Pharmacologic reduction of mean arterial pressure does not adversely affect regional cerebral blood flow and intracranial pressure in experimental intracerebral hemorrhage.Crit Care Med. 1999 May; 27(5):965-71.CC
To determine the effect of mean arterial pressure (MAP) reduction on regional cerebral blood flow and intracranial pressure (ICP) in intracerebral hemorrhage. We tested the hypothesis that there is ischemia in the perihematoma region after intracerebral hemorrhage, which can be exacerbated by a pharmacologic reduction of MAP.
Prospective, controlled, laboratory trial.
Animal research laboratory.
Eighteen mongrel dogs, weighing 15 to 25 kg.
We introduced intracerebral hemorrhage in 12 anesthetized dogs by autologous blood injection under arterial pressure in the deep white matter adjacent to the left caudate region. We measured serial regional cerebral blood flow using radiolabeled microspheres in animals with two different volumes of injected blood (2.8 mL [Group A, n = 6] and 4.4 mL [Group B, n = 6]) and compared them with control animals (n = 6). Intravenous labetalol was administered 90 mins after administration of hematoma, while maintaining cerebral perfusion pressure >65 mm Hg. Regional cerebral blood flow measurements were repeated 10 and 30 mins after labetalol administration. MAP and ICP were monitored continuously using intra-arterial and cisterna magna catheters, respectively.
MEASUREMENTS AND MAIN RESULTS
Compared with control animals, significant elevation in ICP was observed in Groups A and B and elevation in MAP was observed in Group B at 45 mins after injection of blood. These hemodynamic alterations were not accompanied by any significant differences in regional cerebral blood flow in any group. Administration of labetalol resulted in a decrease in MAP (mm Hg+/-SEM) in Groups A (119.0+/-9.2 to 103.0+/-9.1) and B (124.5+/-7.4 to 100.5+/-4.8) and controls (103.5+/-4.3 to 85.0+/-8.0). No differences were observed in regional cerebral blood flow after MAP reduction in both Groups A and B compared with controls in regions around or distant to the hematoma. There were no changes in ICP in Groups A and B both at 10 and 30 mins after reduction in MAP compared with pretreatment values.
In our model, pharmacologic reduction of MAP within the normal autoregulatory limits of cerebral perfusion pressure, 90 mins after onset, had no adverse effect on ICP and regional cerebral blood flow in regions around or distant to the hematoma. These results support the controlled use of antihypertensive treatment in intracerebral hemorrhage in the initial time period.