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Cardiac and systemic sympathetic activity in response to clonidine in human heart failure

^a Division of Cardiology, Department of Medicine, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada

View larger version (15K): [in a new window]   Figure 1 Hemodynamic responses to 50 and 100 µg of clonidine. FAmean = mean femoral artery pressure; LVEDP = left ventricular end-diastolic pressure; LV+dP/dt = rate of rise in left ventricular peak positive pressure; TL = rate of isovolumic relaxation measured by the method of Weiss (18). *p < 0.05 versus control. p < 0.01 versus control. Data are expressed as the mean value ± SEM.

View larger version (9K): [in a new window]   Figure 2 Cardiac norepinephrine spillover (CANESP) and total body norepinephrine spillover (TBNESP) at control values and in response to 50 and 100 µg of clonidine. *p < 0.05 versus control. p < 0.01 versus control. Data are expressed as the mean value ± SEM.

View larger version (15K): [in a new window]   Figure 3 Arterial (open bars) and coronary sinus (solid bars) plasma norepinephrine at control values and in response to 50 and 100 µg of clonidine. There is a significant reduction in the transcardiac gradient of plasma norepinephrine in response to 100 µg of clonidine. This results from a significantly greater decrease in the coronary sinus plasma norepinephrine level as compared with the arterial plasma norepinephrine level. *p < 0.05 versus control. p < 0.01 versus control. p < 0.05 for comparison between the norepinephrine transcardiac gradient (coronary sinus – arterial) with 100 µg of clonidine and control level. Data are expressed as the mean value ± SEM.