Alterations to the middle cerebral artery of the hypertensive-arthritic rat model potentiates intracerebral hemorrhage

Abstract

AimsWe have recently created an age-dependent hypertensive-mono-arthritic animal model from the stroke-resistant spontaneously hypertensive rat to model populations with autoimmune disease who are hypertensive and are prone to stroke. The model exhibits signs of hemorrhagic stroke (HS) subsequent to chronic inflammation and hypertension. HS is also associated with the inability of middle cerebral arteries to undergo pressure dependent constriction (PDC). We investigated alterations in the cerebrovasculature of our hypertensive mono-arthritic animals that develop stroke.Main MethodsAnimals were fed either a high salt diet (HSD) (4% NaCl) or Purina chow (0.58% NaCl) from weaning. Complete Freund’s Adjuvant (CFA) was injected into the left hind paw at 21–28 weeks; controls received saline and histological and functional studies were performed.ResultsBrain damage was more prominent with the high salt, with inflammation exacerbating the damage. High salt alone significantly decreased middle cerebral artery’s (MCA’s) ability to undergo PDC. Inflammation significantly decreased the ability of cerebrovasculature to respond to pressure step in the regular salt diet. The responses to vasoactive peptides were also significantly attenuated in both inflamed groups regardless of diet.ConclusionInduction of chronic systemic inflammation increases brain damage, and affect the MCA’s vasogenic function, decreasing its ability to respond to intraluminal pressure. HSD further exacerbates organ damage associated with chronic inflammation, further compromising cerebrovascular function, and likely increasing the incidence of intracerebral hemorrhage and injury.

Changes in cellular signaling patterns before and after stroke in the middle cerebral arteries of stroke prone spontaneously hypertensive rats

“…Sigma Aldrich, ON, CAN) and ionized calcium binding adaptor molecule 1[Iba-1; 1:1,000, Wako Chemicals, VA, USA]. Secondary antibody of Cy2 Goat Anti-rabbit (1:200; Jackson Immunoresearch, PA, USA) and DAPI (1:1,000) were applied in the second day according to established protocol (21).…”

Fish-Oil Preconditioning Modulates Plasma McP-1 and Timp-1 Levels After Experimental Induced Transient Cerebral Ischemia

“…Tissue section stained with CV were digitalized and quantified with Image J program [23] the infarct area was expressed as a percentage of total brain volume with correction for brain oedema [19]. Morphometric analysis of specific cells changes was performed by the scoring scheme recommended by Randell at al [14]. Focal acute eosinophilic necrosis associated with neural cell vacuolization, neural degeneration with pycnotic nucleus associated with vacuolization of neuropils, cell edema and the presence of inflammatory cells were considered the most important aspects to be evaluated for analysis, both in core and penumbra.…”

Inflammatory cell populations in early neuroinflammation in the core and peri-ischemic lesions of rat brain after transient focal cerebral ischemia: A morphometric study

“…We focused on these morphological cellular and stromal changes: a) focal acute eosinophilic necrosis associated with neural-cell vacuolation; b) neuronal degeneration (pyknotic nuclei associated with vacuolation of neutrophils); c) areas of oedema; and d) the presence of inflammatory cells. For each variable, scores between 1-10 were assigned, as Randell (Randell et al, 2016) have recommended for quantification of brain-tissue damage. To determine the final score, we examined and quantified these variables in the core and penumbra of each sample, using a magnification of 200 x, the score indicating the degree of neural destruction.…”