Summary: A rare variation in the arterial pattern was found in the right arm of an 87-year-old male cadaver in a student dissection practice. In this case, the superficial brachial and superficial subscapular arteries coexisted in the absence of the normal brachial artery (A. brachialis profunda). After branching off a large-sized superficial subscapular artery, the axillary artery did not penetrate the brachial plexus and gave rise to a superficial brachial artery, which arose from the axillary artery at the point between the ansa pectoralis and ansa mediana, and descended ventral to the median nerve branching off the profunda brachii and superior and inferior ulnar collateral arteries. The superficial brachial artery finally divided into the radial and ulnar arteries in the cubital fossa. The superficial subscapular artery passed inferior and dorsal to the medial cord of the brachial plexus, giving off the lateral thoracic artery, and then branched off into the thoracodorsal, circumflex scapular and posterior circumflex humeral arteries. Thus the main nerves of the brachial plexus were sandwiched between the superficial brachial artery and the superficial subscapular artery system. The morphological and clinical significance of this variant are discussed.

ABSTRACT. We investigated the effect of dexamethasone (DEX) at clinical doses on the pharmacokinetics of quinidine (QN) in dogs. Dogs (5 healthy 1-year-old male beagles) were orally administered DEX once daily for 5 days at 2.5 or 7.5 mg/day. QN (2 mg/kg) was intravenously injected 3 weeks before and one day after the DEX treatment. The plasma concentration of QN was determined by high-performance liquid chromatography with fluorometric detection. Plasma concentrations of albumin and α 1 -acid glycoprotein (AGP) were determined by a bromocresol green method and a single immunodiffusion method, respectively. In order to calculate unbound concentrations of QN in plasma, the binding kinetics of QN in plasma was examined by an ultrafiltration method using pooled plasma from the 5 dogs when they were drug-free. Total body clearance of QN was decreased dose-dependently By the DEX treatment, although the decrease was not statistically significant. Elimination half-lives significantly increased (more than twice at 7.5 mg), and intrinsic clearance significantly decreased (about 50%). The volume of distribution increased significantly (about two-fold). Plasma levels of AGP significantly decreased, and the unbound fraction of QN in plasma significantly increased. Our results demonstrate that clinical doses of DEX significantly affect the pharmacokinetics of QN, a CYP3A substrate in dogs, by decreasing CYP3A activity and plasma AGP levels. There is a possibility that adverse drug-drug interaction occurs during DEX therapy through its effects on CYP3A activity and plasma AGP levels. KEY WORDS: canine, clearance, CYP3A, dexamethasone, quinidine.J. Vet. Med. Sci. 68(9): 903-907, 2006 Drug metabolism is one of the determinant factors of drug disposition. Alterations in drug metabolism are, therefore, a matter of primary concern for many researchers not only in human medicine, but also veterinary medicine. Although altered drug metabolism may result from several factors, enzyme inhibition has been extensively studied and recognized as the most important factor requiring a great deal of attention in the clinical state because it may lead to fetal toxicity of co-administered drugs in some cases [6].DEX is a well-established inducer of the cytochrome P450 (CYP) 3A subfamily. There are many reports that describe induction of CYP3A through in vitro [14,10] and in vivo studies [7,17,19]. However, very high doses (more than 10 times of the clinical dose) were used in most of the in vivo studies. In canine clinics, the recommended doses of DEX are 0.05-0.3 mg/kg/day for anti-inflammatory therapy and 0.5-1 mg/kg/day for acute adrenocortical collapse and immunosuppressive therapy [4]. In our previous study [21], therefore, we examined the inducing effect of DEX on CYP3A using clinical doses in dogs and rats. Although Jayyosi et al. reported that there is no significant induction of CYP3A in dogs treated with DEX (50 mg/kg for 5 days), we observed a decrease of about 70% in the maximum reaction velocities of midazolam 4-hydroxylation in...