Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolation of the causative agent remains the "gold standard" for the early diagnosis of pertussis. For this purpose, the nasopharynx is swabbed with a calcium alginate swab. Cephalexin-containing charcoal horse blood medium is used for the transport of the swabs to the bacteriology laboratory. As an alternative, the isolation of bordetellae can be performed at the paediatrician's office by direct inoculation of charcoal horse blood agar plates. Long-lasting cough of unknown aetiology is the main field for pertussis serology (ELISA). Even today, severe courses of whooping cough requiring hospitalization are not rare, especially in infants. Erythromycin (given in high doses for 14 days) is the antibiotic of choice for pertussis. As an alternative to the macrolides, cotrimoxazole may be administered or amoxycillin. Salbutamol and the corticosteroids have been shown to be useful for the symptomatic treatment of severe pertussis in infants.
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PMID:[Pertussis: diagnosis, clinical aspects and therapy]. 219 59

The value of sound spectrum analysis (sonography) as an indicator of the severity of symptomatic pertussis was assessed in four infants aged 3 weeks to 5 months. Coughing paroxysms and whooping could be clearly distinguished and measured on the sonogram. Sonography was then used to evaluate the effects of oral salbutamol on pertussis. The drug reduced the frequency and shortened the duration of the whoops; however, it did not have corresponding effect on the cough. Salbutamol seemed to relieve the laryngeal spasms and consequently eased the infant's breathing difficulties.
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PMID:Efficacy of salbutamol in treatment of infant pertussis demonstrated by sound spectrum analysis. 612 Mar 15

Although beta(2)-adrenoceptors represent 15-25% of beta-adrenoceptors in the guinea pig heart, their functionality is controversial. We assessed the inotropic effects of beta(2)-adrenoceptor partial agonists in right papillary muscles. Salbutamol induced a small but significant concentration-dependent negative inotropic effect (NIE, -5% at 60 nM) followed by a moderate positive inotropic effect (+36% at 6 microM) due to activation of beta(1)-adrenoceptors. In the presence of 4 microM atenolol, the concentration-dependent NIE (-12% at 6 microM) was biphasic, best described by a double logistic equation with respective EC(50) values of 3 and approximately 420 nM, and was insensitive to SR59230A. In muscles from pertussis toxin-treated guinea pigs, the salbutamol-induced positive inotropic effect was sensitive to low concentrations of ICI-118551 in an unusual manner. Experiments in reserpinized animals revealed the importance of the phosphorylation-dephosphorylation processes. PKA inhibition reduced and suppressed the effects obtained at low and high concentrations, respectively, indicating that its activation was a prerequisite to the NIE. The effect occurring at nanomolar concentrations depended upon PKA/phosphatidylinositol 3-kinase/cytosolic phospholipase A(2) (cPLA(2)) activations leading to nitric oxide (NO) release via the arachidonic acid/cyclooxygenase pathway. NO release via PKA-dependent phosphorylation of the receptor was responsible for the inotropic effect observed at submicromolar concentrations, which is negatively controlled by cPLA(2). The possibility that these effects are due to an equilibrium between different affinity states of the receptor (G(s)/G(i) coupled and G(i) independent with different signaling pathways) that can be displaced by ICI-118551 is discussed. We conclude that beta(2)-adrenoceptors are functional in guinea pig heart and can modulate the inotropic state.
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PMID:Roles of PKA, PI3K, and cPLA2 in the NO-mediated negative inotropic effect of beta2-adrenoceptor agonists in guinea pig right papillary muscles. 1794 37

Clenbuterol, a compound classified as a beta2-adrenoceptor (AR) agonist, has been employed in combination with left ventricular assist devices (LVADs) to treat patients with severe heart failure. Previous studies have shown that chronic administration of clenbuterol affects cardiac excitation-contraction coupling. However, the acute effects of clenbuterol and the signaling pathway involved remain undefined. We investigated the acute effects of clenbuterol on isolated ventricular myocyte sarcomere shortening, Ca2+ transients, and L-type Ca2+ current and compared these effects to two other clinically used beta2-AR agonists: fenoterol and salbutamol. Clenbuterol (30 microM) produced a negative inotropic response, whereas fenoterol showed a positive inotropic response. Salbutamol had no significant effects. Clenbuterol reduced Ca2+ transient amplitude and L-type Ca2+ current. Selective beta1-AR blockade did not affect the action of clenbuterol on sarcomere shortening but significantly reduced contractility in the presence of fenoterol and salbutamol (P < 0.05). Incubation with 2 microg/ml pertussis toxin significantly reduced the negative inotropic effects of 30 microM clenbuterol. In addition, overexpression of inhibitory G protein (Gi) by adenoviral transfection induced a stronger clenbuterol-mediated negative inotropic effect, suggesting the involvement of the Gi protein. We conclude that clenbuterol does not increase and, at high concentrations, significantly depresses contractility of isolated ventricular myocytes, an effect not seen with fenoterol or salbutamol. In its negative inotropism, clenbuterol predominantly acts through Gi, and the consequent downstream signaling pathways activation may explain the beneficial effects observed during chronic administration of clenbuterol in patients treated with LVADs.
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PMID:Effects of clenbuterol on contractility and Ca2+ homeostasis of isolated rat ventricular myocytes. 1877 53

The effects of salbutamol on contractility and cAMP levels were investigated in rat right ventricular myocardium. Salbutamol (1-300 microM), produced a concentration-dependent positive inotropic effect which was not affected by ICI 118551 (50 nM), a beta2-adrenoceptor antagonist but was abolished by CGP 20712A (1 microM) a beta1-adrenoceptor antagonist. However, in rats pretreated with pertussis toxin (30 microg/kg intraperitoneal injection) salbutamol increases contractility (Emax = 9.8 +/- 1.8%, - log EC50 = 6.25 +/- 0.07, n = 5). The combination of salbutamol + CGP 20712A, also produces a concentration-dependent enhancement of contractility (Emax = 43.0 +/- 7.5%, - log EC50 = 6.3 +/- 0.04, n = 6), in the presence of 30 microM of the non selective phosphodiesterase (PDE) inhibitor 3-isobutylmethylxantine (IBMX) which was prevented by ICI 118551 (50 nM). Also, salbutamol + CGP 20712A fail to increase cAMP tissue levels but enhance them in the presence of IBMX. This effect was also prevented by ICI 118551. These results indicate that PDEs blunt contractility and cAMP production mediated by beta2-adrenoceptors in rat ventricular myocardium. Gi protein, although less efficiently than PDEs, also limits inotropic effects of salbutamol mediated by beta2-adrenoceptors in this tissue.
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PMID:Phosphodiesterases inhibition unmask a positive inotropic effect mediated by beta2-adrenoceptors in rat ventricular myocardium. 1923 6