1 nlabeled histamine and by chlorpromazine and phenoxybenzamine.

2 take-1 and norepinephrine uptake-2 inhibitor phenoxybenzamine (50 mg/kg intravenously; n = 4), the se

3                                              Phenoxybenzamine administered intraperitoneally did not

4 ed (Control); alpha-adrenergic blockade with phenoxybenzamine (Alpha); beta-adrenergic blockade with

5 used an irreversible alpha-receptor blocker, phenoxybenzamine (alpha1 > alpha2).

6                                  Exposure to phenoxybenzamine, an irreversible inhibitor of alpha1-ad

7 bined alpha- and beta-adrenergic blockade by phenoxybenzamine and propranolol (Alpha/Beta).

8 Patients premedicated with the alpha-blocker phenoxybenzamine appear to have a reduced risk of hypert

9 of receptor reserve by the alkylating agent, phenoxybenzamine, as it reduced the maximal ACh response

10 A group of proestrous rats were treated with phenoxybenzamine at doses of 20 mg/kg, intraperitoneally

11 (18)F-LMI1195 was significantly inhibited by phenoxybenzamine but not desipramine, suggesting (18)F-L

12 WB4101 and the nonselective alpha antagonist phenoxybenzamine completely blocked increase in bursting

13 e were different, in that at all dose levels phenoxybenzamine completely blocked the LH surge and red

14                   The effects of intravenous phenoxybenzamine could be mimicked by substitution of pr

15 lpha-adrenergic antagonists (phentolamine or phenoxybenzamine) increased spontaneous release of iCGRP

16                            Pretreatment with phenoxybenzamine markedly reduced the (18)F-LMI1195 card

17 , or alpha-adrenergic receptor blockade with phenoxybenzamine (PBZ), on the nor-BNI-induced LH respon

18 ntinuous superior vena cava oximetry (SvO2), phenoxybenzamine (POB), strategies to minimize the durat

19 ither unaffected or only slightly reduced by phenoxybenzamine treatment intraperitoneally.

20                   The effects of intravenous phenoxybenzamine were different, in that at all dose lev