Canines were among the earliest-used animals for studying experimental ICH. A 1975 study of the tolerance of the dog's brain to blood injection in different sites—the brain parenchyma and the ventricles—found different lethal volumes for each specific ICH site (55). The authors found that 8 mL was lethal in the dog brain parenchyma and concluded that that death was not a random event but was due to the failure of vital functions as a result of elevated ICP. Further detailed studies demonstrated the evolution of brain injury following ICH in a canine parietal lobe hematoma model by high-resolution sonography, CT, and neuropathologic examinations (56). These authors found a correlation between the sequence of changes on CT and sonography images in their ICH model and the findings following ICH in patients. In early MRI studies in canine ICH models, venous and arterial blood infusions and intraventricular locations of blood were compared, and it was concluded that gradient-echo sequences would be highly useful in detecting and delineating hemorrhages in human ICH patients (57).

In histologic and CT studies of internal capsule hematomas conducted in dogs, 3 distinct stages were identified on histology and CT: (i) in the acute stage (< 5 days), homogeneous high density was present at the periphery of the hematoma on CT, while histologically, a necrotic layer of tissue existed at the boundary of the clot; (ii) in the subacute stage (5-14 days), perihemato-mal density was decreased with ring enhancement after contrast injection and corresponded to the appearance of immature connective tissue with argentophilic fibers; (iii) in the chronic stage (>15 days), contraction of the enhancing ring was noted, corresponding to the development of mature connective tissue with collagen fibers ( 58 ).

Using a mongrel dog ICH model, another study (59) determined the effect of massive ICH on regional CBF (rCBF) and metabolism by testing the hypothesis put forward by Mendelow and coworkers from their studies in rats (27-34) regarding intracerebral bleed-induced peri-hematomal ischemia. Interestingly, these investigators found no evidence for an ischemic penumbra within the first 5 hr after hemorrhage, despite prominent increases in ICP and mean arterial blood pressure (MABP) following hematoma induction, indicative of a Cushing response.

Other investigators found that hypertonic saline, at 3% and 23.4% concentrations, was as effective as mannitol in controlling intracranial hypertension in a dog model (60). In addition, 3% hypertonic saline appeared to have a longer effect than either 23.4% saline or mannitol. No effect on rCBF or cerebral metabolism was observed with any of the agents. In their study of the pharmacologic reduction of MABP, the same group using the same canine model found that reducing MABP with intravenous labetalol within the normal autoregulatory curve of CPP had no adverse effects on ICP and perihematomal or distant rCBF (54). They concluded that MABP reduction is safe within autoregulation limits in the acute period after ICH.

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