Eight adult female cattle (6 Holstein, 1 Jersey, 1 Brown Swiss) were used to determine the antagonistic effects of tolazoline, an alpha 2-adrenoceptor antagonist, on xylazine-induced (via caudal epidural administration) depression of CNS, respiratory, and cardiovascular activity and rumen motility. A 2% solution of xylazine HCl was injected into the epidural space at the first coccygeal interspace, using a dosage of 0.05 mg/kg of body weight, diluted to a 5-ml volume with sterile water, and administered at a rate of approximately 1 ml/30 s. Eight minutes after xylazine injection, either tolazoline (0.3 mg/kg) or saline solution (4 ml) was administered IV. All 8 cattle were treated, using both regimens in a random sequence; at least 1 week elapsed between treatments. Epidurally administered xylazine induced caudal analgesia (S3 to coccyx), as evaluated by no response to superficial and deep muscular pinprick, and induced sedation, cardiopulmonary depression, and inhibition of rumen motility, but all cattle remained standing. Tolazoline effectively reversed xylazine-induced rumen hypomotility, and partially antagonized xylazine-induced cardiopulmonary depression without affecting sedation and desirable local (S3 to coccyx) analgesic effects.

This study has been carried out to investigate the augmenting or inhibiting effects of histamine, 5-hydroxytryptamine and their antagonists on the uterine motility. The uterine motility was represented by the magnitude of impulse and the frequency of uterine contraction which was counted by the number of waves on the recording paper. The inhibitory effect of phenoxybenzamine on the response to 5-hydroxytryptamine is the result of drug antagonism. Histamine stimlates or inhibits the motility of smooth muscle through H1 or H2-receptor. The uterine motility was increased through H1-receptor. Histamine induced relaxation by acting through H2-receptor.

Magnesium(Mg2+) is one of the most abundant intracellular divalent cation. Although recent studies demonstrate that adrenergic receptor stimulation evokes marked changes in Mg2+ homeostasis, the regulation of Mg2+ by dopaminergic receptor stimulation is not yet known. In this work, we uwed dopaminergic agents to identify which type(s) of receptors were involved inthe mobilization of Mg2+ by dopaminergic receptor stimulation in the perfused rat gearts, isolated myocytes and circulating blood. The mg2+ content was measured by atomic absorbance spedtrophotometry. Dopamine(DA), apomorphine(APO) and pergolide stimulated Mg2+ efflux in the perfused rat hearts and these effects were inhibited by haloperidol or fluphenazine, nonselective dopaminergic antagonists. SKF38393, a selective doparminergic agonist, increased Mg2+ efflux from the perfused hearts in dose dependant manners and SKF38393-induced Mg2+ efflux was potentiated in the presence of sulpiride or eticlopride, D2-selective antagonist, from the perfused hearts. This increase of Mg2+ efflux was blocked by haloperidol or imipramine. DA or pergolide increased in circulating Mg2+ from blood. By contrast, PPHT stimulated Mg2+ influx(a decrease in efflux) from the perfused hearts and circulating blood. PPHT-induced Mg2+ influx was blocked by fluphenazine in the perfused hearts. DA-stimulated Mg2+ efflux was inhibited by dopaminergic antagoinst in the isolated myocytes. In conclusion, the flux of Mg2+ is modulated by DA receptor activation in the rat hearts. The efflux of Mg2+ can be increased by D1-receptor stimulation and decreased by D2-receptor stimulation, respectively.

This study was performed to evaluate anesthetic and cardiovascular effects of xylazine/fentanyl/azaperone and medetomidine/midazolam as preanesthetics and their combinations with antagonists in halothane-anesthetized dogs. Eight clinically healthy dogs(4.54+_2.16kg) were used at the interval of more than 14 days between experiments in turn for propionyl promazine(PP 0.3mg/kg, IM), xylazine/fentanyl/azaperone(XFA 2mg/kg, 0.0137mg/kg, 0.11mg/kg, IM), medetomidine/midazolam(MM 0.02mg/kg, 0.3mg/kg, IM), combination of XFA and their antagonists (yohimbine 0.05mg/kg, naloxon 0.0005 mg/kg, IV) and combination of MM and their antagonist(atipamezole 0.08mg/kg IM). The sedation induction times in XFA(2.56+_1.01 min) and MM(5.44+_2.07 min) groups were sighificantly better than that of PP group(10.75+_2.38 min)(p0.05). The thiopental sodium dose required for tracheal intubation in XFA(2.38+_3.38mg/kg) and MM(3.91+_3.47mg/kg)groups were significantly less than that of PP group(12.57+_2.13mg/kg)(p0.05). All time indices expressing the recovery(pedal refles recurrence time, extubation time, arousal time, standing time and walking time) were significantly shorter in the combination groups of XFA or MM with their antagonistis than in PP, XFA and MM groups(p0.05). The suppressions of cardiovascular function of XFA and MM were more than that of PP. Heart rate and cardiac output were recovered by the antagonists of XFA and MM, but mean arterial pressure were not recovered by the antagonists.