Biomedical subjects

I Danner

Publications and source records attributed to I Danner.

5 recordsLinked to original sources

PubMed2001

Beta(3)-adrenoceptors control Cl(-) conductance in rabbit nasal epithelium.

We have investigated the effects of beta(3)-adrenoceptor stimulation in vivo on nasal epithelium. We have recorded the transepithelial potential difference in New Zealand white rabbit nostrils. Superfusion of the nasal epithelial surface with a Cl(-)-free medium supplemented with amiloride, hyperpolarized the nasal potential difference. Isoprenaline produced a hyperpolarization of the nasal potential difference that was not prevented by nadolol, a potent beta(1)-/beta(2)-adrenoceptor antagonist, but was abolished by bupranolol, a nonselective beta(1-3)-adrenoceptor antagonist. SR 58611 ((RS)-N-[(25)-7-ethoxycarbonylmethoxy-1,2,3,4-tetrahydronapht-2-yl]-(2R)-2-(3-chlorophenyl)-2 hydroethanamine hydrochloride) and CGP 12177 (4-[3-t-butylamino-2-hydroxypropoxy]benzimidazol-2-1), a preferential and a partial beta(3)-adrenoceptor agonists, respectively, also produced hyperpolarization of the nasal potential difference. SR 59230 (3-(2-ethylphenoxy)-1-[(1S)1,2,3,4-tetrahydronaphth-1-ylaminol]-(2S)-2-propanol oxalate), a selective beta(3)-adrenoceptor antagonist, abolished the effects of CGP 12177. We conclude that beta(3)-adrenoceptor stimulation resulted in modifications in the nasal potential difference. These findings strengthen the view that beta(3)-adrenoceptors are implicated in controlling water and salt transport in the normal respiratory epithelium.

Adrenergic beta-3 Receptor Agonists↗

PubMed2001

[Bronchopulmonary aspergillosis: new developments].

Bronchopulmonary aspergillosis are in the news. Invasive pulmonary aspergillosis raise early diagnostic problems and prevention problems in immunocompromised patients. These infections are no unusual in chronic obstructive pulmonary disease. The diagnosis between aspergilloma and chronic necrotizing pulmonary aspergillosis can be difficult. In allergic bronchopulmonary aspergillosis, epidemiology and therapy are questionable. Real progress has been made due to thoracic computed tomographic scan and mycological methods. Better use of amphotericin B, of amphotericin B lipid formulations and of azole antifungal agents, combined with surgical resection if necessary should improve aspergillosis prognosis.

Amphotericin B↗

PubMed1999

Respiratory epithelial ion transport in patients with disseminated bronchiectasis.

The nosological limits between disseminated bronchiectasis and cystic fibrosis (CF) remain unclear. In patients with isolated congenital bilateral absence of the vas deferens, a forme fruste of the CF disease, a normal baseline nasal transepithelial potential difference (PD) but an impaired response to pharmacological interventions have been reported. The purpose of the present study was to explore ion transport in respiratory epithelium from patients with disseminated bronchiectasis. The PD under both baseline and pharmacological interventions was investigated in 13 healthy subjects, six patients with genetically proven CF and 15 patients with disseminated bronchiectasis as confirmed by computed tomography scan. Baseline PD was similar in the control and bronchiectasis groups but, as expected, was significantly more negative in the CF group. Patients with bronchiectasis responded to pharmacological tests (sequential perfusion with amiloride, chloride-free solution, isoprenaline and uridine triphosphate (UTP) similarly to healthy subjects. In contrast, CF patients exhibited an increased response to amiloride and an impaired response to chloride-free solution and isoprenaline. The data show that patients with disseminated bronchiectasis exhibit normal electrophysiological properties in their nasal epithelium. Nasal transepithelial potential difference including pharmacological tests may appear a valuable diagnostic procedure for cystic fibrosis with disseminated bronchiectasis.

Adolescent↗

PubMed1998

[A rare dyspnea in internal medicine: platypnea-orthodeoxia after pneumonectomy].

BACKGROUND: A right-to-left shunting across a patent foramen ovale is a rare cause of acute respiratory failure after pneumonectomy. CASE REPORTS: We report two cases of posture dependent dyspnea (platypnea-orthodeoxia) secondary to postoperative right-to-left shunting across a patent foramen ovale. Both cases occurred three months after pneumonectomy, the first in a 63-year-old man and other in a 52-year-old man. CONCLUSION: A platypnea-orthodeoxia (dyspnea induced by the upright position with arterial deoxygenation relieved by recumbency) should lead to the diagnosis which is confirmed by echography or cardiac catheterization. The prognosis is good after surgical closure of the patent foramen ovale. The physiopathologic mechanism is poorly understood. We report two cases of platypnea-orthodeoxia.

Adenocarcinoma↗

PubMed1995

[Pharmacology of ion channels in mucoviscidosis. Physiological bases and therapeutic applications].

Phenotypical expression of cystic fibrosis (CF) includes decreased epithelial chloride secretion and increased sodium absorption. These anomalies produce increased water absorption and a dehydrated mucus responsible for decreased mucociliary clearance. Identification of the gene responsible for the genetic disease (CFTR for cystic fibrosis transmembrane conductance regulator) together with a more accurate comprehension of complexes interactions that exist between the CFTR gene product and other epithelial ionic channels has created novel opportunities for discovering specific pharmacological drugs to treat the disease. Amiloride, which limits sodium hyperabsorption, has demonstrated both efficacy and safety in vivo in a restricted number of adult patients. Nucleotides such as ATP or UTP, prescribed in association with amiloride, increase chloride secretion. Potassium channel openers, by stimulating transepithelial chloride transport, may represent an additional innovative approach. Specific pharmacology to CF is not competitive but rather complementary to gene therapy.

Adenosine Triphosphate↗