Hematoxylin and eosin staining in the anterior horn of spinal cord.

<p>(A) The sham group showed no specific histopathological change. (B) The I/R group showed marked vacuolization and significant loss of α-motor neurons. (C) The NS group showed a similar histopathological appearance to the I/R group. (E–H) Histopathological damage was attenuated in C_0.01, C_0.05, C_0.1, and C_0.5 groups. The α-motor neurons were preserved most in the C_0.1 group. (D and I) The C_0.005 and C₁ groups showed no significant neuroprotection (original magnification, 40× object lens). I/R = ischemia-reperfusion; NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg.</p

Neurological and histopathological outcome at 48 hours after repercussion.

<p>Incidence is expressed as absolute numbers. Number of viable α-motor neurons is expressed as median (25th and 75th percentiles).</p><p>NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg. * <i>P</i><0.05 vs. the NS group.</p

Changes of hemodynamics among different dosage groups.

<p>Clenbuterol (1 mg/kg) reduced DBP from T4 to T9, especially at T7, accompanied with the decrease of MAP. There were no significant differences in HR and SBP. NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg; HR = heart rate; SBP = systolic blood pressure; DBP = diastolic blood pressure; MAP = mean arterial pressure; T0 = baseline; T1 = the onset of ischemia; T2 = 5 minutes after ischemia; T3 = 10 minutes after ischemia; T4 = 15 minutes after ischemia; T5 = 20 minutes after ischemia; T6 = the onset of reperfusion; T7 = 5 minutes after reperfusion; T8 = 10 minutes after reperfusion; T9 = 15 minutes after reperfusion; T10 = 20 minutes after reperfusion; T11 = 30 minutes after reperfusion.</p

Incidence of paraplegia and neurological dysfunction.

<p>Data are expressed as absolute numbers.</p><p>I/R = ischemia-reperfusion; 6 h = 6 hours after reperfusion; 24 h = 24 hours after reperfusion; 48 h = 48 hours after reperfusion. * <i>P</i><0.05 vs. the sham group.</p

Numbers of viable α-motor neurons in the anterior horn of spinal cord.

<p>The numbers of viable α-motor neurons were greater in C_0.01-C_0.5 groups than in the NS group. The best dosage was 0.1 mg/kg. There was no significant difference among the C_0.005, C₁, and NS groups. NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg. * <i>P</i><0.05 vs. the NS group.</p

Tarlov scores at different time points after reperfusion.

<p>Tarlov scores were significantly higher in C_0.01-C_0.5 groups than in the NS group at 24 and 48 hours after reperfusion. The best dosage was 0.1 mg/kg. There was no significant difference among the C_0.005, C₁, and NS groups. Tarlov score: 0 = paraplegia with no lower-extremity movement; 1 = poor lower-extremity movement but unresistant to gravity; 2 = good lower-extremity motor function with resistance to gravity, but unable to draw legs or hop; 3 = ability to draw leg and hop but not normally; 4 = normal lower-extremity motor function. NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg; 6 h = 6 hours; 24 h = 24 hours; 48 h = 48 hours. * <i>P</i><0.05 vs. the NS group.</p

Serum electrolytes concentration (mmol/L).

<p>Data are expressed as mean ± SD.</p><p>NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg; T0 = baseline; T1 = 30 minutes after ischemia; T2 = 30 minutes after reperfusion; T3 = 1 hour after reperfusion. * <i>P</i><0.05 vs. the NS group. # <i>P</i><0.05 vs. before aortic occlusion.</p

Age and gender stratified values of the 2MWD.

<p>Age and gender stratified values of the 2MWD.</p

The effect of activity on the 2MWD in males and females.

<p>The effect of activity on the 2MWD in males and females.</p

Pearson correlations between the variables and 2MWD.

<p>Pearson correlations between the variables and 2MWD.</p