The diphenhydramine-induced decrease in general open-field activity of female rats is gonadal steroid dependent.

The effect of ovarian steroids on sedative effects of diphenhydramine (D), a histamine H1 receptor blocker, was determined. Seventy-five female Wistar rats were randomly divided into three groups: Group 1 (N = 54) was ovariectomized, group 2 (N = 7) was sham-operated, and group 3 (N = 14) was intact. The ovariectomized rats were then subdivided into 4 groups. Two groups received peanut oil 54 and 6 h before treatment with saline solution (group OS) or 20 mg/kg D (group OD). The other two groups received 50 micrograms/kg 17-beta-estradiol and 2 mg/kg progesterone, respectively, 54 and 6h before treatment with saline solution (group OHS) or 20 mg/kg D (group OHD). The sham-operated animals were treated as the OS group. Intact animals were injected with saline (group IS) or 20 mg/kg D (group ID) on the day of estrus, as determined by vaginal smears taken in the morning before the behavioral observations. Rats were observed for 6 min in the open field during the dark period of the cycle, 15 min after the administration of saline or D. There was a similar decrease in locomotion and rearing frequencies in OHS vs OHD and IS vs ID groups. Nevertheless, a lack of D sedative effect was observed in OD rats (locomotion and rearing frequencies, 56.0 +/- 3.3 vs 46.1 +/- 3.8 and 15.5 +/- 1.6 vs 15.2 +/- 1.6., for OS and OD groups, respectively). The results suggest that the sedative effect of diphenhydramine depends on the presence of ovarian steroids.

The diphenhydramine-induced decrease in general open-field activity of female rats is gonadal steroid dependent

The effect of ovarian steroids on sedative effects of diphenhydramine (D), a histamine H1 receptor blocker, was determined. Seventy-five female Wistar rats were randomly divided into three groups: Group 1 (N = 54) was ovariectomized, group 2 (N = 7) was sham-operated, and group 3 (N = 14) was intact. The ovariectomized rats were then subdivided into 4 groups. Two groups received peanut oil 54 and 6 h before treatment with saline solution (group OS) or 20 mg/kg D (group OD). The other two groups received 50 micrograms/kg 17-beta-estradiol and 2 mg/kg progesterone, respectively, 54 and 6h before treatment with saline solution (group OHS) or 20 mg/kg D (group OHD). The sham-operated animals were treated as the OS group. Intact animals were injected with saline (group IS) or 20 mg/kg D (group ID) on the day of estrus, as determined by vaginal smears taken in the morning before the behavioral observations. Rats were observed for 6 min in the open field during the dark period of the cycle, 15 min after the administration of saline or D. There was a similar decrease in locomotion and rearing frequencies in OHS vs OHD and IS vs ID groups. Nevertheless, a lack of D sedative effect was observed in OD rats (locomotion and rearing frequencies, 56.0 +/- 3.3 vs 46.1 +/- 3.8 and 15.5 +/- 1.6 vs 15.2 +/- 1.6., for OS and OD groups, respectively). The results suggest that the sedative effect of diphenhydramine depends on the presence of ovarian steroids

Postadulticide pulmonary hypertension of canine heartworm disease: successful treatment with oxygen and failure of antihistamines.

Postadulticide pulmonary hypertension mechanisms and treatment with antihistamines and supplemental oxygen were studied in eight dogs with heartworm disease. To ensure severe postadulticide thromboembolism, additional heartworms (either 20 or 40 into 4 dogs each) were transplanted into naturally infected dogs before thiacetarsamide treatment. During pentobarbital anesthesia, 2 pulmonary hemodynamic studies were conducted on each dog with a sequence of baseline, hypoxia with FlO2 = 10%, hyperoxia with FlO2 = 100%, a second baseline, treatment with either diphenhydramine (D) or cimetidine (C), and another hypoxia. All dogs were pulmonary hypertensive, with each dog having a mean pulmonary arterial pressure (PPA) greater than 20 mm of Hg. Mean PPA increased from baseline conditions (25.0 +/- 4.5 SD for D and 24.3 +/- 4.4 for C) to hypoxia (28.5 +/- 4.7 for D and 28.4 +/- 3.7 for C), and decreased during hyperoxia (16.9 +/- 3.0 for D and 17.4 +/- 3.0 for C), respectively. Neither antihistamine reduced PPA at normoxia. The degree of pulmonary hypertension when breathing room air increased even more during hypoxia, and this increase was not attenuated by either antihistamine. Histamine did not appear to mediate pulmonary hypertension during postadulticide thromboembolism, nor to modify the hypoxia-mediated pulmonary hypertension at this disease stage. Because baseline PO2 was low (66.6 +/- 11.7 mm of Hg for D and 69.4 +/- 14.2 for C) and because PPA decreased during administration of oxygen, the pulmonary hypertension was mostly hypoxia-induced. In addition to the arterial lesions, much of the pulmonary hypertensive mechanism was an active and reversible vasoconstriction in response to hypoxia caused by the secondary lung disease.(ABSTRACT TRUNCATED AT 250 WORDS)