K (ATP) + Channels in Neonatal Pulmonary Vessels during Normal Development and Chronic Hypoxia

1994 ◽  
pp. 213-224
Author(s):  
Piet J. Boels ◽  
Robert M. Tulloh ◽  
Sheila G. Haworth
1994 ◽  
Vol 267 (6) ◽  
pp. L667-L678 ◽  
Author(s):  
C. Xue ◽  
A. Rengasamy ◽  
T. D. Le Cras ◽  
P. A. Koberna ◽  
G. C. Dailey ◽  
...  

Expression and localization of nitric oxide synthase (NOS) in the lungs of chronically hypoxic and normoxic rats were studied using both immunohistochemistry and NADPH diaphorase (NADPH-d) staining techniques. In the normoxic and in the hypoxic rat, NOS was detected by both methods in the endothelium of large pulmonary vessels and in the epithelium of bronchi and bronchioli. NOS expression was not detected in the endothelium of normoxic pulmonary resistance vessels but was prominently expressed in the endothelium of these vessels after 2-4 wk of chronic hypoxia. In contrast to small pulmonary vessels, the endothelium of small bronchial vessels exhibited NOS immunostaining in both normoxic and hypoxic lungs. Hypoxia was also found to induce de novo NOS expression in the smooth muscle of large and small pulmonary vessels and in bronchial smooth muscle. NOS enzyme activity in lung homogenates was assessed by [3H]arginine to [3H]citrulline conversion. The activity of soluble NOS, but not particulate NOS, was increased in the hypoxic lungs. These results demonstrate chronic hypoxia-induced upregulation of NOS protein expression and activity in the rat lung, suggesting a potentially important role of nitric oxide in adaptation of the pulmonary circulation to chronic hypoxia. The lack of immunostaining in small pulmonary resistance vessels is also consistent with physiological studies suggesting that NO may not be involved in the mechanism for maintaining the normally low pulmonary vascular resistance.


2013 ◽  
pp. 589-595 ◽  
Author(s):  
H. AL-HITI ◽  
M. CHOVANEC ◽  
V. MELENOVSKÝ ◽  
O. VAJNEROVÁ ◽  
A. BAŇASOVÁ ◽  
...  

Chronic hypoxia induces an increased production of nitric oxide (NO) in pulmonary prealveolar arterioles. Bioavailability of the NO in the pulmonary vessels correlates with concentration of L-arginine as well as activity of phosphodiesterase-5 enzyme (PDE-5). We tested a hypothesis whether a combination of L-arginine and PDE-5 inhibitor sildenafil has an additive effect in reduction of the hypoxic pulmonary hypertension (HPH) in rats. Animals were exposed to chronic normobaric hypoxia for 3 weeks. In the AH group, rats were administered L-arginine during chronic hypoxic exposure. In the SH group, rats were administered sildenafil during chronic hypoxic exposure. In the SAH group, rats were treated by the combination of L-arginine as well as sildenafil during exposure to chronic hypoxia. Mean PAP, structural remodeling of peripheral pulmonary arterioles (%DL) and RV/LV+S ratio was significantly decreased in the SAH group compared to hypoxic controls even decreased compared to the AH and the SH groups in first two measured parameters. Plasmatic concentration of cGMP and NOx were significantly lower in the SAH group compared to hypoxic controls. We demonstrate that NO synthase substrate L-arginine and phosphodiesterase-5 inhibitor sildenafil administered in combination are more potent in attenuation of the HPH compared to a treatment by substances given alone.


1993 ◽  
Vol 85 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Paul A. Woodmansey ◽  
Fan Zhang ◽  
Kevin S. Channer ◽  
Alyn H. Morice

1. Isolated rat aorta and pulmonary arteries were maximally precontracted with 100 mmol/l KCl, and the vasorelaxation due to the dihydropyridine calcium antagonist amlodipine was measured. The response of large pulmonary arteries (mean lumen diameter 983 μm) was directly compared with that of isolated pulmonary resistance vessels (mean lumen diameter 259 μm) from both normoxic animals and animals exposed to chronic hypoxia. 2. Amlodipine caused a significant relaxation of aorta (P <0.001). A significant relaxation of large and resistance pulmonary arteries from both normoxic and chronically hypoxic animals was also demonstrated at all doses tested (P <0.05) or less). 3. Amlodipine produced significantly more relaxation in pulmonary resistance vessels than in large pulmonary arteries from both normoxic and chronically hypoxic rats (P <0.02). 4. The action of amlodipine was slow in onset and persistent in all vessels studied. In the pulmonary vessels from normoxic animals both the rate of onset and the magnitude of effect was proportional to the drug concentration (P <0.001). 5. These results demonstrate that amlodipine is a potent inhibitor of KCl-induced contractions in rat pulmonary arteries with a preferential action in pulmonary resistance vessels.


2013 ◽  
pp. 585-588
Author(s):  
M. ŽALOUDÍKOVÁ ◽  
J. HERGET ◽  
M. VÍZEK

Chronic hypoxia causes oxidative injury of pulmonary vessels and attenuates their reactivity to different stimuli. When combined with hypercapnia, biochemical markers of this injury are reduced but the effect of concomitant hypoxia and hypercapnia on vascular reactivity is not fully understood. This study was therefore designed to test whether hypercapnia can prevent also the hypoxia-induced loss of reactivity of pulmonary vessels. The reactivity of vessels from rats exposed either to hypoxia or hypoxia combined with hypercapnia was tested using a small vessel myograph (M 500A, Linton, Norfolk, GB). The second and third intrapulmonary branches of pulmonary arteries were isolated under a dissecting microscope from lungs of 8 control rats (group N), 6 rats exposed to hypoxia for 5 days (isobaric, 10 % O2, group H) and 7 rats exposed to hypoxia combined with hypercapnia for 5 days (10 % O2, 5 % CO2, group H+CO2). The transmural pressure was set by automatic normalization to 30 mm Hg. The vessel size did not vary among the groups. After stabilization we challenged the vessels twice with KCl (80 mM) and once with PGF2α (0.1 mM). There were no significant differences in KCl induced contractions among the groups. The responses to PGF2α were expressed as a ratio to the maximal tension obtained by the exposure to 80 mM KCl. Contractions induced by PGF2α were markedly reduced in group H (0.07±0.02) and in group H+CO2 (0.26±0.03) in comparison with group N (0.83±0.07). The vessels of group H responded to PGF2α less than those of group H+CO2. However we observed the attenuated reactivity also in group H+CO2 in comparison with N. Hypercapnia therefore partially blunted the hypoxia-induced loss of reactivity in pulmonary arteries. This finding supports the hypothesis that hypercapnia significantly alters the nature of lung injury induced by chronic hypoxia.


1991 ◽  
Vol 80 (s24) ◽  
pp. 7P-7P
Author(s):  
C J Emery ◽  
D Bee ◽  
A J Stewart ◽  
G R Barer

1977 ◽  
Vol 53 (4) ◽  
pp. 397-400 ◽  
Author(s):  
A. J. Suggett ◽  
J. Herget

1. Groups of young rats were kept in a hypoxic chamber or in air as control animals for 28 days. 2. Hypoxic and control animals were treated with either α-methyl-3,4-dihydroxyphenylalanine (α-methyldopa) or distilled water. 3. α-Methyldopa significantly reduced the increase in pulmonary artery pressure and right ventricular hypertrophy induced by chronic hypoxia and partially prevented the histological changes in the small pulmonary vessels.


Author(s):  
Michael T. Postek

Silicon occurs naturally in plants in the form of its hydrated oxide (SiO2.nH2O) commonly called silica. Silica has been shown to be a necessary element in the normal development of many plants, playing an array of roles including strengthening, protection, and reduction of water loss. Deposition of silica in various portions of the plant body, especially the leaves, may also be viewed as a way for the plant to dispose of any excess silica taken up beyond that necessary for normal metabolism.Studies of this “opaline” silica have thus far been limited to species of the Cyperaceae and Gramineae known to possess significant quantities of silica. Within the Magnoliaceae, certain “glistening” idioblast cells at the foliar veinlet termini and vein sheaths of Magnolia grandiflora (1) have been suspected to be siliceous in nature.


Author(s):  
Thomas T.F. Huang ◽  
Patricia G. Calarco

The stage specific appearance of a retravirus, termed the Intracisternal A particle (IAP) is a normal feature of early preimplantation development. To date, all feral and laboratory strains of Mus musculus and even Asian species such as Mus cervicolor and Mus pahari express the particles during the 2-8 cell stages. IAP form by budding into the endoplasmic reticulum and appear singly or as groups of donut-shaped particles within the cisternae (fig. 1). IAP are also produced in large numbers in several neoplastic cells such as certain plasmacytomas and rhabdomyosarcomas. The role of IAP, either in normal development or in neoplastic behavior, is unknown.


1994 ◽  
Vol 3 (1) ◽  
pp. 79-88 ◽  
Author(s):  
Theresa A. Kouri

Lexical comprehension skills were examined in 20 young children (aged 28–45 months) with developmental delays (DD) and 20 children (aged 19–34 months) with normal development (ND). Each was assigned to either a story-like script condition or a simple ostensive labeling condition in which the names of three novel object and action items were presented over two experimental sessions. During the experimental sessions, receptive knowledge of the lexical items was assessed through a series of target and generalization probes. Results indicated that all children, irrespective of group status, acquired more lexical concepts in the ostensive labeling condition than in the story narrative condition. Overall, both groups acquired more object than action words, although subjects with ND comprehended more action words than subjects with DD. More target than generalization items were also comprehended by both groups. It is concluded that young children’s comprehension of new lexical concepts is facilitated more by a context in which simple ostensive labels accompany the presentation of specific objects and actions than one in which objects and actions are surrounded by thematic and event-related information. Various clinical applications focusing on the lexical training of young children with DD are discussed.


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