin vivoExperimental Models Reflect Human Cerebral Small Vessel Disease? a Systematic Review

“…The mildly neuroprotective anaesthesic agent, pentobarbitone, was used in 12 reports on SHR-SP (Sadoshima et al, 1983;Tamaki et al, 1984;Werber and Heistad, 1984;Mayhan et al, 1987Mayhan et al, , 1988Baumbach et al, 1988Baumbach et al, , 1994Hajdu et al, 1991;Yang et al, 1991Yang et al, , 1993Chillon and Baumbach, 1999;Maguire et al, 2004) and in 4 other studies (Rosenberg et al, 1990;Toshima et al, 2000;Whitehead et al, 2005a, b). The primate aortic coarctation studies used ketamine anaesthesia (Kemper et al, 1999(Kemper et al, , 2001Moore et al, 2002), though this is unlikely to affect the data, given the prolonged pathogenesis of the lesions. Compliance with animal welfare regulations (domain no.…”

“…This produced cerebrovascular lesions and some myocardial hypertrophy and retinopathy, but no obvious change in lifespan. Tiny infarcts were seen-discrete regions < 0.5 mm diameter-with loss of neurons and myelin (Kemper et al, 1999(Kemper et al, , 2001). These were most abundant in forebrain white matter (more rarely in periventricular white matter) and also scattered in cerebral cortex, hippocampus, striatum, midbrain, and cerebellum (Garcia et al, 1981;Kemper et al, 1999Kemper et al, , 2001.…”

Age effects on atrophy rates of entorhinal cortex and hippocampus

“…A recent clinical study demonstrated that elderly individuals with silent brain infarcts were at greater risk for dementia and cognitive decline than elderly individuals without such lesions [53]. In addition to the subcortical cerebral vascular lesions visible on MRI, microinfarctions, which are usually not visible on MRI, may also be present, especially in subjects with hypertension [28]. Hypertension has been shown as a risk factor for late-life cognitive impairment [12,32].…”