Relevant bibliographies by topics / And Rat aorta rings

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Academic literature on the topic 'And Rat aorta rings'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "And Rat aorta rings"

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Nurullahoğlu-Atalık, KE, S. Kutlu, H. Solak, and R. Özen Koca. "Cilostazol enhances atorvastatin-induced vasodilation of female rat aorta during aging." Physiology International 104, no. 3 (September 2017): 226–34. http://dx.doi.org/10.1556/2060.104.2017.3.3.

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Statins have cholesterol-independent effects including an increased vascular nitric oxide activity and are commonly used by patients with cardiovascular disease. Such patients frequently have cardiovascular diseases, which may be treated with cilostazol, a platelet aggregation inhibitor. This study was designed to investigate whether combined use of cilostazol would increase the inhibitory effect of statin on vascular smooth muscle and how maturation would affect these responses. Female Wistar rats, aged 3–4 months (young) and 14–15 months (adult), were sacrificed by cervical dislocation and the thoracic aorta was dissected and cut into 3- to 4-mm-long rings. The rings were mounted under a resting tension of 1 g in a 20-ml organ bath filled with Krebs–Henseleit solution. Rings were precontracted with phenylephrine (10−6 M), and the presence of endothelium was confirmed with acetylcholine (10−6 M). Then, the concentration–response curves were obtained for atorvastatin alone (10−10 to 3 × 10−4 M; control) and in the presence of cilostazol (10−6 M) in young and adult rat aortas. This experimental protocol was also carried out in aorta rings, which had been pretreated with NG-nitro-l-arginine methyl ester (l-NAME, 10−4 M). Atorvastatin induced concentration-dependent relaxations in young and adult rat thoracic aorta rings precontracted with phenylephrine. The pIC50 value of atorvastatin was significantly decreased in adult rat aortas. In addition, pretreatment of aortas with cilostazol enhanced the potency of atorvastatin in both young and adult aortas. Incubation with l-NAME did not completely eliminate the relaxations to atorvastatin in the presence of cilostazol. These results suggest that combined application of cilostazol with atorvastatin was significantly more potent than atorvastatin alone. Combined drug therapy may be efficacious in delaying the occurrence of cardiovascular events.
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Pieper, G. M., D. A. Mei, P. Langenstroer, and S. T. O'Rourke. "Bioassay of endothelium-derived relaxing factor in diabetic rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 3 (September 1, 1992): H676—H680. http://dx.doi.org/10.1152/ajpheart.1992.263.3.h676.

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The bioassay technique was utilized to quantitate endothelium-derived relaxing factor (EDRF) released from perfused donor segments of control and diabetic rat aorta. In the presence of indomethacin, perfusates of donor segments with endothelium were allowed to superfuse recipient detector rings of normal rat aorta without endothelium. Under basal conditions, relaxations of the bioassay rings to perfusates of control and diabetic donor segments were similar. Perfusion of donor segments with acetylcholine produced relaxation of bioassay rings, which was decreased from endothelial perfusion of diabetic donor segments. These relaxations were inhibited by addition of methylene blue to the detector ring or by perfusion of donor segments with nitro-L-arginine. Infusion of superoxide dismutase (SOD) at a site proximal to the donor segment normalized relaxations induced by acetylcholine addition to diabetic donors. In contrast, infusion of SOD distal to the donor had no effect on acetylcholine-stimulated relaxations of detector rings from control donors while attenuating, paradoxically, the relaxations of detector rings from diabetic donors. These results suggest that diabetic rat aortas release similar levels of EDRF in response to acetylcholine, but the action of EDRF arising from diabetic donors is attenuated by enhanced release of oxygen-derived free radicals, which limits EDRF-mediated relaxation of vascular smooth muscle.
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Langenstroer, P., and G. M. Pieper. "Regulation of spontaneous EDRF release in diabetic rat aorta by oxygen free radicals." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 1 (July 1, 1992): H257—H265. http://dx.doi.org/10.1152/ajpheart.1992.263.1.h257.

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The interaction of endothelium-derived relaxing factor (EDRF) and oxygen-derived free radicals may potentially play an important role in the pathophysiology of complications associated with diabetes. In the present study, we investigated spontaneous EDRF release in diabetic rat aorta that is unmasked by the addition of superoxide dismutase (SOD). SOD produced a significantly greater relaxation in diabetic aorta compared with control aorta using both aortic ring and bioassay preparations. This relaxation was unaltered by pretreatment with catalase or indomethacin. Removal of the endothelium or pretreatment with either NG-monomethyl-L-arginine or methylene blue eliminated SOD-induced relaxation in both control and diabetic rings. Measurement of antioxidant enzymes revealed an elevation in catalase in diabetic aorta, with no difference in the SOD or glutathione peroxidase activity. The increase in catalase activity suggests increased exposure of diabetic aorta to hydrogen peroxide. Pretreatment of rings with the catalase inhibitor, 3-amino-1,2,4-triazole, attenuated the SOD-induced relaxation in diabetic aortic rings but had no effect in control aortic rings. In summary, our observations suggest that the diabetic rat aorta releases more spontaneous EDRF than control aorta; however, the activity of EDRF on vascular smooth muscle tone is masked by increased destruction by oxygen-derived free radicals.
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Kutchai, Howard, and Lisa M. Geddis. "Lactate Transport in Rat Aorta." Journal of Vascular Research 22, no. 2 (1985): 84–93. http://dx.doi.org/10.1159/000158587.

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1. Ouabain (10 mM) and gramicidin (5 µg/ml) do not inhibit lactate uptake by rat aortic rings. This supports the integretation that a Na<sup>+</sup> gradient is not involved in lactate transport. 2. Dinitrophenol (25 µM) fails to inhibit lactate uptake, suggesting that oxidative metabolism is not required for lactate uptake. 3. DIDS (4,4’-diisothiocyano-2,2’-stilbenedisulfonate), quercetin, and α-cyano-4-hydroxycinnamate – agents that have been reported to inhibit lactate transport in other cell types -were ineffective in inhibiting lactate transport in rat aortic rings.4. Inhibition of lactate uptake by glyceraldehyde is not stereospecific, does not involve inhibition of glucose phosphorylation, and does not appear to involve interaction with membrane sulfhydryls. PCMBS (p-chloromercuribenzenesulfonate) does not markedly inhibit the initial rate of lactate uptake, but diminishes the lactate space at later times.5. Pyruvate, phenylpyruvate, and thiolactate inhibit lactate uptake, but propionate and glycolate are poor inhibitors.
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Bouchard, Jean-François, Éric C. Dumont, and Daniel Lamontagne. "Modification of vasodilator response in streptozotocin-induced diabetic rat." Canadian Journal of Physiology and Pharmacology 77, no. 12 (November 15, 1999): 980–85. http://dx.doi.org/10.1139/y99-106.

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Functional dilatory response in streptozotocin-induced diabetic rats was investigated using thoracic aortas, isolated hearts, and mesenteric beds. Dose-response curves to the PGI2 analogue iloprost on phenylephrine-preconstricted rings of diabetic rats and controls were comparable. In contrast, decreased vasodilation in diabetic rats was observed when dose-response curves to iloprost were performed in hearts and on phenylephrine-preconstricted mesenteric beds. Dose-response curves to forskolin, an adenylyl cyclase activator, performed with hearts and phenylephrine-preconstricted aortic rings and isolated mesenteric beds of diabetic rats and controls were comparable. However, a decreased vasodilation to the ATP-sensitive potassium channel (KATP) activator lemakalim was observed in diabetic hearts, but not in aortic rings and mesenteric beds. In conclusion, under our experimental conditions, diabetes mellitus affects the vasodilation to iloprost in both coronary and mesenteric beds, but not in the aorta. In the heart, this modification of vascular reactivity may be due to a decrease in KATP channel mediated response and not to a decreased activity of adenylyl cyclase. At this time, in the isolated mesenteric bed, the mechanism of this modification in vascular reactivity remains unknown.Key words: diabetes mellitus, iloprost, KATP channels, adenylyl cyclase, aorta, coronary circulation, mesenteric bed.
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Chakraborty, Indrani, Nirmal Chandra Sukul, Rungrapa Mesripong, Nattaya Chaothanaphat, Prasan Dhummaupakorn, and Anirban Sukul. "High dilutions of homeopathic remedies induce relaxation of rat aorta precontracted with Noradrenalin." International Journal of High Dilution Research - ISSN 1982-6206 12, no. 43 (December 2, 2021): 44–51. http://dx.doi.org/10.51910/ijhdr.v12i43.627.

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BACKGROUND Homeopathic potencies have been reported to produce alteration of contraction in isolated rat ileum in an organ bath. Potentized homeopathic drugs like Lycopus V and Aurum met are used for the treatment of hypertension. AIM The purpose of this study is to see whether Lycopus V 30 CH and Aurum met 30 CH could produce relaxation of isolated rat aorta in the organ bath. METHODS The aorta of rats were dissected out, placed in Krebs-Henseleit solution, cleared of connective tissue and endothelium and cut into 2-2.5 mm long rings. The rings were fixed in organ baths with the upper end connected by a string to an isometric transducer which was finally attached through a data acquisitation equipment to a computer. Aurum met 30 CH Lycopus V 30 CH, and their medium 90% ethanol were added separately to the bathing fluid containing the aorta rings which were precontracted with noradrenalin (NA). RESULTS Both the drugs produced significant relaxation of the aorta (p
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Tsakadze, Nina L., Sanjay Srivastava, Sunday O. Awe, Ayotunde S. O. Adeagbo, Aruni Bhatnagar, and Stanley E. D'Souza. "Acrolein-induced vasomotor responses of rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 2 (August 2003): H727—H734. http://dx.doi.org/10.1152/ajpheart.00269.2003.

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Acrolein is a highly reactive aldehyde pollutant and an endogenous product of lipid peroxidation. Increased generation of, or exposures to, acrolein incites pulmonary and vascular injury. The effects of acrolein on the vasomotor responses of rat aortic rings were studied to understand its mechanism of action. Incubation with acrolein (10–100 μM) alone did not affect the resting tone of aortic vessels; however, a dose-dependent relaxation of phenylephrine-precontracted aortic rings was observed. Acrolein-induced relaxation was slow and time dependent and the extent of relaxation after 100 min of application was 44.7 ± 4.1% (10 μM), 56.0 ± 5.6% (20 μM), 61.0 ± 7.9% (40 μM), and 96.1 ± 2.1 (80 μM), respectively, versus 14.2 ± 3.3% relaxation in the absence of acrolein. Acrolein-induced vasorelaxation was prevented by endothelial denudation and was abolished on pretreatment with the nitric oxide synthase inhibitor Nω-nitro-l-arginine methyl ester, the guanylyl cyclase inhibitor 1 H-[1,2,4]oxidazolo[4,3- a]quinoxaline-1-one, or the cyclooxygenase inhibitor indomethacin. Inhibition of K+ channels (by tetrabutylammonium) or Na+-K+-ATPase (by ouabain) did not significantly prevent acrolein-mediated vasorelaxation. Exposure to acrolein in the presence or absence of other compounds elicited slow wave vasomotor effect in 77% of aortic vessels versus 1.4% in control. Vasomotor responses were also studied on aortic rings prepared from rats fed 2 mg · kg–1 · day–1 acrolein for 3 alternate days by oral gavage. These vessels developed a significantly lower contractile response to phenylephrine compared with controls. Together, these results indicate that acute acrolein exposure evokes delayed vasorelaxation due to a nitric oxide- and prostacyclin-dependent mechanism, whereas in vivo acrolein exposure compromises vessel contractility.
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Omanwar, S., B. Saidullah, K. Ravi, and M. Fahim. "Vasorelaxant effects of mercury on rat thoracic aorta." Human & Experimental Toxicology 33, no. 9 (December 17, 2013): 904–10. http://dx.doi.org/10.1177/0960327113512341.

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Mercury, a heavy metal, is widespread and persistent in the environment and has been elucidated as a possible risk factor in cardiovascular diseases. Mercury has been reported to selectively impair the nitric oxide (NO) pathway in the vascular endothelium as a consequence of oxidative stress. Conversely, mercury per se causes endothelium-dependent vasorelaxation at lower concentration via the NO pathway. Little is known about the effects of mercury per se on other endothelial mediators. To elucidate possible mechanisms involved in this action, isometric tension was measured in aortic rings precontracted with phenylephrine (10 µM) from Wistar rats. Responses to increasing concentrations of inorganic mercuric chloride (10−12–10−5 M) were obtained in the presence and absence of endothelium. Inorganic mercury produced a biphasic response in endothelium-intact aortic rings and produced only vasoconstriction in endothelium-denuded aortic rings. To study the possible underlying mechanisms for the biphasic response of mercury, increasing concentrations of mercuric chloride (10−12–10−5 M) were used before and after NG-nitro-l-arginine methyl ester (L-NAME (10−4 M)), glybenclamide (10−5 M), superoxide dismutase (10 U/ml) + catalase (100 U/ml), and nifedipine (10−4 M) treatment. Results suggest that mercury produces endothelium-dependent relaxation at low concentration mediated by endothelial-generated NO and endothelium-derived hyperpolarizing factor and endothelium-independent contraction resulting from the blockade of l-type Ca2+ channels by generation of free radicals.
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Delp, M. D., T. Holder-Binkley, M. H. Laughlin, and E. M. Hasser. "Vasoconstrictor properties of rat aorta are diminished by hindlimb unweighting." Journal of Applied Physiology 75, no. 6 (December 1, 1993): 2620–28. http://dx.doi.org/10.1152/jappl.1993.75.6.2620.

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Prolonged bed rest and exposure to weightlessness in humans result in cardiovascular alterations that are characterized by orthostatic intolerance and decreased exercise capacity. Modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Rat hindlimb unweighting (HU) was used as an animal model to determine whether prolonged decreases in weight-bearing activity induce changes in vasoreactivity of peripheral arterial vessels. Responses to vasoactive compounds were examined in vitro using isolated abdominal and thoracic aortic rings. Maximal isometric contractile tension evoked by the vasoconstrictors KCl (10–100 mM), norepinephrine (NE; 10(-9)-10(-4) M), phenylephrine (10(-9)-10(-4) M), arginine vasopressin (10(-13)-3 x 10(-5) M), and CaCl2 (10(-6)-10(-2) M) was lower in abdominal aortic rings from HU rats. Sensitivity [agonist concentration that produced 50% of maximal vasoconstrictor response (EC50)] to KCl was enhanced in segments from HU animals but was not different for the other constrictors. Maximal contractile responses of thoracic aortic rings to KCl (10–100 mM) and NE (10(-9)-10(-4) M) were also attenuated by HU. In abdominal aortic rings preconstricted with 10(-4) M NE, maximal vasodilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and 8-bromoguanosine 3',5'-cyclic monophosphate (10(-6)-10(-2) M) were greater in vessel rings from HU rats. However, with 10(-7) M NE preconstriction, maximal dilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and acetylcholine (10(-9)-10(-4) M) were not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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Jing, Ming, Saiid Bina, Ajay Verma, Jayne L. Hart, and Sheila M. Muldoon. "Effects of Halothane and Isoflurane on Carbon Monoxide-induced Relaxations in the Rat Aorta." Anesthesiology 85, no. 2 (August 1, 1996): 347–54. http://dx.doi.org/10.1097/00000542-199608000-00017.

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Background Halothane and isoflurane previously were reported to attenuate endothelium-derived relaxing factor/nitric oxide-mediated vasodilation and cyclic guanosine monophosphate (cGMP) formation in isolated rat aortic rings. Carbon monoxide has many chemical and physiologic similarities to nitric oxide. This study was designed to investigate the effects of halothane and isoflurane on carbon monoxide-induced relaxations and cGMP formation in the isolated rat aorta. Methods Isometric tension was recorded continuously from endothelium denuded rat aortic rings suspended in Krebs-filled organ baths. Rings precontracted with submaximal concentrations of norepinephrine were exposed to cumulative concentrations of carbon monoxide (26-176 microM). This procedure was repeated three times, with anesthetics delivered 10 min before the second procedure. Carbon monoxide responses of rings contracted with the same concentration of norepinephrine (10(-6) M and 2 x 10(-6) M) used in the anesthetic-exposed preparations also were examined. The concentrations of cGMP were determined in denuded rings using radioimmunoassay. The rings were treated with carbon monoxide (176 microM, 30 s) alone, or carbon monoxide after a 10-min incubation with halothane (0.34 mM or 0.72 mM). To determine whether the sequence of anesthetic delivery influenced results, vascular rings pretreated with halothane were compared with nonpretreated rings. Results Carbon monoxide (26-176 microM) caused a dose-dependent reduction of norepinephrine-induced tension, with a maximal relaxation of 1.51 +/- 0.07 g (85 +/- 7% of norepinephrine-induced contraction). Halothane (0.34 mM and 0.72 mM) significantly attenuated the carbon monoxide-induced relaxations, but only the highest concentration of isoflurane (0.53 mM) significantly attenuated the carbon monoxide-induced relaxations. Carbon monoxide (176 microM) significantly increased cGMP content (+88.1 +/- 7.1%) and preincubation of the aortic rings with halothane (0.34 mM and 0.72 mM) inhibited this increase (-70.7 +/- 6.8% and -108.1 +/- 10.6%, respectively). When aortic rings and carbon monoxide were added simultaneously to Krebs solution equilibrated with halothane (0.72 mM), no inhibition of cGMP formation occurred. Conclusion Carbon monoxide-induced endothelium-independent relaxations of rat aortic rings were decreased by clinically relevant concentrations of halothane and isoflurane. The carbon monoxide-induced elevations of cGMP were attenuated by halothane only when the anesthetic was incubated with aortic rings before carbon monoxide treatment. The possible clinical significance of the actions of the anesthetics on this endogenous vasodilator is yet to be determined.
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Dissertations / Theses on the topic "And Rat aorta rings"

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Ghalb, Faraa Amer Ahmed. "IN VITRO FUNCTIONAL INTERPLAY BETWEEN PERIVASCULAR ADIPOSE TISSUE AND FLAVONOIDS: CRITICAL ROLE OF BETA3 RECEPTOR AND SUPEROXIDE ANION." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1207163.

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Flavonoids, a class of natural polyphenols abundantly present in our diet, have been shown to exert in vitro vasorelaxant activity. This was ascribed to a direct effect on the smooth muscle or factors released by the endothelium. Nowadays, perivascular adipose tissue (PVAT) is emerging as a fine regulator of blood vessel contractility. Therefore, it is conceivable to hypothesize that flavonoids vasoactivity may occur also through or is influenced, either positively or negatively, by PVATreleased factors. This hypothesis was assessed in vitro on rat aorta rings. Several flavonoids proved to display both antispasmodic and spasmolytic activity towards noradrenaline-induced contraction of rings deprived of PVAT (-PVAT). However, when PVAT was present (+PVAT), both activities of some flavonoids were lost and/or much decreased. In rings-PVAT, the superoxide donor pyrogallol mimicked the effect of PVAT, whereas in rings+PVAT the antioxidant mito-tempol restored both activities of the two most powerful flavonoids, namely apigenin and chrysin. The Rho-kinase inhibitor fasudil, or apigenin and chrysin concentration-dependently relaxed the vessel active tone induced by the Rho-kinase activator NaF; the presence of PVAT counteracted apigenin spasmolytic activity though only in the absence of mito-tempol. Similar results were obtained in rings pre-contracted with phenylephrine. Finally, when β3 receptors were blocked by SR59230A, the vasorelaxant activity of both flavonoids was no more affected by PVAT. These findings are coherent with the hypothesis that both noradrenaline and apigenin activated adipocyte β3 receptors with the ensuing release of mitochondrial superoxide anion, which once diffused toward myocytes counteracted flavonoid vasorelaxant activity, thus underlining the control of adipocytes upon the vascular tone. This phenomenon might limit the beneficial health effects of this class of natural compounds in patients affected by either obesity and/or other pathological conditions characterized by sympathetic nerve overactivity.
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Al-Zobaidy, Mohammed. "Differential actions of methlyarginines in the rat aorta." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3838/.

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The PhD project is about the Regulation of vascular tone by endothelium. It involves studying the effects of methylated arginine analogues such as monomethyl arginine (L-NMMA) and asymmetric dimethylarginine (ADMA) on nitric oxide (NO) activity in rat aorta using organ baths containing Krebs solution at 37 ˚C and gassed with 95% O2 and 5% CO2. These two inhibitors of endothelial nitric oxide synthase enzyme (eNOS) showed an anomalous action, as they inhibited basal NO activity (assessed by enhancement of phenylephrine-induced tone and by blocking relaxations produced by superoxide dismutase or the PDE5 inhibitor; T0156) but not that is stimulated by agonists like acetylcholine or the calcium ionophore A23187. After establishing these findings I will try to find the reason(s) for these paradoxical actions of these two endogenously synthesized inhibitors of eNOS.
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藍志洪 and Chi-hung Nam. "Effect of cerivastatin on endothelial function in rat aorta." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B42575837.

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Nam, Chi-hung. "Effect of cerivastatin on endothelial function in rat aorta." Click to view the E-thesis via HKUTO, 2001. http://sunzi.lib.hku.hk/hkuto/record/B42575837.

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Vinh, Vu Huu. "Comparative contractile effects of halothane and sevoflurane in rat aorta." Kyoto University, 2001. http://hdl.handle.net/2433/150545.

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Gorp, Adrianus Wilhelmus van. "The relationship between structural and in vivo dynamic mechanical properties of the thoracic aorta in rats influence of ageing and hypertension /." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=7537.

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Rice, Kevin M. "Effects of aging on pressure-induced MAPK activation in the rat aorta." Huntington, WV : [Marshall University Libraries], 2005. http://www.marshall.edu/etd/descript.asp?ref=526.

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管漢偉 and Hon-wai Michael Koon. "Potentiating effects of platelet activating factor on endothelin-1 induced rat arota vasoconstriction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31221014.

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Koon, Hon-wai Michael. "Potentiating effects of platelet activating factor on endothelin-1 induced rat arota vasoconstriction /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20565689.

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Ferreira, Iolanda João Mora Cruz de Freitas. "Pre and postjunctional effects of rosiglitazone on the isolated rat aorta and heart." Master's thesis, Faculdade de Medicina da Universidade do Porto, 2010. http://hdl.handle.net/10216/61097.

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Books on the topic "And Rat aorta rings"

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Alatawi, Abdulrahman *. The synthesis and accumulation of elastin in rat aorta during development of systemic hypertension. 1988.

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Rohman, Carrie. Strange Prosthetics: Rachel Rosenthal’s Rats and Rings. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190604400.003.0005.

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Rosenthal’s book, Tatti Wattles: A Love Story, reveals her aesthetic practice itself to be animated by the discourse of species. The drawings in this text, especially, suggest that Rosenthal’s self-identification as an artist is mediated by animality. The images also efface the human yet “en-face” the rat, de-emphasizing human power and privilege. These images are also marked by Rosenthal’s “auto-graphy” as a mover or dancer, by an alimentary tropology highlighting the body, by the concept of mediation, and by the taming of human exceptionalism. The argument follows that all of these elements in Rosenthal’s view of her artistic practice, self, and process are mediated by animality, and they challenge our received notions of art as a centrally human practice.
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Archer, Nick, and Nicky Manning. Left-sided abnormalities. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198766520.003.0010.

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This chapter explores left-sided abnormalities, discussing venoatrial abnormalities (including partial anomalous pulmonary venous drainage, total anomalous pulmonary venous drainage, and left-sided SVC), atrioventricular abnormalities (mitral atresia and mitral hypoplasia), ventriculoarterial abnormalities (including aortic stenosis, aortic atresia, and hypoplastic le. heart syndrome), and arterial abnormalities (coarctation of the aorta, interrupted aortic arch, right aortic arch, aberrant subclavian artery, double aortic arch, persistent fifth aortic arch, vascular rings, and aorto-pulmonary window).
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Book chapters on the topic "And Rat aorta rings"

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St-Louis, Jean, Benoit Sicotte, Eric Breton, and Ashok K. Srivastava. "Contractile effects of vanadate on aorta rings from virgin and pregnant rats." In Vanadium Compounds: Biochemical and Therapeutic Applications, 145–50. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-1251-2_18.

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Backer, Carl L. "Vascular Rings." In Diseases of the Aorta, 97–109. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11322-3_7.

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Nishida, Seiichiro, and Hiroyasu Satoh. "Vascular Modulation of Rat Aorta by Taurine." In Advances in Experimental Medicine and Biology, 37–46. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-75681-3_4.

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Nicosia, Roberto Francesco. "The Rat Aorta Model of Angiogenesis and Its Applications." In Vascular Morphogenesis: In Vivo, In Vitro, In Mente, 111–29. Boston, MA: Birkhäuser Boston, 1996. http://dx.doi.org/10.1007/978-1-4612-4156-0_9.

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Nicosia, Roberto F. "The Rat Aorta Model of Angiogenesis: Methodology and Applications." In Angiogenesis, 47–53. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-9185-3_6.

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Reid, Julianne J., Ng-Hi Tran, Geoffrey W. Tregear, and Peter J. Roche. "The effect of relaxin on vascular function in rat aorta." In Relaxin 2000, 183–84. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-017-2877-5_26.

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Plante, Gérard E., Stéphanie Lehoux, and Pierre Sirois. "Drug-Induced Alteration of Endothelial Permeability in the Rat Aorta." In Advances in Experimental Medicine and Biology, 249–53. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0179-8_41.

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Sanz, F., J. Rodríguez, E. Lozoya, F. Manaut, T. G. Ferreiro, M. I. Loza, J. A. Fontela, I. Cadavid, and E. Raviña. "Antiserotoninergic activity of 2-aminoethylbenzocyclanones in rat aorta: Structure-activity relationships." In Trends in QSAR and Molecular Modelling 92, 552–53. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1472-1_153.

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Motley, Evangeline D., Robert R. Ruffolo, Douglas W. P. Hay, and Andrew J. Nichols. "Role of Phosphatidylinositol Turnover in the Contraction of the Rat Aorta." In Advances in Experimental Medicine and Biology, 211–16. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6015-5_18.

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Quast, Ulrich, Claudia Linde, Cornelia Löffler, and Friedrich Metzger. "Modulation of ATP-Sensitive K+ Channels in Rat Aorta and Kidney." In Molecular and Cellular Mechanisms of Cardiovascular Regulation, 111–21. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-65952-5_10.

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Conference papers on the topic "And Rat aorta rings"

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Katušić, Z. S., and M. K. Krstić. "ENDOTHELIUM-INDEPENDENT PARTIAL AGONISTIC ACTIVITY OF VASOPRESSIN IN THE RAT COMMON CAROTID ARTERY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644600.

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It has been shown that vasopressin causes endothelium-dependent relaxations of the canine basilar artery, suggesting that_increased circulating concentrations of vasopressin can produce redistribution of the blood from the peripheral to the cerebral circulation (Katušić et al., 1984). The present experiments were done to examine effect of vasopressin on the rat peripheral arteries* The experiments were performed on rings (4 mm long) of aorta, common carotid and renal arteries* The arteries were placed in Krebs-Ringer-bicarbonate solution gassed with 95%O2-5%co2 gas mixture and kept at 37°c. In certain rings the endothelium was removed mechanically by gentle rubbing of the intimal surface. Isometric tension was continously recorded (IPM electronic).Vasopressin (10-11 to 3×10-8 M) caused concentration-dependent contraction being full agonist in aorta and renal artery, but partial agonist in common carotid artery. After removal of endothelium vasopressin-induced contractions were not significantlly afected in any of the tested arteries. Gyclooxygenase inhibitor indomethacin (10-5 M; contact time = 40 min) did not affect partial agonistic activity of vasopressin in common carotid artery. This results indicate that partial agonistic activity of vasopressin in common carotid artery is not related to increased production of "EDRF" or prostacyclin from endothelium. In addition, our findings are consistent with the hypothesis that vasopressin may contribute to redistribution of the blood flow from the peripheral to the cerbral circulation.Z.S. Katušić, J.T. Shepherd and P.M. Vanhoutte. Circ. Res., 55: 575-579, 1984
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Martinez-Sales, V., J. Valles, M. T. Santos, and J. Aznar. "1-14C-ARACHIDONIC ACID INCORPORATION INTO THE LIPIDS OF RAT AORTA.EFFECT OF EXHAUSTION ON PGI2 PRODUCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643372.

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Prostacyclin (PGI2) production in rat aortic rings incubated in Tris-buffer decreases with time.It has been shown that this decrease is not dependent on the total arachidonate concentration in the arterial lipids, and it has been suggested that it may be due to a partial enzymatic inactivation of cyclooxygenase and / or PGI2-synthethase. However, there is a possibility that although the total l-14C-arachidonate (AA*) incorporation increases with exhaustion, this incorporation into the different lipid fractions may be different before and after the exhaustion process.In this study we evaluate this possibility by assessing the incorporation of AA* into rat aorta lipids in control samples and after 180 min exhaustion in 10mM Tris-buffer saline pH=7.4 or human plasma. In addition 6-keto-PGFl (6K) formation from endogenous AA was also evaluated inα the above mentioned experimental conditions by RIA. The results show that this 6K production is drastically reduced by the exhaustion in Tris-buffer (91%) and to a lower extent in arteries exhausted in plasma (52%). With regard to AA* incorporation into the total lipid fractions, it was found that in control arteries 67% was incorporated in phospholipids (PL),19% in triglycerides (TG) and 4.2% in esterified cholesterol. The AA* incorporation into the different PL was: 31% in phosphatidyl-choline (PC), 28% in P-ethanolamine (PE), 25% in P-serine+P-inositol, 8% sphingomyeline and 6% lisolecitine.When the arteries are exhausted in Tris-buffer the AA* incorporation decreases in TG and increases in total PL when compared to control samples. Additionally, a very significant increase of AA* in PE and a decrease in PC were found. In plasma-exhausted sairples the AA* incorporation into the arterial lipids shows the same trend as in Tris-buffer exhausted samples, although these differences were lower in the former when compared to the control. When rat aortic rings are exhausted in Tris-buffer there is a remarkable reduction in PGI2 production and an alteration in the AA* incorporation into the arterial lipids.Plasma has a protective effect on rat aorta during the exhaustion process.
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Moreno, A., J. P. de la Cruz, J. Garcia Campos, and F. Sanchez de la Cuesta. "EFFECT OF DIPYRIDAMOLE + ASA ON THE RETINE VASCULAR PATTERN OF ESTREPTOZOTOCIN-DIABETIC RATS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643098.

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INTRODUCTIONWe have used an experimental model which allows the evaluation of the qualitative differences in the retinal vascular pattern by means of the labeling of the retine vascular tree with radish peroxidase (HRP) in estreptozotocin-diabetic rats. The aim of the study was to evaluate the effect of ASA and DIP + ASA on the vessels platelet behaviour of said retine pattern in a group of rats in t-hich the diabetes had 3 months of evolution.PROCEDURE22 Wistar male rats were divided into A groups; 1) control group, 2) diabetic rats without antiaggregant, 3) dietetic rats treated with 6 mg/day ASA p.o., 4) diabetic rats treated with 6 mg/day ASA +12 mg/day DIP p.o. For inducing diabetes 30 mg/Kg of i.v. estreptozotocine were administered. The animals were considered “diabetic” when glucemia was over 200 mg/100 ml. After 3 months of treatment with 4IU insuline and ASA, or ASA + DIP, the animals were sacrified. Samples of blood and rings of descending aorta were extracted. Platelet aggregation in IJB in front of 1 μg/ml of collagen and the prostacycline-like activity of the aorta ring were evaluated. The configuration of the retine vascular tree labeled with HRP was observed.RESULTS AND CONCLUSIONSMaximal aggregation intensity: 11.1 Ω in the control group,10.9Ω in the diabetic non-treated group, 4.8Ω in rats receiving ASA and 4.6Ω in rats treated with DIP + ASA. The incUbation during 10 min. of aorta rings in blood samples produced 38.7% inhibition in the control group, 12.8% in the non treated-diabetic group 0% in the ASA group and 49.3% in the group treated with DIP + ASA.The qualitative changes in the diabetic rats retinal vascular network non treated with antiaggregants showed a scarce visibility of capillars as well as large zones of tortuous vessels. The rats treated with ASA showed a continuous vascular bed and less tortuous vessels than the ones in the non treated group but the vascular diameters were smaller than the ones observed in non-diabetic rats; the rats treated with DIP + ASA showed a continuous vascular bed, scarce tortuous vessels and vascular diameters similar to the ones found in non-diabetic rats. Mortality rates: 0% in the control group, 50% in the non-treated diabetic group, 16% in the ASA group and 0% in the DIP + ASA group. The administration of DIP + ASA normalized the prostacycline-like activity and the retinal vascular pattern in estreptozotocin-diabetic rats.
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Ocal, I., A. Demirkazik, M. Emre, and I. Gunay. "The effects of chronic AC magnetic field on contraction and relaxation of isolated thoracic aorta rings of healthy and diabetic rats." In 2003 IEEE International Symposium on Electromagnetic Compatibility, 2003. EMC '03. IEEE, 2003. http://dx.doi.org/10.1109/icsmc2.2003.1429135.

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Cerletti, C., M. C. Gombino, S. Possaghe, F. Bucchi, Z. M. Chen, and G. de Gaetano. "EFFECTS OF ORAL ASPIRIN ON PLATELET AND VASCULAR CYCLOOXYGENASE ACTIVITY IN RATS WITH PORTACAVAL SHUNT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643417.

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Oral aspirin can be extensively hydrolysed to salicylate in stomach and liver before entering the systemic circulation. “Pre-systemic” acetylation of the platelets may thus occur during aspirin absorption. This may result in concomitant sparing of peripheral vascular cyclooxygenase mainly exposed to salicylate. We tested whether the “biochemical selectivity” of oral aspirin as an inhibitor of platelet vs. vascular cyclooxygenase would be reduced by elimination of the “first-pass” hepatic metabolism. A portacaval shunt was inserted in anaesthetized rats by connecting the portal vein to the inferior vena cava through a “Y” heparinized polyethylene PE 60-160 cannula. Sham operated rats acted as controls. 90 min after recovery from anaesthesia rats were given aspirin orally (10 mg/kg) and 45 min later serum TxB2 and 6-keto-PGF la formation by vascular rings were evaluated by radioimmunoassay. Serum TxB2 was completely suppressed in all animals; in contrast, vascular 6-keto-PGF la was significantly reduced (by 40-60* in aorta and vena cava) in rats with portacaval shunt but not in controls. The results in rats with portacaval shunt were similar to those previously obtained after i.v. aspirin. 15 min after aspirin administration, plasma levels of unmetabolized drug measured by HPLC were significantly higher in rats with portacaval shunt (0.56±0.16 μg/ml; n= 5) than in sham operated controls (0.16±0.22 }μg/ml; n= 5). This study directly supports the role of “ first-pass” hepatic metabolism in determining the “biochemical selectivity” of oral aspirin.
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Kumrungsee, Thanutchaporn, Norihisa Kato, Toshiro Matsui, and Yongshou Yang. "Plant and gut microbiota-derived protein metabolites and potential health functions." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/envt3719.

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Bioactive peptides can be obtained from protein hydrolysates through in vitro enzymatic hydrolysis, gastrointestinal digestion, and microbial fermentation. Recent emerging research suggests that prebiotic-stimulated gut microbiota also plays a role in generating bioactive peptides and amino acids in gut. In this study, we examined if enzymatic hydrolysis of soybean and wheat germ, plant materials often used in oil industry, can generate antihypertensive peptides and determined if prebiotic digestive enzymes can induce the production of gut microbiota-derived amino acids. In the first experiment, soybean and wheat germ were hydrolyzed by protease enzymes. Then, their hydrolysates were subjected to peptide isolation and identification. Identified peptides were subjected to test for their potential antihypertensive activities. For the second experiment, rodents were fed an Aspergillus-derived protease- or lipase-mixed diet for 2 weeks. Then, cecum contents were collected for bacteria and metabolite analyses. As a result, we found that His-Gly-Lys from soybean hydrolysate strongly inhibited angiotensin II-induced elevated intracellular Ca2+ concentration in vascular smooth muscle cells (VSMCs). Trp-Val and Trp-Ile from wheat germ hydrolysate were found to inhibit Ca2+-calmodulin (CaM)-dependent protein kinase II (CaMK II), a protein kinase promoting hypertension by inducing Ca2+ influx into VSMCs, in rat thoracic aorta rings. These findings suggest the potential of the plant-derived peptides in preventing hypertension and vascular-related diseases. In the second experiment, we found that the dietary protease and lipase increased Bifidobacterium and Lactobacillus probiotics and induced the production of probiotic-derived amino acids, taurine, ornithine, and γ-aminobutyric acid. Since these amino acids have versatile functions including in gut health modulation and brain functions, it can be hypothesized that the dietary prebiotic-digestive enzymes may be beneficial for gut health and brain functions. This study suggests the possibility of applying oil processing by-products in the production of functional food ingredients including bioactive peptides and amino acids.
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Lin, Xingsun, Fei Sun, Hui Ma, Jingbo Zhao, Lei Jin, and Die Yan Chen. "Two-photon fluorescence imaging of rat aorta." In Optics and Optoelectronic Inspection and Control: Techniques, Applications, and Instruments, edited by Hong Liu and Qingming Luo. SPIE, 2000. http://dx.doi.org/10.1117/12.403959.

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Lv, Mei, Bin Li, Wenjun Shi, Junchao Zou, Xiaowei Fei, Zile Yu, Yibing Bu, and Shiyue Tang. "TFCM Induced Vasodilation of Isolated Rat Thoracic Aorta." In 2014 International Conference on Education Reform and Modern Management (ERMM-14). Paris, France: Atlantis Press, 2014. http://dx.doi.org/10.2991/ermm-14.2014.52.

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Xia, Manli, and Min Wang. "Relaxation effect of total flavonoids from peanut hull on rat thoracic aorta." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027990.

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"Changes of Endothelin-1 Receptors Activity in Induced-Hyperthyroid Isolated Rat Aorta." In 2nd Hawler Pharmaceutical Sciences Conference. Hawler Medical University, 2020. http://dx.doi.org/10.15218/hpsc.02.02.

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Reports on the topic "And Rat aorta rings"

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Zhang, Jing. Platelet-Derived Growth Factor-BB Stimulates Fibronectin Gene Expression in Fibroblasts Isolated from Rat Thoracic Aorta. Fort Belvoir, VA: Defense Technical Information Center, May 1994. http://dx.doi.org/10.21236/ad1011392.

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