What causes strokes in rats? - briefly
Ischemic strokes in rodents are typically produced by occluding the middle cerebral artery—using filament insertion, photothrombosis, or embolic particles—while hemorrhagic strokes result from direct vessel rupture induced by collagenase injection or blood infusion. Both models replicate the primary pathological mechanisms that lead to cerebral infarction and bleeding in rats.
What causes strokes in rats? - in detail
Stroke in rodents is produced by a combination of vascular, metabolic, and genetic factors that mimic human cerebrovascular disease. Experimental models isolate specific mechanisms, allowing precise identification of causative agents.
Vascular occlusion is the primary inducer. Mechanical blockage of the middle cerebral artery using an intraluminal filament creates focal ischemia by compressing the arterial lumen. The filament’s diameter and insertion depth determine infarct size and reproducibility. Photothrombotic injury employs a photosensitizing dye activated by focused light; the resulting platelet aggregation occludes microvessels within a defined cortical region. Embolic models inject autologous blood clots or microspheres into the carotid artery, generating distal emboli that lodge in arterioles and produce heterogeneous infarcts.
Hemorrhagic injury arises from vessel rupture. Intracerebral injection of collagenase degrades the basal lamina, weakening vessel walls and causing spontaneous bleed. Direct infusion of autologous blood into brain parenchyma reproduces the mass effect and secondary inflammation seen in intracerebral hemorrhage.
Systemic hypertension, often induced by high‑salt diets or chronic infusion of angiotensin II, predisposes rats to spontaneous lacunar infarcts and enhances susceptibility to occlusive insults. Genetic strains such as spontaneously hypertensive rats (SHR) and stroke‑prone SHR develop chronic vascular remodeling, endothelial dysfunction, and increased oxidative stress, all of which contribute to stroke pathology.
Metabolic disturbances amplify injury. Hyperglycemia, achieved by glucose loading or streptozotocin‑induced diabetes, intensifies infarct volume through exacerbated oxidative damage and impaired reperfusion. Dyslipidemia, induced by high‑fat diets, promotes atherosclerotic plaque formation in cerebral arteries, facilitating thrombus development.
Inflammatory and neurotoxic pathways act as secondary contributors. Endothelin‑1 microinjection causes potent vasoconstriction, leading to rapid ischemia. Systemic administration of lipopolysaccharide primes microglia, heightening post‑ischemic inflammation and worsening tissue loss.
Key determinants of rodent stroke
- Mechanical arterial blockage (filament, photothrombosis, emboli)
- Enzymatic vessel degradation (collagenase)
- Elevated blood pressure (dietary salt, angiotensin II, hypertensive strains)
- Metabolic imbalances (hyperglycemia, hyperlipidemia)
- Vasoconstrictive peptides (endothelin‑1)
- Pro‑inflammatory stimuli (lipopolysaccharide)
Understanding these factors enables controlled replication of ischemic and hemorrhagic events, facilitating the evaluation of therapeutic strategies and the translation of findings to human cerebrovascular disease.