OBJECTIVE: Elevated uterine artery resistance has been associated with the development of preeclampsia. We sought to determine if the human uterine arterial circulation was more sensitive to alpha-adrenergic blockade than a control vascular bed. METHODS: We studied 38 healthy nulliparous women during the follicular phase of the menstrual cycle. Arteriolized venous blood was measured for plasma epinephrine and norepinephrine. Doppler ultrasound of the uterine and upper extremity radial artery was performed before and after intravenous administration of phentolamine. Heart rate and volumetric flow were calculated. Data are presented as means +/- SD. RESULTS: Mean heart rate before and after administration of phentolamine was 63 +/- 11 and 68 +/- 12 beats per minute (7.5% increase, P <.001). Mean radial artery blood flow before and after administration of phentolamine was 4.6 +/- 4.7 mL/min and 5.8 +/- 5.9 mL/min (19.9% increase, P =.071). Mean uterine blood flow before and administration of phentolamine was 15.4 +/- 10.1 mL/min and 27.3 +/- 17.5 mL/min (43.7% increase, P <.001). The uterine response (43.7% increase) and radial response (19.9% increase) were significantly different (P <.001). The increase in uterine blood flow after phentolamine administration was linked with resting norepinephrine (r = 0.394, P =.063). CONCLUSION: We found evidence that uterine alpha-adrenergic tone is more sensitive to blockade by phentolamine than upper extremity radial circulation. This provides evidence for a differential responsiveness and sensitivity to alpha-adrenergic blockade in different vascular beds. We theorize that the increased adrenergic tone associated with preeclampsia may contribute disproportionately to decreased uterine blood flow.
OBJECTIVE: Elevated uterine artery resistance has been associated with the development of preeclampsia. We sought to determine if the human uterine arterial circulation was more sensitive to alpha-adrenergic blockade than a control vascular bed. METHODS: We studied 38 healthy nulliparous women during the follicular phase of the menstrual cycle. Arteriolized venous blood was measured for plasma epinephrine and norepinephrine. Doppler ultrasound of the uterine and upper extremity radial artery was performed before and after intravenous administration of phentolamine. Heart rate and volumetric flow were calculated. Data are presented as means +/- SD. RESULTS: Mean heart rate before and after administration of phentolamine was 63 +/- 11 and 68 +/- 12 beats per minute (7.5% increase, P <.001). Mean radial artery blood flow before and after administration of phentolamine was 4.6 +/- 4.7 mL/min and 5.8 +/- 5.9 mL/min (19.9% increase, P =.071). Mean uterine blood flow before and administration of phentolamine was 15.4 +/- 10.1 mL/min and 27.3 +/- 17.5 mL/min (43.7% increase, P <.001). The uterine response (43.7% increase) and radial response (19.9% increase) were significantly different (P <.001). The increase in uterine blood flow after phentolamine administration was linked with resting norepinephrine (r = 0.394, P =.063). CONCLUSION: We found evidence that uterine alpha-adrenergic tone is more sensitive to blockade by phentolamine than upper extremity radial circulation. This provides evidence for a differential responsiveness and sensitivity to alpha-adrenergic blockade in different vascular beds. We theorize that the increased adrenergic tone associated with preeclampsia may contribute disproportionately to decreased uterine blood flow.