Large-sized Arteries Research Articles

Rare variation of the arm artery: coexistence with the superficial brachial and superficial subscapular arteries in the absence of the normal brachial artery.

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.

Coronary arterial lesions induced by endothelin antagonists

Endothelins are potent vasoconstrictors and pressor peptides and are important mediators of cardiac, renal and endocrine functions. Increased ET-1 levels in disease states such as congestive heart failure, pulmonary hypertension, acute myocardial infarction, and renal failure suggest the endothelin system as an attractive target for pharmacotherapy. A non-peptidic, selective, competitive endothelin receptor antagonist with an affinity for the ET A receptor in the subnanomolar range was administered by continuous intravenous infusion to beagle dogs, rats, and Goettingen minipigs. It caused mild arteriopathy characterised by segmental degeneration in the media of mid- to large-size coronary arteries in the heart of dog, but not rat or minipig. The lesions only occurred in the atrium and ventricle. Frequency and severity of the vascular lesions was not sex or dose related. No effects were noted in blood vessels in other organs or tissue. Plasma concentrations at steady state, and overall exposure in terms of AUC (0–24h) were higher in minipig and rat than the dog but did not cause cardiac arteriopathy. These findings concur with those caused by other endothelin anatagonists, vasodilators and positive inotropic/vasodilating drugs such as potassium channel openers, phosphodiesterase inhibitors and peripheral vasodilators, and confirm that dogs appear to be uniquely sensitive to the development of cardiac vascular lesions.

Theophylline-induced mesenteric periarteritis in F344/N rats.

The toxicity and carcinogenic potential of theophylline (an alkaloid bronchodilator drug) was investigated in male and female F344/N rats in 16-day, 14-week, and 2-year gavage and feeding studies. In 16-day studies, rats were fed diets containing 0, 500, 1000, 2000, 4000, and 8000 ppm of theophylline or given 0, 12.5 (twice daily), 25 (once daily), 50 (once daily), 50 (twice daily), 100 (once daily), 200 (once daily), 200 (twice daily), and 400 (once daily) mg theophylline/kg body weight in corn oil by gavage. In 14-week studies, rats were fed diets containing 0, 1000, 2000, and 4000 ppm theophylline or given 0, 37.5, 75, and 150 mg/kg body weight theophylline in corn oil by gavage. In 2-year gavage studies, rats were given 0, 7.5, 25, and 75 mg/kg body weight in corn oil. In 16-day gavage studies, treatment-related periarteritis occurred in arteries of the pancreas and adjacent to the mesenteric lymph nodes of early death male and female rats given 400 mg/kg once daily. In the 14-week studies, treatment-related periarteritis occurred at similar sites and in male rats exposed to 75 and 150 mg/kg, and in all exposed female rats (gavage studies), in females exposed to 1000 ppm, and in both sexes exposed to 2000 and 4000 ppm (feeding studies). In the 2-year study, chronic periarteritis was significantly increased only in the males receiving 75 mg/kg of theophylline. The adventitia, media and intima of medium- and large-sized mesenteric arteries were involved. Similar to other vasodilator chemicals, the pathogenesis of theophylline-induced vascular lesions may be a consequence of hemodynamic changes induced in the vascular wall.

Glucocorticoid-mediated repression of cytokine gene transcription in human arteritis-SCID chimeras.

Giant cell arteritis (GCA) is a vasculitic syndrome that preferentially affects medium and large-sized arteries. Glucocorticoid therapy resolves clinical symptoms within hours to days, but therapy has to be continued over several years to prevent disease relapses. It is not known whether and how glucocorticoids affect the function of the inflammatory infiltrate or why the disease persists subclinically despite chronic treatment. GCA is self-sustained in temporal arteries engrafted into SCID mice, providing a model in which the mechanisms of action and limitations of glucocorticoid therapy can be examined in vivo. Administration of dexamethasone to temporal artery-SCID chimeras for 1 wk induced a partial suppression of T cell and macrophage function as indicated by the reduced tissue concentrations of IL-2, IL-1beta, and IL-6 mRNA, and by the diminished expression of inducible NO synthase. In contrast, synthesis of IFN-gamma mRNA was only slightly decreased, and expression of TGF-beta1 was unaffected. These findings correlated with activation of the IkappaBalpha gene and blockade of the nuclear translocation of NFkappaB in the xenotransplanted tissue. Dose-response experiments suggested that steroid doses currently used in clinical medicine are suboptimal in repressing NFkappaB-mediated cytokine production in the inflammatory lesions. Chronic steroid therapy was able to deplete the T cell products IL-2 and IFN-gamma, whereas the activation of tissue-infiltrating macrophages was only partially affected. IL-1beta transcription was abrogated; in contrast, TGF-beta1 mRNA synthesis was steroid resistant. The persistence of TGF-beta1-transcribing macrophages, despite paralysis of T cell function, may provide an explanation for the chronicity of the disease, and may identify a novel therapeutic target in this inflammatory vasculopathy.

Giant cell arteritis

Giant cell arteritis is a form of vasculitis affecting medium- and large-size arteries, with a predilection for vessels arising from the aortic arch. The origins of giant cell arteritis are unknown. However, ethnic affinities are prominent, with the majority of cases involving white, elderly patients. In addition, there is evidence of a familial pattern and an association with HLA-DR4, suggesting a genetic predisposition in select cases. With an increase in the elderly population, clinicians must become cognizant of this age-related malady and its treatment to ensure quality care for elderly patients.

Arterial Occlusive Disease in Systemic Lupus Erythematosus

The lesions of middle- and large-sized arteries due to systemic lupus erythematosus have been infrequently reported, but vasculitis of small arterioles has been seen more commonly. Herein, a forty-four-year-old woman with lower extremity arterial occlusive disease secondary to systemic lupus erythematosus is presented, and the results of sympathectomy are described.

Takayasu's Arteritis and Temporal Arteritis

The giant cell arteritides, temporal arteritis and Takayasu’s arteritis, are granulomatous vasculitides affecting medium and large-sized arteries. Temporal arteritis is a systemic panarteritis affecting the elderly, with greater than 95% of patients being over 50 years of age, although a few case reports in young adults and adolescents exist. The etiology is unknown, but evidence suggests an autoimmune phenomenon. Generalized constitutional symptoms usually precede diagnosis, and the symptom complex is often consistent with polymyalgia rheumatica, thus raising the prospect of a relationship between the two entities. The hallmark of diagnosis is an elevated erythrocyte sedimentation rate and a positive arterial biopsy. Involvement of the subclavian-axillary arterial segment may produce ischemic symptoms of the upper extremities, and carotid and retinal artery involvement may lead to blindness. Prompt steroid therapy may resolve both the anatomic and clinical pictures. Takayasu’s arteritis produces stenosis and aneurysms of medium and large arteries of the aortic arch, abdominal aorta, their branches or a combination in young women. Its etiology, like that of temporal arteritis, is unknown, although an autoimmune-mediated etiology is a distinct possibility in Takayasu’s arteritis, also. There is an acute and chronic phase of the disease. During the acute inflammatory phase, the erythrocyte sedimentation rate is elevated, and this phase may last months to years. Reduced or absent pulses, presence of bruits

Binding of [3H]Isradipine (PN 200-110) on Smooth Muscle Cell Membranes from Different Bovine Arteries

The binding of [3H]isradipine [( 3H]PN 200-110), a new dihydropyridine (DHP) calcium blocker on smooth muscle cell (SMC) membranes from different bovine arteries was saturable with comparable high affinities but different binding site densities (Bmax). The data were fitted to a model that provided a common estimation for the dissociation constant (Kd = 0.46 nM, SD = 0.03) but different Bmax values. Two groups of arteries could be distinguished, large-sized with high Bmax (aorta, 149 fmol/mg, SD = 4; intrapulmonary, 134 fmol/mg, SD = 4) and medium-sized with lower Bmax (mesenteric, 67 fmol/mg, SD = 2; internal carotid, 50 fmol/mg, SD = 2; renal artery, 29 fmol/mg, SD = 2). The Kd values were similar to those previously reported, but the Bmax value on aorta SMC was higher than usually reported with other DHPs, showing that isradipine was a high full antagonist of calcium channel. Our results also suggest that the increase in arterial compliance induced by DHPs will probably be more important on large-sized arteries than on medium-sized arteries because of higher DHP binding.

When and why do ulcers bleed and what can be done about it?

This article reviews the pathophysiology and management of bleeding peptic ulcer. Ulcers bleed when and because they erode into a blood vessel, and bleed massively when they erode into a medium- or large-sized artery. Focal pathology at the bleeding point (such as arteritis, aneurysmal dilatation or recanalized thrombus) contributes to the timing and clinical pattern of ulcer bleeding. Big bleeds are probably associated with erosion into big arteries. The identification of a visible vessel in the floor of an ulcer that has recently bled is predictive of further bleeding, while the absence of a visible vessel or stigmata of recent haemorrhage is strongly predictive that further bleeding will not occur. Unfortunately, no conventional method of managing gastrointestinal bleeding from ulcers has been convincingly shown to be better than placebo in controlled clinical trials. The value of transfusion and surgery has never been tested in controlled trials, while many small studies of drug therapy, especially of H2-receptor blocking agents, and a few small studies of early surgery afford generally negative or equivocal results. There is some evidence that new physical methods such as lasers or bipolar probes applied at endoscopy are superior to placebo though negative trials have also been reported. Studies randomizing larger numbers of patients with bleeding ulcers are required if therapeutic benefit of any aspect of management is to be demonstrated or refuted.

The Regional Difference of Relaxations Induced by Various Vasodilators in Isolated Dog Coronary and Mesenteric Arteries

Relaxant responses to vasodilators, including nitroglycerin, sodium nitroprusside, prostaglandin I2 sodium salt (PGI2), prostaglandin E1 (PGE1), diltiazem hydrochloride and adenosine, were compared in heiical strips of dog coronary arteries of different sizes and in coronary and mesenteric arterial strips. The relaxant responses to nitroglycerin, sodium nitroprusside, diltiazem and adenosine were significantly greater in coronary arteries than in mesenteric arteries, whereas the responses to PGI2 and PGEt in these arteries did not significantly differ. In coronary arteries of different sizes, the relaxation induced by nitroglycerin was in the order of large>medium>small-size, while in contrast, the relaxations by adenosine, PGI2 and PGE1 were greatest in the small-size arteries and least in the large-size arteries. The relaxant responses to sodium nitroprusside and diltiazem did not differ in the coronary arteries of different sizes. Nitroglycerin, sodium nitroprusside and diltiazem appear to dilate coronary arteries more predominantly than mesenteric arteries. The preferential dilator action of PGI2 and PGE1 on distal coronary arteries, like that of adenosine, may lead more blood to re-distribute to the non-ischemic region of the heart in anginal patients.