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Tail Artery (tail + artery)

Distribution by Scientific Domains
Medical Sciences55%
Life Sciences44%

Selected Abstracts

Tail arteries from chronically spinalized rats have potentiated responses to nerve stimulation in vitro

THE JOURNAL OF PHYSIOLOGY, Issue 2 2004
Melanie Yeoh
Patients with severe spinal cord lesions that damage descending autonomic pathways generally have low resting arterial pressure but bladder or colon distension or unheeded injuries may elicit a life-threatening hypertensive episode. Such episodes (known as autonomic dysreflexia) are thought to result from the loss of descending baroreflex inhibition and/or plasticity within the spinal cord. However, it is not clear whether changes in the periphery contribute to the exaggerated reflex vasoconstriction. The effects of spinal transection at T7,8 on nerve- and agonist-evoked contractions of the rat tail artery were investigated in vitro. Isometric contractions of arterial segments were recorded and responses of arteries from spinalized animals (,spinalized arteries') and age-matched and sham-operated controls were compared. Two and eight weeks after transection, nerve stimulation at 0.1,10 Hz produced contractions of greater force and duration in spinalized arteries. At both stages, the ,-adrenoceptor antagonists prazosin (10 nm) and idazoxan (0.1 ,m) produced less blockade of nerve-evoked contraction in spinalized arteries. Two weeks after transection, spinalized arteries were supersensitive to the ,1 -adrenoceptor agonist phenylephrine, and the ,2 -adrenoceptor agonist, clonidine, but 8 weeks after transection, spinalized arteries were supersensitive only to clonidine. Contractions of spinalized arteries elicited by 60 mm K+ were larger and decayed more slowly at both stages. These findings demonstrate that spinal transection markedly increases nerve-evoked contractions and this can, in part, be accounted for by increased reactivity of the vascular smooth muscle to vasoconstrictor agents. This hyper-reactivity may contribute to the genesis of autonomic dysreflexia in patients. [source]

Vibration Causes Acute Vascular Injury in a Two-Step Process: Vasoconstriction and Vacuole Disruption

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 8 2008
Sandya R. Govindaraju
Abstract Hand,arm vibration syndrome is a vasospastic and neurodegenerative occupational disease. In the current study, the mechanism of vibration-induced vascular smooth muscle cell (SMC) injury was examined in a rat-tail vibration model. Tails of male Sprague Dawley rats were vibrated continuously for 4 hr at 60 Hz, 49 m/s2 with or without general anesthesia. Ventral tail arteries were aldehyde fixed and embedded in epoxy resin to enable morphological analysis. Vibration without anesthesia caused vasoconstriction and vacuoles in the SMC. Anesthetizing rats during vibration prevented vasoconstriction and vacuole formation. Exposing tail arteries in situ to 1 mM norepinephrine (NE) for 15 min induced the greatest vasoconstriction and vacuolation. NE induced vacuoles were twice as large as those formed during vibration. When vibrated 4 hr under anesthesia after pretreatment with NE for 15 min, the SMC lacked vacuoles and exhibited a longitudinal banding pattern of dark and light staining. The extracellular matrix was filled with particulates, which were confirmed by electron microscopy to be cellular debris. The present findings demonstrate that vibration-induced vasoconstriction (SMC contraction) requires functioning central nervous system reflexes, and the physical stress of vibration damages the contracted SMC by dislodging and fragmenting SMC vacuoles. Anat Rec, 291:999,1006, 2008. © 2008 Wiley-Liss, Inc. [source]

Changes in reactivity of rat arteries subjected to dynamic stretch

ACTA PHYSIOLOGICA, Issue 1 2000
Dvoretsky
The effect of dynamic stretch on the reactivity of the rat tail and mesenteric artery segments was studied. Segments mounted on a myograph were stretched by a computer-controlled motorized micromanipulator. Dynamic stretch (1, 5 or 7 Hz) inhibited the artery constriction induced by noradrenaline (10 ,M), 5-hydroxytryptamine (0.7 ,M), or electrical field stimulation of intramural nerves. In contrast, dynamic stretch enhanced the tetrodotoxin-insensitive dilation induced by electrical field stimulation of noradrenaline-contracted arteries. Maximal increase of dilation evoked by electrical field stimulation (24.5 ± 5.0% in mesenteric and 50.3 ± 15.6% in the tail artery) was observed at a dynamic stretch-frequency of 5 Hz. An inhibitor of nitric oxide synthesis, NG -nitro- L -arginine (100 ,M), abolished the difference in reactivity between static and dynamic conditions. The results indicate that dynamic stretch of the arteries activates nitric oxide synthesis/secretion, thus reducing constrictor and increasing dilator responses to the stimuli used. [source]

Tail arteries from chronically spinalized rats have potentiated responses to nerve stimulation in vitro

THE JOURNAL OF PHYSIOLOGY, Issue 2 2004
Melanie Yeoh
Patients with severe spinal cord lesions that damage descending autonomic pathways generally have low resting arterial pressure but bladder or colon distension or unheeded injuries may elicit a life-threatening hypertensive episode. Such episodes (known as autonomic dysreflexia) are thought to result from the loss of descending baroreflex inhibition and/or plasticity within the spinal cord. However, it is not clear whether changes in the periphery contribute to the exaggerated reflex vasoconstriction. The effects of spinal transection at T7,8 on nerve- and agonist-evoked contractions of the rat tail artery were investigated in vitro. Isometric contractions of arterial segments were recorded and responses of arteries from spinalized animals (,spinalized arteries') and age-matched and sham-operated controls were compared. Two and eight weeks after transection, nerve stimulation at 0.1,10 Hz produced contractions of greater force and duration in spinalized arteries. At both stages, the ,-adrenoceptor antagonists prazosin (10 nm) and idazoxan (0.1 ,m) produced less blockade of nerve-evoked contraction in spinalized arteries. Two weeks after transection, spinalized arteries were supersensitive to the ,1 -adrenoceptor agonist phenylephrine, and the ,2 -adrenoceptor agonist, clonidine, but 8 weeks after transection, spinalized arteries were supersensitive only to clonidine. Contractions of spinalized arteries elicited by 60 mm K+ were larger and decayed more slowly at both stages. These findings demonstrate that spinal transection markedly increases nerve-evoked contractions and this can, in part, be accounted for by increased reactivity of the vascular smooth muscle to vasoconstrictor agents. This hyper-reactivity may contribute to the genesis of autonomic dysreflexia in patients. [source]

A Nonsurgical Technique for Blood Access in Extracorporeal Affinity Adsorption of Antibodies in Rats

ARTIFICIAL ORGANS, Issue 4 2007
Linda Mårtensson
Abstract:, Monoclonal antibodies for targeting cytotoxic conjugates to tumor cells are currently being evaluated together with extracorporeal affinity adsorption. The aim of the adsorption was to reduce undesired side effects in normal organs and to increase the tumor-to-normal tissue ratios. This technique is also applicable to several other therapeutic areas such as immune-mediated disorders, that is, autoimmunity, allergy, and transplantation rejection. We describe an improved technique for extracorporeal affinity adsorption of radiolabeled biotinylated antibodies in rats. Blood access is established through the tail artery and tail vein, without surgical insertion of permanent catheters. This technique is simple, does not require surgery, and causes only minimal stress to the animals. In addition, experiments can be carried out on several animals simultaneously. This new technique is of considerable benefit for studying extracorporeal affinity adsorption in rats, as experiments can be carried out with negligible anatomical and physiological interventions, compared to previously used techniques. [source]

Rho kinase inhibitors reduce neurally evoked contraction of the rat tail artery in vitro

BRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2005
Melanie Yeoh
The effects of Rho kinase inhibitors (Y27632, HA-1077) on contractions to electrical stimulation and to application of phenylephrine, clonidine or ,,, -methylene adenosine 5,-triphosphate (,,, -mATP) were investigated in rat tail artery in vitro. In addition, continuous amperometry and intracellular recording were used to monitor the effects of Y27632 on noradrenaline (NA) release and postjunctional electrical activity, respectively. Y27632 (0.5 and 1 ,M) and HA-1077 (5 ,M) reduced neurally evoked contractions. In contrast, the protein kinase C inhibitor, Ro31-8220 (1 ,M), had little effect on neurally evoked contraction. In the absence and the presence of Y27632 (0.5 ,M), the reduction of neurally evoked contraction produced by the , -adrenoceptor antagonists prazosin (10 nM) and idazoxan (0.1 ,M) was similar. The P2-purinoceptor antagonist, suramin (0.1 mM), had no inhibitory effect on neurally evoked contraction in the absence or the presence of Y27632 (1 ,M). In the presence of Y27632, desensitization of P2X-purinoceptors with ,,, -mATP (10 ,M) increased neurally evoked contractions. Y27632 (1 ,M) and H-1077 (5 ,M) reduced sensitivity to phenylephrine and clonidine. In addition, Y27632 reduced contractions to ,,, -mATP (10 ,M). Y27632 (1 ,M) had no effect on the NA-induced oxidation currents or the purinergic excitatory junction potentials and NA-induced slow depolarizations evoked by electrical stimulation. Rho kinase inhibitors reduce sympathetic nerve-mediated contractions of the tail artery. This effect is mediated at a postjunctional site, most likely by inhibition of Rho kinase-mediated ,Ca2+ sensitization' of the contractile apparatus. British Journal of Pharmacology (2005) 146, 854,861. doi:10.1038/sj.bjp.0706377 [source]

Quercetin as a novel activator of L-type Ca2+ channels in rat tail artery smooth muscle cells

BRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2002
Simona Saponara
The aim of this study was to investigate the effects of quercetin, a natural polyphenolic flavonoid, on voltage-dependent Ca2+ channels of smooth muscle cells freshly isolated from the rat tail artery, using either the conventional or the amphotericin B-perforated whole-cell patch-clamp method. Quercetin increased L-type Ca2+ current [ICa(L)] in a concentration- (pEC50=5.09±0.05) and voltage-dependent manner and shifted the maximum of the current-voltage relationship by 10 mV in the hyperpolarizing direction, without, however, modifying the threshold and the equilibrium potential for Ca2+. Quercetin-induced ICa(L) stimulation was reversible upon wash-out. T-type Ca2+ current was not affected by quercetin. Quercetin shifted the voltage dependence of the steady-state inactivation and activation curves to more negative potentials by about 5.5 and 7.5 mV respectively, in the mid-potential of the curves as well as increasing the slope of activation. Quercetin slowed both the activation and the deactivation kinetics of the ICa(L). The inactivation time course was also slowed but only at voltages higher than 10 mV. Moreover quercetin slowed the rate of recovery from inactivation. These results prove quercetin to be a naturally-occurring L-type Ca2+ channel activator. British Journal of Pharmacology (2002) 135, 1819,1827; doi:10.1038/sj.bjp.0704631 [source]