Rodent stroke models

In rodent stroke models, statin pretreatment has been shown to reduce infarct volumes and improve outcomes. Similarly, several clinical studies have shown that prior statin use reduced the severity of acute ischemic stroke and myocardial infarction. Recent studies indicate that beneftt can be achieved even when treatment is initiated after the onset of symptoms. In rodents, atorvastatin and simvastatin have been shown to reduce the growth of ischemic lesions, enhance functional outcome, and induce brain plasticity when administered after stroke onset. A retrospective analysis of the population-based Northern Manhattan Stroke Study (NOMASS) showed that patients using lipid-lowering agents at the time of ischemic stroke have a lower incidence of in-hospital stroke progression and reduced 90-day mortality rates. Retrospective analysis of data of the phase III citicoline trial showed... 

The NgR antibody can be covalently attached to a HA hydrogel by a hydrolytically unstable hydrazone linkage, and this modified HA hydrogel can serve as an antibody releasing system for grafting into the injured brain [39]. By use of this system in rodent stroke models, the distribution of the antibody and differentiation of neurons in the injured area can be seen, accompanied by certain behavioral recovery [40]. There has been a study by Wei and co-workers [41] showing that HA hydrogels modified with poly(L-lysine) (PLL) and... 

At this time, however, we are not aware of any compounds selected primarily by their neuroprotection activity on rodent models that have established clinical efficacy for dementias or related neurodegenerative diseases. This may be partially explained by their priority development for stroke, and clinicians have found it is difficult or unlikely to slow the ischemia in patients if they are not treated aggressively within 3 h of the initial ischemic event. The speed of neurodegeneration in stroke (cerebral ischemia) makes it a much more difficult target for drug intervention than neurodegeneration from slower pathologies such as Alzheimer s, Parkinson s, and malfunctions in neurotransmitters. 

Neuroprotective Effect of Nitroglycerin in a Rodent Model of Ischemic Stroke Evaluation of Bel-2 Expression... 

Schmidt-Kastner R, Paschen W, Ophoff BG, Hossmann KA (1989) A modified four-vessel occlusion model for inducing incomplete forebrain ischemia in rats. Stroke 20 938-946 Schmitz B, Bottiger BW, Hossmann KA (1997) Functional activation of cerebral blood flow after cardiac arrest in rat. J Cereb Blood FlowMetab 17 1202-1209 Schmitz B, Bock C, Hoehn-Berlage M, Kerskens CM, Bottiger BW, Hossmann KA (1998) Recovery of the rodent brain after cardiac arrest a functional MRI study. Magn Reson Med 39 783-788... 

Stem cell-based therapy for cerebral ischemia will be more complicated, because the extensive cell death and massive inflammatory response make these brains a more hostile environment for cell grafts. Various sources of cells have been tested for their ability to reconstruct the forebrain and improve function after transplantation in animal models of stroke (Lindvall and Kokaia, 2004). In most cases, only a few grafted cells could survive. Some recent exciting findings in rodents suggest that stroke can induce an increase in neurogenesis thus, a new therapeutic approach based on self-repair has been brought forth, as discussed in Sect. 13.11.1. 

The beneficial effects of potassium on blood pressure should reduce the occurrence of blood pressure-related cardiovascular disease. Potassium may also have protective effects that are independent of blood pressure reduction. This possibility has been tested in experimental studies conducted in rodents. In a series of animal models, the addition of either potassium chloride or potassium citrate markedly reduced mortality from stroke. Interestingly, these reductions occurred when blood pressure was held constant. Such data indicate that potassium has both blood pressure-dependent and blood pressure-independent properties that are cardioprotective. 

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