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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of calcium channel antagonists, felodipine and cadmium, as well as pertussis toxin on noradrenaline-induced contractions in pulmonary artery rings from rats with pulmonary hypertension induced by monocrotaline (MCT) were examined. MCT-treated rats had pulmonary hypertension, right ventricular hypertrophy and lung oedema, as compared to corresponding vehicle-treated rats. The MCT-treated animals did not have polycythemia as compared to vehicle-treated rats. Pre-treatment of pulmonary artery rings from MCT-treated rats with felodipine and cadmium significantly reduced the maximum response without altering the EC50 or the Hill coefficient of concentration-response curve to noradrenaline. In pulmonary artery rings from vehicle-treated rats, felodipine significantly increased the EC50 and reduced the maximum response and the Hill coefficient of the concentration-response curve to noradrenaline. In contrast, cadmium did not alter these parameters in pulmonary artery rings from vehicle-treated rats. Pertussis toxin did not affect noradrenaline-induced contractions in pulmonary artery rings from vehicle- or MCT-treated rats. Felodipine, cadmium and pertussis toxin were ineffective in inhibiting noradrenaline-induced contractions in aortic rings from either vehicle- or MCT-treated rats. Our results can be interpreted to indicate that alteration to voltage operated, felodipine-sensitive, calcium channels as well as, cadmium-sensitive sites contribute to the changes observed in the functional behavior of pulmonary blood vessels from pulmonary hypertensive rats.
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PMID:Effects of calcium channel antagonists and pertussis toxin on noradrenaline-induced contractions in pulmonary artery from pulmonary hypertensive rats. 747 94

To determine whether platelet-activating factor (PAF)-induced release of cyclooxygenase products might be dependent on G proteins in vivo, we administered pertussis toxin (PTX) (9.7-10.0 micrograms/kg iv) to conscious pigs approximately 48 h before bolus infusions of PAF (10 ng/kg). Autoradiography of ADP-ribosylated lung cell membrane proteins from PTX-treated pigs demonstrated marked reduction in the amount of radiolabel ([32P]NAD) incorporated, indicating that PTX induced ADP-ribosylation of G proteins in vivo. PAF, infused at hourly intervals from 0-4 h, caused increases in plasma concentrations of thromboxane B2 (TxB2) concomitant with pulmonary hypertension and vasoconstriction in anesthetized pigs. These physiological changes were blocked or markedly attenuated by indomethacin, indicating they were dependent on cyclooxygenase products. In PTX-treated pigs, the PAF-induced pulmonary hypertension and vasoconstriction were modestly attenuated, whereas the increases in plasma TxB2 were markedly attenuated. PTX prevented PAF-induced aggregation of platelets in vivo as evidenced by blockade of thrombocytopenia. However, in vitro, PAF-induced aggregation of platelets was independent of PTX. Moreover, incubation of platelet-rich plasma with 50 microM PAF failed to increase TxB2 levels. These findings suggested that a PTX-sensitive cell other than the platelet was responsible for triggering release of TxA2 and thrombocytopenia in vivo. We conclude that PAF-induced release of TxA2, pulmonary vasoconstriction, and thrombocytopenia in anesthetized pigs are dependent on a PTX-sensitive G protein; however, the residual hemodynamic effects indicate involvement of a PTX-insensitive G protein, or alternatively, G protein independent pathways.
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PMID:Pertussis toxin attenuates platelet-activating factor-induced pulmonary hemodynamic alterations in pigs. 846 Jul 10

Bordetella pertussis causing severe respiratory failure in infants that is unresponsive to treatment is well described. Pulmonary hypertension is a prominent feature of such cases. In this series of 13 critically ill infants with B. pertussis, hyperleukocytosis ( > 100 x 10(9)/l) was an independent predictor of death. We suggest that such extreme leukocytosis may contribute to disease severity via the formation of aggregates in the pulmonary vasculature.
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PMID:Is leukocytosis a predictor of mortality in severe pertussis infection? 1112 65

Despite widespread immunization against Bordetella pertussis, whooping cough remains potentially fatal in susceptible populations such as neonates. A case of neonatal pertussis with severe pulmonary hypertension (PH) requiring extracorporal membrane oxygenation (ECMO) is described. PH associated with pertussis severe enough to require ECMO is frequently irreversible and associated with a poor prognosis.
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PMID:Neonatal pertussis requiring extracorporeal membrane oxygenation. 1131 88

Hypoxia causes pulmonary hypertension and induces oxygen radicals in pulmonary artery smooth muscle cells (PASMCs). Since oxidative stress regulates gaddl53 expression, we examined gaddl53 mRNA in PASMCs cultured in a hypoxic environment. Gadd153 mRNA content was increased in PASMCs cultured for 24 hours in 1% oxygen. This increase was not abrogated by inhibition of protein synthesis. To explore the signaling pathways mediating hypoxic regulation of gaddl53 mRNA, the impact of calcium channel blockade by verapamil, G protein inhibition by pertussis toxin, and protein kinase C (PKC) down-regulation, was examined. Although none of these interventions reduced basal expression of gaddl53 mRNA in PASMCs, all of them suppressed the induction by hypoxia. In contrast, antioxidants had no effect. These observations indicate hypoxia induces gaddl53 expression in PASMCs through common signaling pathways.
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PMID:Regulation of gadd153 mRNA expression by hypoxia in pulmonary artery smooth muscle cells. 1175 72

Severe B. pertussis infection in infants is characterized by severe respiratory failure, pulmonary hypertension, leukocytosis, and death. This retrospective case analysis highlights the course and outcome of severe B. pertussis infection treated with extracorporeal membrane oxygenation (ECMO) at a single center. Over the last decade, out of a total caseload of nearly 800 infants and children, 12 infants with severe B. pertussis have been referred for ECMO therapy to our center. All infants with pertussis infection who received ECMO therapy were less than 3 months of age at presentation and unvaccinated. There was a high mortality rate (7 of 12 infants died), which was associated with an elevated neutrophil count at presentation and multiorgan dysfunction characterized by intractable pulmonary hypertension, persistent systemic hypotension, renal insufficiency, and fits. ECMO should be offered to children with pertussis infection and respiratory failure refractory to mechanical ventilation. However, further research is required to determine the optimal management for infants receiving ECMO therapy with this disease.
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PMID:Extracorporeal life support in pertussis. 1295 44

A 3-month-old infant of 33 weeks' gestation was hospitalized with pneumonia caused by Bordetella pertussis. Respiratory insufficiency worsened, and on hospital day 3, there was severe pulmonary dysfunction (arterial oxygen pressure/fraction of inspired oxygen ratio: 120), extreme leukocytosis (white blood cell count 104,000/mm3), and severe pulmonary hypertension as assessed by 2-dimensional echocardiogram. A double volume exchange transfusion was performed to reduce the leukocyte mass. Oxygenation began to improve during the exchange and continued to improve over the ensuing 31 hours (arterial oxygen pressure/fraction of inspired oxygen ratio: 280). The white blood cell count fell dramatically after the exchange, and the rate of rise was slower after exchange therapy compared with preexchange.
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PMID:Pertussis pneumonia, hypoxemia, hyperleukocytosis, and pulmonary hypertension: improvement in oxygenation after a double volume exchange transfusion. 1528 67

Infection with Bordetella pertussis can cause severe illness with neurological and pulmonary complications in children. Pulmonary hypertension is an early sign of potentially fatal disease and can cause failure of conventional respiratory therapy in severe acute respiratory distress syndrome (ARDS). We report a 4 1/2-year-old boy with B. pertussis infection who developed severe ARDS and pulmonary hypertension. Because of severe neurological signs the patient did not qualify for extracorporal membrane oxygenation (ECMO). After conventional ventilation, surfactant and high frequency oscillation ventilation (HFOV) failed, treatment with nitric oxide (NO) improved oxygenation, allowing recovery without the need for ECMO. The patient survived with few sequelae. Thus, this treatment may be an option in high-risk children who meet the criteria for ECMO but are excluded because of poor neurological status, as in our patient.
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PMID:Successful treatment of ARDS and severe pulmonary hypertension in a child with Bordetella pertussis infection. 1562 48

Fatal myocardial failure secondary to pulmonary hypertension is reported in 5 young infants who presented with Bordetella pertussis infection. All cases showed severe leukocytosis. Three of the 5 patients died early despite intensive management. The autopsy revealed signs of pulmonary hypertension. In addition to acquiring further knowledge of its pathogenesis, it is necessary to develop some new therapeutic approaches to Bordetella pertussis infection in susceptible populations.
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PMID:Pertussis and fatal pulmonary hypertension: a discouraged entity. 1576 5

Pertussis, or "whooping cough," is a highly communicable disease caused by the coccobacillus Bordetella pertussis. Pertussis remains one of the most common causes of death from infectious diseases worldwide. We describe a 5-week-old infant girl who presented with severe pertussis infection associated with extreme leukocytosis and required prolonged extracorporeal membrane oxygenation (ECMO). Nitric oxide therapy resolved the pulmonary hypertension, and she was successfully weaned from ECMO and discharged home after 3 months. We report successful application of ECMO for severe pertussis-induced respiratory failure despite multiple grave prognostic indicators (<1 year age, leukocytosis, pulmonary hypertension) and discuss the role of extracorporeal life support in treating pertussis.
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PMID:Pertussis with severe pulmonary hypertension and leukocytosis treated with extracorporeal membrane oxygenation. 1593 56


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