Inhibition of Brain Swelling after Ischemia-Reperfusion by β-Adrenergic Antagonists: Correlation with Increased K⁺ and Decreased Ca²⁺ Concentrations in Extracellular Fluid

Table 3

Brain water content in MCAO model after 3 hr ischemia and 8 hr reperfusion in the right hemisphere under control conditions (intracerebral saline only) and after injection of inhibitors of either the - or the -adrenergic pathway in astrocytes.

	Left hemisphere	Right hemisphere
Saline	77.97 ± 0.17 ( = 8)	81.28 ± 0.34 ( = 8)^*
H89	77.00 ± 0.42 ( = 3)	77.19 ± 0.09 ( = 3)
PTX	77.19 ± 0.11 ( = 4)	77.51 ± 0.26 ( = 4)
GM6001	77.08 ± 0.11 ( = 4)	77.15 ± 0.13 ( = 4)
AG1478	77.14 ± 0.11 ( = 3)	77.27 ± 0.04 ( = 3)
U0126	77.39 ± 0.10 ( = 4)	78.22 ± 0.67 ( = 4)
PP1	77.52 ± 0.26 ( = 5)	80.04 ± 0.33 ( = 5)^*

In rats with MCAO in the right hemisphere drugs were added 15 min before the occlusion as described in Methods. Water content was calculated as (wet weight − dry weight)/wet weight × 100%. In control animals (the same value as in Table 1) an increase in the ipsilateral hemisphere was significant ( < 0.05), as marked with *. This was also the case after treatment with PP1, an inhibitor of Src, an intermediate in -adrenergic signaling, but not after administration of any of the other inhibitors, which interrupt - but not -adrenergic signaling as shown and discussed in Figure 1. Most but not all inhibitors used to delineate the signaling pathways shown in that Figure were tested in this table. Since PP1 was the only -adrenergic inhibitor tested, an was used, whereas each the other inhibitors, which all act on the same, -adrenergic were tested in fewer experiments.