Table 3. Carbon dioxide reactivity of cerebral blood flow in nonoperated controls, in vehicle-, leptin-, and GM-CSF-treated animals after three-vessel occlusion (3-VO).
|
Carbon dioxide reactivity (% per mm Hg apCO2) |
Microsphere perfusion (% occluded/non-occluded hemisphere) | |||
|---|---|---|---|---|
| Total | Ipsilateral | Contralateral | ||
| Nonischemic control (n=8) | 1.29±0.10 | 1.48±0.15 | 1.10±0.09 | |
| 1 Week 3-VO | ||||
| Vehicle (n=9) | 0.54±0.09# | 0.42±0.08# | 0.65±0.12# | 64.9±1.4 |
| Leptin (n=10) | 1.05±0.20 | 1.11±0.24* | 0.99±0.24 | 66.3±2.2 |
| GM-CSF (n=10) | 1.13±0.25 | 1.25±0.28* | 1.12±0.41 | 79.2±2.6‡ |
GM-CSF, granulocyte–macrophage colony stimulating factor.
Blood flow was measured during ventilation with 6% CO2 by laser Doppler flowmetry (LDF) of the ipsilateral and contralateral hemispheres. The CO2 reactivity is expressed as percent change of LDF per mm Hg increase of arterial pCO2. Total CO2 reactivity is the average cerebrovascular reactivity of both hemispheres. Note suppression of CO2 reactivity at 1 week of 3-VO (#P<0.05 vehicle-treated versus nonischemic control group), followed by almost complete recovery after leptin and GM-CSF treatment (*P<0.05 compared with vehicle treatment). Only GM-CSF treatment lead to a significant improved microsphere perfusion under maximal vasodilation (‡P<0.05, vehicle- compared with leptin-treated animals).