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8 ng/mL, corresponding to a ?85 �� 2% decrease from baseline) as compared to GW786034 cost LZ (��2 �� 0.3 ng/mL, corresponding to a ?65 �� 4% decrease from baseline). After hemorrhage, OZ had significantly higher plasma insulin levels as compared to LZ in both saline�\ and ICI�\treated groups. There were no differences in plasma insulin in ICI�\treated animals compared to the respective saline�\treated group after hemorrhage. Figure 5. Plasma insulin levels at control levels, after hemorrhage (Hem), and after hemorrhage with ICI treatment (Hem + ICI; *P this website ICI treatment blocked the decrease in hepatic glycogen in OZ after hemorrhage with a no significant effect in LZ, suggesting a greater ��2�\adrenoceptor�\mediated glycogenolysis in OZ after hemorrhage; and (4) as compared to LZ, insulin, and glucagon levels were suppressed to a greater extent after hemorrhage in OZ and likely contributed to the altered hyperglycemic responses. Altered hemodynamic response in OZ after hemorrhage is insufficient to Adenosine explain the exacerbated hyperglycemia Hemorrhage can cause a rapid fall in MAP resulting in an increase in SNA. MAP was significantly reduced throughout the recovery period in all animal groups (Fig. ?(Fig.1).1). Consistent with our previous work, OZ had an impaired blood pressure recovery at only 30 min after hemorrhage (Xiang et al. 2013), with this one point in the recovery unlikely to cause significant biological differences between LZ and OZ. A reduction in blood pressure is a well�\known factor that activates the baroreflex to cause a sympathetic�\induced acute hyperglycemia. However, how this contributes to the increased plasma glucose in OZ after hemorrhage is unknown. This is complicated by the fact that OZ has impaired baroreflex sensitivity and decreased SNA in response to reductions in blood pressure (Schreihofer et al. 2007).