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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 32 (2005), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Chronic hypoxia causes sustained pulmonary hypertension and, although impairment of the pulmonary endothelial nitric oxide (NO) pathway has been implicated, no study has described the central role of NO in modulating pulmonary vascular tone and reactivity. Centrally, NO inhibits sympathetic outflow, so we hypothesised that central NO would modulate pulmonary vascular tone and its reactivity to acute hypoxia, especially in the hypertensive state.2. Male adult Sprague-Dawley rats were exposed to normoxia (N) or chronic hypoxia (CH; 12% O2) for 14 days. Mean pulmonary arterial pressure (MPAP), systemic mean arterial blood pressure (MABP), cardiac output and heart rate were then measured in pentobarbitone-anaesthetized, artificially ventilated rats. The N and CH rats were exposed to acute hypoxia (10% O2 for 4 min) after the intracerebroventricular (i.c.v.) administration of artificial cerebrospinal fluid (control) and then again after either i.c.v. NG-nitro-l-arginine methyl ester (l-NAME; 150 μg in 10 μL) or 3-morpholino-sydnonimine hydrochloride (SIN-1; 100 μg in 10 μL).3. Chronic hypoxia caused pulmonary hypertension (MPAP 20 ± 1 vs 30 ± 1 mmHg in N and CH rats, respectively) and attenuated acute hypoxic pulmonary vasoconstriction (HPV). Central inhibition of NO synthesis (by l-NAME) did not alter baseline MPAP or the acute HPV in either N or CH rats, but it did elevate MABP. The NO donor SIN-1 did not alter baseline MPAP, but it did enhance (N rats) or restore (CH rats) the HPV and decreased MABP.4. The results of the present study indicate that central NO has a limited role in the tonic modulation of MPAP during normoxia and after chronic hypoxia. However, the acute HPV seems to be enhanced by exogenous NO.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Mesenchymal stem cells are multipotent cells that can differentiate into cardiomyocytes and vascular endothelial cells. Here we show, using cell sheet technology, that monolayered mesenchymal stem cells have multipotent and self-propagating properties after transplantation into infarcted rat ...
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1600-5775
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Geosciences , Physics
    Notes: The usefulness of a synchrotron microangiography system for depicting, quantitating and therapeutically evaluating angiogenic vessels in cancer is illustrated. In 20 mice transplanted with murine colon cancer, sequential changes in the angiogenic vessels were determined by using synchrotron microangiography, using changes in tumor volume for reference. This system allowed the depiction and quantification of angiogenic vessels in the period from one to four weeks after transplantation. The effects of antiangiogenic therapy were evaluated by using a neutralizing antibody against vascular endothelial growth factor. The neutralizing antibody partially suppressed angiogenesis and tumor growth. Synchrotron microangiography is shown to be useful for the depiction, quantification and evaluation of angiogenic vessels in cancer.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1600-5775
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Geosciences , Physics
    Notes: A HARPICONTM camera has been applied to a digital angiography system with fluorescent-screen optical-lens coupling. It uses avalanche multiplication in the photoconductive layer for high-sensitivity imaging. The limiting spatial resolutions in the 1050 scanning-line mode of the camera are about 30 and 50 µm at input field sizes of 20 × 20 and 50 × 50 mm on the screen, respectively. For high-speed imaging, the 525 scanning-line mode at a rate of 60 images s−1 can be selected. High-quality images of coronary arteries in dogs were obtained by intra-aortic coronary angiography and superselective coronary angiography using a single-energy X-ray above the iodine K-edge energy.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-7241
    Keywords: nisoldipine ; calcium channel blocker ; coronary vessels ; myocardium ; Na+-H+ exchange ; amiloride ; cellular acidosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined whether nisoldipine, a calcium (Ca) channel blocker, increases coronary blood flow (CBF) without decreasing aortic blood pressure (AoP) with ischemic and nonischemic hearts, and whether the presence of cellular acidosis in ischemic myocardium contributes to the augmentation of coronary vasodilation due to nisoldipine. In 42 dogs, coronary perfusion pressure (CPP) was reduced so that CBF decreased to 60% of the baseline, and CPP was maintained constant thereafter. First, we administered nisoldipine into a systemic vein in the ischemic and nonischemic hearts. Second, nisoldipine was administered into the canine coronary artery of the ischemic myocardium with and without administration of either sodium bicarbonate (NaHCO3), sodium hydroxide (NaOH), or amiloride. Nisoldipine (0.25–4.0 mg/kg, IV) increased CBF by 59% in the ischemic myocardium more than the nonischemic myocardium (by 34%) without reducing AoP. The infusion of nisoldipine (40 ng/kg/min, IC) increased CBF markedly by about 55% in the ischemic myocardium with increases in fractional shortening (FS; 11 ± 2% to 21 ± 2%) and lactate extraction ratio (LER; −19 ± 4% to 15 ± 2%). Increases in CBF, FS, and LER were markedly attenuated during administration of nisoldipine with concomitant administration of either NaHCO3 or NaOH. Furthermore, the extent of increases in CBF (54 ± 2 mL/100 g/min), FS (13 ± 2%), and LER (−17 ± 4%) were also markedly attenuated due to the concomitant treatment with amiloride. We conclude that myocardial cellular acidosis plays an important role in mediating coronary vasodilation affected by nisoldipine in the ischemic myocardium. H+ may modulate the property of voltage-dependent Ca channels via Na+–H+ exchange.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-7241
    Keywords: dogs ; ischemic myocardium ; endocardium ; epicardium ; recovery time ; myocardial blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the response of refractory periods and blood flow to blockade of α1- and β-adrenoceptors alone, or in combination on endocardium and epicardium, during myocardial ischemia. Dogs were anesthetized with α-chloralose and divided into bunazosin (an α1-blocking agent)-treated (0.1–0.2 mg/kg, IV, n = 14), propranolol-treated (0.2 mg/kg, IV, n = 12), and vehicle-control (n = 10) groups. The diagonal branches of the left anterior descending artery were ligated. The refractory period (ERP) and blood flow (RMBF) were determined by an S1-S2 extrastimulus method and a nonradioactive microsphere technique, respectively. The duration of regional electrograms (DRE) was measured in the endocardial and epicardial sites. Bunazosin alone reversed the ischemia-related shortening of ERPs at both the endocardial and epicardial sites, with a greater effect seen epicardially (P 〈 .05). Subsequent administration of propranolol further prolonged ERPs in both sites, although the effect was greater in the epicardial surface (P 〈 .05). Bunazosin reduced RMBF to a greater degree at the endocardial site than at the epicardial site in the ischemic zone (P 〈 .01 and P 〈 .05, respectively), but the magnitude of the reduction in RMBF and the difference in RMBF between sites were similar to the control group (P 〈 .01). Propranolol alone and subsequent administration of bunazosin prolonged the ERP more at the epicardial site (P 〈 .01) than at the endocardial sites in the ischemic zone. Propranolol produced no significant difference in RMBF between both sites. DREs in animals treated with bunazosin and propranolol alone, or in combination, were similar to those in animals treated with vehicle. These results suggest that differences in ERPs between endocardium and epicardium with blockade of α1- and/or β-adrenoceptor are not due to concomitant alterations in RMBF, but to differences in electrophysiological properties of the endocardial and epicardial cells during the acute phase of myocardial ischemia.
    Type of Medium: Electronic Resource
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