Fig. 2.

Evaluation of VMH lactate and the counterregulatory hormone responses. Plasma glucose (a) and GIR (b) during the hypoglycaemic clamp; control group (n=6); recurrently hypoglycaemic (RH) rats (n=7); carvedilol-treated RH rats (n=7). GIRs at the end of the clamp were significantly higher in the RH group compared with the control group (*p<0.05, control vs RH, for time points shown below the bar). Carvedilol treatment reduced the GIR of RH animals to normal (^†p<0.05, RH vs RH + carvedilol, for time points shown below the bar). (c) Basal extracellular (VMH) lactate levels were 66% elevated in the RH rats (n=7; *p<0.05 vs control) compared with the controls (n=6) and these levels were reduced to normal with carvedilol treatment (n=6; *p<0.05 vs RH). (d) Baseline plasma lactate concentrations were lower in RH animals (n=7) compared with controls (n=6; *p<0.05, control vs RH and RH + carvedilol). No differences were observed between carvedilol-treated RH animals (n=8) and the RH group. (e) In comparison with controls (n=6), peak plasma glucagon levels were reduced by 42% in the RH (n=7) group (*p<0.05 vs control). (f) Peak adrenaline concentrations during the hypoglycaemic clamp were significantly suppressed by 75% in the RH (n=7) group compared with controls (n=6) (*p<0.05 vs control). Treatment with carvedilol (n=7) restored these hormone responses to normal (***p<0.001 vs RH animals). Plasma glucose and GIR data were analysed using two-way repeated measures ANOVA and microdialysate and hormone data were analysed using one-way ANOVA with post hoc Tukey honest significant difference (HSD) test. Data are presented as mean ± SEM. RH, recurrently hypoglycaemic