Rocastine (AHR-11325), a rapid acting, nonsedating antihistamine. The effect of trypsin of rate, force and cyclic AMP in guinea pig atria. Evaluation of fetal heart rate in relation to the intrauterine 20 mm Hg level. Rx drugs

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Agents Actions. 1989 Aug;28(1-2):53-61.
Rocastine (AHR-11325), a rapid acting, nonsedating antihistamine.

Nolan JC, Stephens DJ, Proakis AG, Leonard CA, Johnson DN, Kilpatrick BF, Foxwell MH, Yanni JM.

Pharmacology Department, A.H. Robins Co., Richmond VA 23261.

Rocastine [AHR-11325, 2-[2-(dimethylamino)ethyl]-2,3-dihydro-4-methylpyrido-[3,2-f]-1,4- oxazepine-5(4H)-thione (E)-2-butenedioate)] is a rapid-acting, potent, nonsedating antihistamine. In guinea pigs challenged with a lethal dose of histamine, rocastine is as effective [based on 1 hr. oral, protective dose (PD50S)] as brompheniramine, chlorpheniramine, pyrilamine, and promethazine and superior to astemizole, diphenhydramine, terfenadine, and oxatomide. Rocastine has a faster onset of action than does terfenadine; rocastine being as effective with a 15 min pretreatment time (PD50 = 0.13 mg/kg) as it is with a 1 hr pretreatment time (PD50 = 0.12 mg/kg), while the 15 min PD50 of terfenadine (PD50 = 44.0 mg/kg) is 22 times greater than the 1 hr PD50 (PD50 = 1.93 mg/kg). Against aerosolized histamine, rocastine was 7.12 x, 2.63 x, and equipotent to pyrilamine in preventing histamine-induced prostration at pretreatment times of 1,3, and 6 hr, respectively. Rocastine protected guinea pigs from collapse induced by aerosolized antigen; rocastine was approximately 36 x more potent (based on 1 hr PD50) than diphenhydramine and as potent as oxatomide and terfenadine. Rocastine did not alter the EEG of cats at doses in vast excess (150x) of its antihistaminic dose nor did it potentiate yohimbine toxicity in mice. Further, rocastine possesses no anticholinergic, antiadrenergic, or antiserotonergic properties in vitro. Rocastine is a selective, nonsedating, H1-antagonist with a rapid onset of action.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2571244&dopt=Abstract

Eur J Pharmacol. 1981 Aug 27;74(1):95-9.
The effect of trypsin of rate, force and cyclic AMP in guinea pig atria.

Cros GH, Serrano JJ, McNeill JH.

Trypsin (10(-6)M produced a positive inotropic and chronotropic effect in left and right atria respectively and an increase in cyclic AMP. The effects were blocked by aprotinine while propranolol, phentolamine, promethazine and cimetidine and reserpine pretreatment did not alter trypsin activity. Trypsin effects were potentiated by RO 20,1724, a phosphodiesterase inhibitor. The cardiac effects of trypsin may be due to increase in cyclic AMP and are in agreement with previous work indicating that trypsin can activate cardiac adenylate cyclase.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6274653&dopt=Abstract

Eur J Obstet Gynecol Reprod Biol. 1975;5(5):263-72.
Evaluation of fetal heart rate in relation to the intrauterine 20 mm Hg level.

Wladimiroff JW, Eskes TK, Drogendijk AC, van Elteren P.

The purpose of the author's study was to investigate whether any changes in fetal heart rate (FHR) and in fetal acid-base status could be observed when the intrauterine pressure rises above 20 mm Hg. 16 primigravidae were studied. In 11 out of 16 patients labor was induced by amniotomy, in 9 cases oxytocin was given, and in 12 patients pethidine and promethazine (Phenergan) was administered. Two new parameters were introduced into the study of the collected material: the peak variation in FHR (bpm) i.e. the difference between the highest and lowest FHR over a given period of time; the contraction energy, i.e. the product of duration and intensity of intrauterine contractions as measured from the 20 mm Hg level. In 15 out of 16 women the mean peak variation in FHR was highest during a uterine contraction (greater than 20 mm Hg). After a uterine contraction (less than 20 mm Hg) the mean peak variation did not immediately return to control values. It is suggested that in the 16 patients studied, the increase in FHR peak variation during uterine contraction is basically caused by a slight transient fetal hypoxia, exaggerated during the expulsion period of labor by cord entanglement.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1053519&dopt=Abstract

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