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1.
J Int Med Res ; 40(2): 601-11, 2012.
Article in English | MEDLINE | ID: mdl-22613421

ABSTRACT

OBJECTIVE: The characteristics of sleep apnoea syndrome (SAS) in the elderly, including subtype classification and association with mortality, have not been fully elucidated. This study examined these factors in an elderly Japanese inpatient population. METHODS: Overnight polysomnography was used to diagnose and classify SAS in 145 elderly inpatients (mean ± age 81 ± 8 years). Clinical data, including brain computerized tomography findings, were recorded. The study population included nine inpatients with obstructive SAS, 12 with central SAS, 25 with mixed SAS and 99 controls (no SAS). RESULTS: Increased body mass index and grade of aortic arch calcification independently contributed to risk of all subtypes of SAS combined. There was an independent association between SAS and increased risk of mortality from all causes as well as from pneumonia and from cardiovascular disease. Only mixed SAS was independently and positively associated with increased risk of death from pneumonia. CONCLUSIONS: Obstructive, central and mixed SAS were associated with increased risk of cardiovascular related and all-cause mortality. Mixed SAS was associated with an increase in mortality from pneumonia. There was no relationship between mortality and severity of SAS.


Subject(s)
Cardiovascular Diseases/mortality , Cause of Death , Pneumonia/mortality , Sleep Apnea Syndromes , Sleep Apnea, Obstructive , Aged , Aged, 80 and over , Body Mass Index , Female , Humans , Inpatients , Japan , Male , Polysomnography , Risk Factors , Sleep Apnea Syndromes/complications , Sleep Apnea, Obstructive/complications
2.
J Appl Physiol (1985) ; 91(4): 1766-74, 2001 Oct.
Article in English | MEDLINE | ID: mdl-11568161

ABSTRACT

There is little information regarding the effect of hypoxia on alveolar fluid clearance capacity. We measured alveolar fluid clearance, lung water volume, plasma catecholamine concentrations, and serum osmolality in rats exposed to 10% oxygen for up to 120 h and explored the mechanisms responsible for the increase in alveolar fluid clearance. The principal results were 1) alveolar fluid clearance did not change for 48 h and then increased between 72 and 120 h of exposure to hypoxia; 2) although nutritional impairment during hypoxia decreased basal alveolar fluid clearance, endogenous norepinephrine increased net alveolar fluid clearance; 3) the changes of lung water volume and serum osmolality were not associated with those of alveolar fluid clearance; 4) an administration of beta-adrenergic agonists further increased alveolar fluid clearance; and 5) alveolar fluid clearance returned to normal within 24 h of reoxygenation after hypoxia. In conclusion, alveolar epithelial fluid transport capacity increases in rats exposed to hypoxia. It is likely that a combination of endogenous norepinephrine and nutritional impairment regulates alveolar fluid clearance under hypoxic conditions.


Subject(s)
Hypoxia/metabolism , Lung/metabolism , Pulmonary Alveoli/metabolism , Adrenergic alpha-Antagonists/pharmacology , Adrenergic beta-Agonists/pharmacology , Adrenergic beta-Antagonists/pharmacology , Algorithms , Animals , Biological Transport, Active/drug effects , Body Fluids/drug effects , Body Fluids/metabolism , Catecholamines/blood , Extravascular Lung Water/drug effects , Extravascular Lung Water/metabolism , Food Deprivation/physiology , Lung/drug effects , Pulmonary Alveoli/drug effects , Rats , Rats, Sprague-Dawley , Sodium Channel Blockers/pharmacology
3.
Exp Lung Res ; 27(6): 485-504, 2001 Sep.
Article in English | MEDLINE | ID: mdl-11558966

ABSTRACT

Alveolar type II cells (type II cells) play a crucial role in the progression and repair of lung inflammation and injury. We investigated whether inducible nitric oxide synthase (iNOS) was expressed and nuclear factor-kappaB (NF-kappaB) was activated in type II cells in lung injury. After injecting lipopolysaccharide (LPS) or saline in the rat, the lungs were excised and type II cells were isolated. iNOS and its mRNA were expressed both in lung tissue and isolated type II cells in response to LPS. The lungs from saline-treated rats showed only minimal expression of iNOS. Electrophoretic mobility shift assay revealed that expression of NF-kappaB in the nuclear extracts was augmented by LPS, and p5O/NFkappaB was expressed in type II cells in LPS-treated rats. Intraperitoneal dexamethasone almost completely inhibited the iNOS expression and attenuated the activation of NF-kappaB in the LPS-treated lung. These findings suggest that type II cells can be a source of NO production in lung injury,and that the effects of corticosteroids may be in part through inhibition of both iNOS expression and NF-kappaB activation.


Subject(s)
NF-kappa B/metabolism , Nitric Oxide Synthase/genetics , Pulmonary Alveoli/enzymology , Respiratory Distress Syndrome/metabolism , Tyrosine/analogs & derivatives , Animals , Dexamethasone/pharmacology , Electrophoretic Mobility Shift Assay , Gene Expression Regulation, Enzymologic , Glucocorticoids/pharmacology , Immunohistochemistry , Lipopolysaccharides , Male , NF-kappa B/analysis , NF-kappa B/genetics , NF-kappa B p50 Subunit , Nitric Oxide Synthase/analysis , Nitric Oxide Synthase Type II , Pulmonary Alveoli/cytology , RNA, Messenger/analysis , Rats , Rats, Sprague-Dawley , Respiratory Distress Syndrome/chemically induced , Respiratory Distress Syndrome/drug therapy , Specific Pathogen-Free Organisms , Tyrosine/metabolism
4.
Exp Lung Res ; 27(5): 453-68, 2001.
Article in English | MEDLINE | ID: mdl-11480585

ABSTRACT

Because high-dose terbutaline and isoproterenol (10(-3) M), beta2-adrenergic agonists, failed to increase alveolar fluid clearance, the mechanisms responsible for this effect were examined in ex vivo rat lungs. An isosmolar 5% albumin solution with Evans blue dye was instilled into the distal airspaces in isolated rat lungs that were then inflated with 100% oxygen at an airway pressure of 8 cm H2O in a 37 degrees C incubator. Alveolar fluid clearance was measured by the progressive increase in dye concentrations over 1 hour. The results indicated that: (1) although 10(-5) M terbutaline or isoproterenol increased alveolar fluid clearance, 10(-3) M terbutaline or isoproterenol did not; (2) both concentrations of terbutaline (10(-5), 10(-3) M) increased intracellular adenosine 3',5'-cyclic monophosphate in cultured type II alveolar epithelial cells; (3) instillation of atenolol, a selective beta1-adrenergic antagonist, in the presence of either 10(-3) M terbutaline or isoproterenol was associated with an increase in alveolar fluid clearance. These results suggested that beta1-adrenoceptor stimulation prevented the normal response to a beta2-adrenergic agonist. To further test this hypothesis, a selective beta1-adrenergic agonist, denopamine, was administered; these results showed that (4) 10(-3) M denopamine, a selective beta1-adrenergic agonist, inhibited the increase in alveolar fluid clearance in the presence of 10(-5) M terbutaline; (5) hypoxia for 2 hours did not alter the effects of terbutaline on alveolar fluid clearance. The mechanism for the inability of the alveolar epithelium to respond to high-dose terbutaline or isoproterenol with the normal upregulation of alveolar fluid clearance in ex vivo rats lungs appears to be mediated by beta1-adrenoceptor stimulation that subsequently suppresses the beta2-adrenergic response.


Subject(s)
Adrenergic beta-Agonists/pharmacology , Receptors, Adrenergic, beta-1/drug effects , Terbutaline/pharmacology , Animals , Bronchoalveolar Lavage Fluid , Cell Hypoxia , Epithelial Cells/drug effects , Isoproterenol/pharmacology , Lung/cytology , Lung/drug effects , Lung/metabolism , Male , Organ Culture Techniques , Rats , Rats, Sprague-Dawley , Receptors, Adrenergic, beta-1/metabolism
5.
Am J Pathol ; 158(5): 1665-75, 2001 May.
Article in English | MEDLINE | ID: mdl-11337364

ABSTRACT

The Rab small G protein family participates in intracellular vesicle transport, including exocytosis and endocytosis. The cDNA encoding a novel Rab-related small G protein (Rab38) has been cloned from rat lung cDNA library and recorded in GenBank (accession no. M94043). However, the expression and localization of the protein in the lung remains primarily unknown. We produced polyhistidine-tagged recombinant Rab38 and a polyclonal antibody with a synthetic peptide. Immunohistochemistry demonstrated that the protein is specifically localized in alveolar type II cells and in bronchial epithelial cells. In situ hybridization using a digoxygenin-labeled RNA riboprobe clearly showed that the mRNA of the protein is localized in alveolar type II cells and bronchial epithelial cells, especially terminal airway epithelial cells. Western blot and reverse transcriptase-polymerase chain reaction showed distinct expression of the protein and mRNA in isolated alveolar type II cells, but not in alveolar macrophages. The native protein was predominantly hydrophobic and was enriched in a high-density vesicle fraction but was barely detectable in nuclear and lamellar body fractions in alveolar type II cells. Immunofluorescence cytochemistry performed on cultured alveolar type II cells showed that Rab38 distributed extensively in the cytoplasm with a distribution pattern similar to endoplasmic reticulum rather than other subcellular organelles. These results suggest that this novel rab small G protein (Rab38) mediates vesicular transport in terminal airway epithelium.


Subject(s)
Lung/metabolism , rab GTP-Binding Proteins/genetics , Amino Acid Sequence , Animals , Base Sequence , Cell Line , Gene Expression , Immunohistochemistry , In Situ Hybridization , Lung/chemistry , Macrophages, Alveolar/cytology , Macrophages, Alveolar/metabolism , Male , Molecular Sequence Data , Pulmonary Alveoli/cytology , Pulmonary Alveoli/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Rats , Rats, Sprague-Dawley , Specific Pathogen-Free Organisms , rab GTP-Binding Proteins/metabolism
6.
Jpn J Pharmacol ; 85(2): 161-6, 2001 Feb.
Article in English | MEDLINE | ID: mdl-11286398

ABSTRACT

Because it was still uncertain whether a stimulation of beta1-adrenoceptors accelerated alveolar fluid clearance in hyperoxic lung injury, the effect of denopamine, a selective beta1-adrenergic agonist, on alveolar fluid clearance was determined in rats exposed to 93% oxygen for 48 and 56 h. Alveolar fluid clearance was measured by the progressive increase in the concentration of Evans blue labeled albumin instilled into the alveolar spaces over 1 h at 37 degrees C in isolated rat lungs. The principle results were as follows: 1) Although lung water volume increased in rats exposed to hyperoxia for 48 and 56 h, basal alveolar fluid clearance did not change for up to 56 h; 2) Denopamine increased alveolar fluid clearance in rats exposed to hyperoxia as well as in rats without exposure to hyperoxia; 3) Denopamine primarily increased amiloride-insensitive alveolar fluid clearance in rats exposed to hyperoxia; 4) The potency of denopmaine was similar to that of terbutaline, a selective beta2-adrenergic agonist. In summary, denopamine is a potent stimulator of alveolar fluid clearance in rats exposed to hyperoxia.


Subject(s)
Adrenergic beta-Agonists/pharmacology , Body Fluids , Ethanolamines/pharmacology , Hyperoxia/physiopathology , Pulmonary Alveoli , Terbutaline/pharmacology , Adrenergic beta-1 Receptor Agonists , Amiloride/pharmacology , Animals , Male , Rats , Rats, Sprague-Dawley
7.
J Appl Physiol (1985) ; 90(1): 10-6, 2001 Jan.
Article in English | MEDLINE | ID: mdl-11133887

ABSTRACT

The effect of denopamine, a selective beta(1)-adrenergic agonist, on alveolar fluid clearance was determined in both ex vivo rat and guinea pig lungs. Alveolar fluid clearance was measured by the progressive increase in the concentration of Evans blue-labeled albumin over 1 h at 37 degrees C. Denopamine (10(-6) to 10(-3) M) increased alveolar fluid clearance in a dose-dependent manner in ex vivo rat lungs. Denopamine also stimulated alveolar fluid clearance in guinea pig lungs. Atenolol, a selective beta(1)-adrenergic antagonist, and amiloride, a sodium channel inhibitor, inhibited denopamine-stimulated alveolar fluid clearance. The potency of denopamine was similar to that of similar doses of isoproterenol or terbutaline. Short-term hypoxia (100% nitrogen for 1-2 h) did not alter the stimulatory effect of denopamine. Denopamine (10(-4), 10(-3) M) increased intracellular adenosine 3',5'-cyclic monophosphate levels in cultured rat alveolar type II cells. In summary, denopamine, a selective beta(1)-adrenergic agonist, stimulates alveolar fluid clearance in both ex vivo rat and guinea pig lungs.


Subject(s)
Adrenergic beta-Agonists/pharmacology , Body Fluids/metabolism , Ethanolamines/pharmacology , Pulmonary Alveoli/metabolism , Acute Disease , Adrenergic beta-Antagonists/pharmacology , Animals , Cells, Cultured , Cyclic AMP/metabolism , Guinea Pigs , Hypoxia/metabolism , In Vitro Techniques , Isoproterenol/pharmacology , Lung Diseases/metabolism , Male , Pulmonary Alveoli/cytology , Rats , Rats, Sprague-Dawley , Sodium Channel Blockers , Terbutaline/pharmacology
8.
Transplantation ; 69(9): 1785-93, 2000 May 15.
Article in English | MEDLINE | ID: mdl-10830212

ABSTRACT

BACKGROUND: Because the fluid transport capacity of the alveolar epithelium after lung ischemia with and without lung deflation has not been well studied, we carried out experimental studies to determine the effect of lung deflation on alveolar fluid clearance. METHODS: After 1 or 2 hr of ischemia, we measured alveolar fluid clearance using 125I-albumin and Evans blue-labeled albumin concentrations in in vivo rabbit lungs in the presence of pulmonary blood flow and in ex vivo rat lungs in the absence of any pulmonary perfusion, respectively. RESULTS: The principal results were: (1) lung deflation decreased alveolar fluid clearance while inflation of the lungs during ischemia preserved alveolar fluid clearance in both in vivo and ex vivo studies; (2) alveolar fluid clearance was normal in the rat lungs inflated with nitrogen (thus, alveolar gas composition did not affect alveolar fluid clearance); (3) amiloride-dependent alveolar fluid clearance was preserved when the lungs were inflated during ischemia; (4) terbutaline-simulated alveolar fluid clearance was preserved in the hypoxic rat lungs inflated with nitrogen; (5) lecithinized superoxide dismutase, a scavenger of superoxide anion, and N(omega)-nitro-L-arginine methyl ester, an inhibitor of nitric oxide, preserved normal alveolar fluid clearance in the deflated rat lungs. CONCLUSION: Lung deflation decreases alveolar fluid clearance by superoxide anion- and nitric oxide-dependent mechanisms.


Subject(s)
Ischemia/metabolism , Lung/blood supply , Pulmonary Alveoli/metabolism , Amiloride/pharmacology , Animals , Biological Transport , Epithelium/metabolism , Lung/metabolism , Male , NG-Nitroarginine Methyl Ester/pharmacology , Rabbits , Rats , Rats, Sprague-Dawley , Superoxide Dismutase/pharmacology , Terbutaline/pharmacology
9.
J Appl Physiol (1985) ; 88(4): 1457-66, 2000 Apr.
Article in English | MEDLINE | ID: mdl-10749842

ABSTRACT

The conventional acoustic reflection technique in which acoustic waves are launched through the mouth cannot be applied during sleep, nor can it be applied to the nasopharynx, which is the major site of occlusion in patients with obstructive sleep apnea syndrome. We propose a new technique of nasal acoustic reflection to measure pharyngeal cross-sectional areas including the nasopharynx. The acoustic waves are introduced simultaneously to both nostrils during spontaneous nasal breathing. A new algorithm takes into account the nasal septum with asymmetric nasal cavities on both sides and assumes prior knowledge of the cross-sectional area of the nasal cavities and the position of the nasal septum. This method was tested on an airway model with a septum and on healthy human subjects. The conventional technique gave inaccurate measurements for pharyngeal cross-sectional areas for an airway model with asymmetric branching, whereas the new technique measured them almost perfectly. The oro- and hypopharyngeal cross-sectional area measurements acquired by the new method were not different from those obtained by the conventional method in normal subjects. This new method can be used as a monitor of upper airway dimensions in nocturnal polysomnography.


Subject(s)
Pharynx/physiology , Sleep Apnea, Obstructive/physiopathology , Sleep/physiology , Acoustics , Algorithms , Humans , Models, Theoretical , Nasal Septum/anatomy & histology , Nasal Septum/physiology , Nasal Septum/physiopathology , Nasopharynx/anatomy & histology , Nasopharynx/physiology , Nasopharynx/physiopathology , Pharynx/anatomy & histology , Pharynx/physiopathology
10.
Nihon Rinsho ; 57(9): 1988-94, 1999 Sep.
Article in Japanese | MEDLINE | ID: mdl-10497395

ABSTRACT

The lung is susceptive to excess oxidants from inhaled air and marginated large portion of circulating leukocytes. Oxygen radicals generated from sequestrated leukocytes injure endothelial cells to increase permeability. Excessively generated oxidants in the mitochondria, such as in ischemia-reperfusion injury, changes mitochondrial function and cause Ca++ leak from the organelle, which leads to induction of apoptosis. Reactive oxygen intermediates induce some cytokine gene expression such as IL-8. Hydrogen peroxide activates phospholipase C and the subsequent signal transduction pathways resulting in change of cytoskeletal configuration and cell shape. It is expected that understanding of contribution of oxidant-antioxidant imbalance in lung diseases may develop new strategy of 'antioxidant' therapies.


Subject(s)
Antioxidants/metabolism , Lung Diseases/etiology , Lung/metabolism , Reactive Oxygen Species/metabolism , Cytokines/metabolism , Free Radicals , Humans , Lung Diseases/metabolism , Mitochondria/metabolism , Oxidative Stress
11.
Nihon Kokyuki Gakkai Zasshi ; 37(1): 61-6, 1999 Jan.
Article in Japanese | MEDLINE | ID: mdl-10087879

ABSTRACT

A 52-year-old woman who had undergone a partial mastectomy 1 year earlier because of benign phyllodes tumor was admitted because of dry cough and abnormal chest radiograph findings. Chest computed tomograms demonstrated multiple thin-walled cavities and nodules. Clinical examinations and transbronchial biopsy specimens failed to provide a conclusive diagnosis. However, the pulmonary thin-walled cavities enlarged, and a nodular shadow revealed cavitary formation. An open lung biopsy was performed to diagnose the pulmonary lesions. Although biopsy specimens disclosed the infiltration of poorly differentiated adenocarcinoma cells in pleura and pulmonary parenchyma, no primary site was detected. The patient did not respond to systemic chemotherapy (CDDP and VP-16), and died of respiratory failure due to advanced pulmonary metastasis. Autopsy demonstrated marked tumor invasion of the lungs, myocardium, and bone. We analyzed malignant cells in lung tissues at autopsy by immunohistochemistry, and found identical malignant cells in surgical samples obtained during the patients earlier mastectomy. A diagnosis of pulmonary metastasis from malignant phyllodes tumor of the breast was made. Thin walled cavitary lesions from malignant phyllodes tumor are rare; however, pulmonary metastasis of malignant phyllodes tumor should be considered one disease that exhibits thin-walled cavities as a radiographic manifestation.


Subject(s)
Adenocarcinoma/secondary , Breast Neoplasms/pathology , Lung Neoplasms/secondary , Lung/pathology , Phyllodes Tumor/secondary , Adenocarcinoma/diagnostic imaging , Female , Humans , Lung/diagnostic imaging , Lung Neoplasms/diagnostic imaging , Middle Aged , Phyllodes Tumor/diagnostic imaging , Radiography
12.
Respiration ; 65(6): 458-68, 1998.
Article in English | MEDLINE | ID: mdl-9817960

ABSTRACT

Obstructive sleep apnea syndrome is ascribed to pharyngeal dysfunction, but there are only a few reports about the normal morphological values in this anatomical region. We measured the pharyngeal cross-sectional area and the compliance (collapsibility), using the acoustic reflection technique with air breathing, in 181 healthy subjects (age 21-69 years). We assessed their sex-related differences, and the effects of age, body size and body postures on these parameters. The pharyngeal cross-sectional area, defined as the region from the fauces to the glottis, posturally changed with successive decreases in the sitting, left lateral decubitus and supine positions. The area was significantly greater in male than in female subjects in the sitting position (p < 0.01), but no difference was present in the recumbent positions. The pharyngeal cross-sectional area did not correlate with either age or body size. The specific pharyngeal compliance was greater in the males than in the females (p < 0.01) and increased with age only in the male subjects.


Subject(s)
Pharynx/anatomy & histology , Pharynx/physiology , Adult , Age Factors , Aged , Compliance , Female , Humans , Male , Middle Aged , Pressure , Sex Factors
13.
J Appl Physiol (1985) ; 84(3): 1003-10, 1998 Mar.
Article in English | MEDLINE | ID: mdl-9480963

ABSTRACT

To investigate the effect of alveolar hypoxia on the pulmonary blood flow-segmental vascular resistance relationship, we determined the longitudinal distribution of vascular resistance while increasing blood flow during hyperoxia or hypoxia in perfused cat lungs. We measured microvascular pressures by the micropipette servo-null method, partitioned the pulmonary vessels into three segments [i.e., arterial (from main pulmonary artery to 30- to 50-micron arterioles), venous (from 30- to 50-micron venules to left atrium), and microvascular (between arterioles and venules) segments] and calculated segmental vascular resistance. During hyperoxia, total resistance decreased with increased blood flow because of a reduction of microvascular resistance. In contrast, during hypoxia, not only microvascular resistance but also arterial resistance decreased with increase of blood flow while venous resistance remained unchanged. The reduction of arterial resistance was presumably caused by arterial distension induced by an elevated arterial pressure during hypoxia. We conclude that, during hypoxia, both microvessels and arteries >50 micron in diameter play a role in preventing further increases in total pulmonary vascular resistance with increased blood flow.


Subject(s)
Hypoxia/physiopathology , Lung/physiology , Pulmonary Circulation/physiology , Vascular Resistance/physiology , Animals , Blood Pressure/physiology , Cats , Female , Hyperoxia/physiopathology , In Vitro Techniques , Male , Microcirculation/physiology , Pulmonary Alveoli/physiology , Vascular Capacitance/physiology , Vasoconstriction/physiology
14.
Nihon Kokyuki Gakkai Zasshi ; 36(10): 871-4, 1998 Oct.
Article in Japanese | MEDLINE | ID: mdl-9893429

ABSTRACT

A 69-year-old woman was admitted because of persistent productive cough, low-grade fever and abnormal pulmonary infiltrates. Chest roentgenograms revealed right pulmonary cavitary lesions and infiltrates in both upper pulmonary fields. Digital subtraction bronchography (DSBG) was performed to detect for the presence of pulmonary cavitary lesions. Double-contrast DSBG images clearly revealed marked bronchiectasis in the right pulmonary cavity with aspergilloma in the cavitary lesions. Aspergilloma was not obvious in routine chest roentgenograms and computed tomograms. Asperillus fumigatus was cultured from sputum materials, and aspergilloma of the pulmonary cavity was clinically diagnosed. The infiltrative lesions were thought to be associated with invasive aspergillosis because the patient exhibited persistent low-grade fever and positive inflammatory reactions. Anti-fungal chemotherapy was highly effective in treating these lesions. DSBG is a new, less-invasive bronchographic technique for the evaluation of bronchial trees, and in this case proved useful for the detection of small aspergilloma in pulmonary cavities.


Subject(s)
Aspergillosis/diagnostic imaging , Aspergillus fumigatus , Bronchography/methods , Lung Diseases, Fungal/diagnostic imaging , Aged , Bronchiectasis/diagnostic imaging , Female , Humans
16.
Respir Physiol ; 104(2-3): 197-204, 1996 Jul.
Article in English | MEDLINE | ID: mdl-8893365

ABSTRACT

We compared the effects of acetylcholine (Ach) in intrapulmonary arteries and veins of adult sheep. Preconstricted arterial rings with endothelium relaxed with Ach whereas arteries without endothelium or pretreated with NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, did not dilate. Venous rings with or without endothelium, whether under resting tension or preconstricted, always contracted with Ach. However, preconstricted veins dilated with bradykinin, another endothelium-dependent vasodilator. Preconstricted veins pretreated with indomethacin or SQ29548, a prostaglandin H2 (PGH2)/TxA2 receptor blocker, did not constrict but rather dilated with Ach. This dilation was abolished with removal of endothelium or treatment with L-NAME, indicating that endothelium-derived NO (EDNO) was mediating the dilation. We conclude that Ach is an endothelium-dependent vasodilator in ovine intrapulmonary arteries, whereas in veins, Ach elicits two responses: EDNO-mediated vasodilation and vasoconstriction mediated by TxA2/PGH2.


Subject(s)
Acetylcholine/pharmacology , Pulmonary Artery/drug effects , Pulmonary Veins/drug effects , Animals , Bradykinin/pharmacology , Endothelium, Vascular/drug effects , Endothelium, Vascular/enzymology , Endothelium, Vascular/metabolism , Enzyme Inhibitors/pharmacology , In Vitro Techniques , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide/metabolism , Nitric Oxide Synthase/antagonists & inhibitors , Prostaglandin H2 , Prostaglandin-Endoperoxide Synthases/metabolism , Prostaglandins H/metabolism , Pulmonary Artery/enzymology , Pulmonary Artery/metabolism , Pulmonary Veins/enzymology , Pulmonary Veins/metabolism , Receptors, Muscarinic/drug effects , Receptors, Muscarinic/physiology , Sheep , Thromboxane A2/metabolism , Vasoconstriction/drug effects , Vasodilation/drug effects
17.
Biol Neonate ; 69(2): 84-93, 1996.
Article in English | MEDLINE | ID: mdl-8713653

ABSTRACT

We have studied the differential role of endothelium-derived nitric oxide (EDNO) in the regulation of the systemic and pulmonary circulations of the lamb. Hemodynamic effects of NG-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg i.v.), an inhibitor of NO synthesis, were determined in juvenile (6 +/- 1 weeks old) lambs, under conditions of basal and elevated vasomotor tone. Under basal conditions, L-NAME raised both systemic (SVR) and pulmonary vascular resistances (PVR) by 20-30% (increasing SVR from 0.318 +/- 0.013 to 0.385 +/- 0.015 mm Hg.min.ml-1.kg and PVR from 0.050 +/- 0.003 to 0.067 +/- 0.010 mm Hg.min.ml-1.kg). When tone was elevated in the pulmonary circulation with hypoxia (PVR was elevated by 60%, from 0.059 +/- 0.010 to 0.094 +/- 0.019 mm Hg.min.ml-1.kg), L-NAME treatment resulted in an augmented increase in PVR (PVR increased by greater than 50% to 0.140 +/- 0.024 mm Hg.min.ml-1.kg). However, when tone was elevated to a comparable degree in the systemic circulation with angiotensin infusion (SVR was elevated by 60%, from 0.432 +/- 0.065 to 0.065 to 0.634 +/- 0.113 mm Hg.min.ml-1.kg), the response to L-NAME was not augmented. Our data suggest that the role of EDNO in the modulation of the pulmonary circulation is dependent on the level of vasomotor tone, whereas its role in the systemic circulation is small and is independent of the level of vasomotor tone.


Subject(s)
Blood Circulation/physiology , Nitric Oxide/physiology , Pulmonary Circulation/physiology , Animals , Arginine/analogs & derivatives , Arginine/pharmacology , Enzyme Inhibitors/pharmacology , Hemodynamics/drug effects , Hemodynamics/physiology , Hypoxia/blood , Hypoxia/physiopathology , NG-Nitroarginine Methyl Ester , Sheep , Vascular Resistance/drug effects , Vasomotor System/growth & development , Vasomotor System/physiology
18.
19.
Nihon Kyobu Shikkan Gakkai Zasshi ; 33 Suppl: 184-9, 1995 Dec.
Article in Japanese | MEDLINE | ID: mdl-8752504

ABSTRACT

The sites of action of endogenous and inhaled nitric oxide (NO) were reassured during hypoxic pulmonary vasoconstriction. Lungs of 21 adult cats were perfused in situ with autologous blood in zone-3 conditions. Capillary pressures were measured by the double-occlusion techniques and pressures in arterioles and venules 70-100 microns in diameter were measured by the servo-null micropuncture technique, both during normoxia (FiO2 = 0.3) and during hypoxia (FiO2 = 0.02). The effects of NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg), an inhibitor of NO synthase, and of inhaled NO (5-100 ppm) were also measured. The PO2 of the prefusate decreased from 187.6 +/- 5.3 mmHg during normoxia to 25.7 +/- 1.3 mmHg during hypoxia, and further decreased to 20.8 +/- 2.2 mmHg during hypoxia with 50 ppm NO (p < 0.05, compared with hypoxia only). Increases in pulmonary vascular pressure drop in response to hypoxia were 4.8 +/- 1.0 cmH2O and 9.1 +/- 1.4 cmH2O in non-treated and L-NAME-treated lungs, respectively (p < 0.05). L-NAME significantly increased hypoxic construction in the venous segment. The concentration of exhaled NO increased from 13 +/- 4 ppb during normoxia to 18 +/- 4 ppb during hypoxia (p < 0.1). Inhaled NO lowered not only pulmonary artery pressure but also capillary pressure in a dose-dependent manner, which reduced hypoxic pulmonary vasoconstriction. Pulmonary veins were more sensitive to inhaled NO than were arteries. Inhaled NO (50 ppm) dilated vessels smaller than 70 to 100 microns in diameter, by 39% (p < 0.05), and dilated venules greater than 100 microns in diameter by 26% (p < 0.05), but did not significantly dilate arterioles greater than 100 microns in diameter (11%). Inhaled NO did not significantly change the ratio of wet weight to dry weight. We conclude that both endogenous and inhaled NO attenuate hypoxic pulmonary vasoconstriction, with significant pulmonary venous dilation. The main site of action of inhaled NO is vessels smaller than 100 microns in diameter and venules greater than 100 microns in diameter. Inhaled NO (5-100 ppm) does not cause interstitial edema.


Subject(s)
Microcirculation/drug effects , Nitric Oxide/physiology , Pulmonary Circulation/drug effects , Vasoconstriction/drug effects , Administration, Inhalation , Animals , Cats , Hypoxia/physiopathology , Nitric Oxide/administration & dosage , Nitric Oxide/pharmacology , Vascular Resistance/drug effects
20.
Nihon Kyobu Shikkan Gakkai Zasshi ; 33(2): 150-5, 1995 Feb.
Article in Japanese | MEDLINE | ID: mdl-7731119

ABSTRACT

A 23-year-old man was admitted because of an attack of chest pain and dry cough. Chest roentogenogram showed a solitary pulmonary nodule in the left upper lobe. Chest CT showed a nodule and a small pleural effusion on the same side. Pulmonary thrombosis was diagnosed by pulmonary Ventilation/perfusion scintigraphy and pulmonary arteriography. Deep vein thrombosis was not detected except in a distal pulmonary artery. The solitary nodule disappeared spontaneously without thrombolytic therapy. An anticardiolipin antibody (IgG) test was positive. Primary antiphospholipid syndrome was diagnosed, because of the absence of physical findings suggesting other collagen vascular diseases. Patients with antiphospholipid syndrome have a high frequency of pulmonary complications that include pulmonary hypertension and pulmonary embolism. Most of the patients with pulmonary embolism have deep vein thrombosis, and pulmonary vessel thrombosis as seen in the present case is a rare complication.


Subject(s)
Antiphospholipid Syndrome/complications , Pulmonary Embolism/etiology , Adult , Antibodies, Anticardiolipin/analysis , Humans , Immunoglobulin G/analysis , Male , Pulmonary Embolism/diagnostic imaging , Radiography
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