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Doxycycline protects against right ventricular dysfunction and dilatation caused by acute pulmonary thromboembolism
Author(s) -
Neves Evandro Manoel Neto,
Santos Ozelia Sousa,
Ferraz Karina Coutinho,
Ceron Carla Speroni,
Romano Minna Dias,
Gali Luis Gustavo,
Maciel Benedito Carlos,
Santos Jose Eduardo Tanus
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.669.1
Subject(s) - medicine , doxycycline , dobutamine , ventricle , cardiology , pulmonary artery , matrix metalloproteinase , vascular resistance , blood pressure , hemodynamics , antibiotics , biology , microbiology and biotechnology
We examined whether pretreatment with doxycycline (a matrix metalloproteinase MMP inhibitor) protects against acute pulmonary thromboembolism (APT)‐induced right ventricular dysfunction and dilatation. APT (350 mg/kg of autologous blood clots) increased mean pulmonary artery pressure (MPAP) and pulmonary vascular resistance index (PVRI) by approximately 186% and 196% respectively. Ecocardiography showed that right ventricle (RV) diameter increased in animals with APT (from 10.7±0.8 to 18.3±1.6 mm, P<0.05), but not in embolized animals pretreated with doxycycline at 10 mg/kg i.v. (from 13.3±0.9 to 14.4±1.0 mm, P>0.05). Dobutamine stimulation induced minor improvements in RV function in embolized animals. However, doxycycline improved the RV contractile reserve. APT increased serum cardiac troponin I concentrations and RV gelatinolytic activity, and doxycycline prevented theses increases (P<0.05). These results suggest that MMPs are involved in APT‐induced cardiomyocyte injury, RV dysfunction and dilatation, and degrade contractile proteins. Doxycycline improves the responses to dobutamine during APT. Funded by FAPESP, CNPq, and CAPES (Brazil).