- Meeting abstract
Protection of spinal cord ischemic injury with the β-agonist Clenbuterol
Critical Care volume 4, Article number: P184 (2000)
We studied Clenbuterol, a selective β-2 agonist, in preventing ischemic injury to the spinal cord.
We used 30 New Zealand rabbits for their unique segmental arterial supply to the spinal cord. Fifteen animals in the study arm were given Clenbuterol 9 mg PO 24 h before clamping. Fifteen (control arm) received water only. Heparin (70 IU/kg) was given 5 min before the incision. Ischemic injury was reproduced by cross-clamping the infrarenal aorta for either 22 or 30 min. Direct aortic blood flow measurements were taken with the transonic flowmeter before and after cross-clamping. Paralysis was assessed by the Tarlov's neurological scale.
All animals (2 control, 2 study arm; n=4) subjected to a clamping time of 30 min developed complete paraplegia. Of the control group with 22-min clamping time 77% developed paraplegia (Tarlov 0, n=9; Tarlov 1, n=1) and 23% did not (Tarlov 3, n=1; Tarlov 4, n=2). In the experimental (Clenbuterol) group with 22-min clamping time 38% developed paraplegia (Tarlov 0, n=3; Tarlov 1, n=2) and 62% did not (Tarlov 3, n=2; Tarlov 4, n=6). A consistent observation was that animals which developed paraplegia had a marked increase in post-declamping blood flow, i.e., hyperperfusion, suggesting that variations in aortic blood flow post-declamping may play a role in the development of paraplegia.
We concluded that Clenbuterol had a protective effect on the spinal cord in 62% (experimental group) vs 23% (control) in animals subjected to a clamping time of 22 min. Furthermore, controlling variations in aortic blood flow post-declamping may help to prevent paraplegia.