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  <front>
    <journal-meta>
      <journal-id journal-id-type="nlm-ta">Arq Bras Cardiol</journal-id>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id specific-use="scielo-v3" pub-id-type="publisher-id">rKvQd7B8yB6S8qWmjMmCpxt</article-id>
      <article-id specific-use="scielo-v2" pub-id-type="publisher-id">S0066-782X2021001401113</article-id>
      <article-id pub-id-type="publisher-id">abc.20210935</article-id>
      <article-id pub-id-type="doi">10.36660/abc.20210935</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Minieditorial</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Uma Nova Alternativa Terap&#234;utica para o Tratamento da Hipertens&#227;o Pulmonar?</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="editor">
          <contrib-id contrib-id-type="orcid">0000-0001-6491-9209</contrib-id>
          <name>
            <surname>Gelpi</surname>
            <given-names>Ricardo J</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
          <xref ref-type="corresp" rid="c1"/>
        </contrib>
        <aff id="aff1">
          <label>1</label>
          <institution content-type="orgname">Universidade de Buenos Aires</institution>
          <institution content-type="orgdiv1">Faculdade de Medicina</institution>
          <institution content-type="orgdiv2">Departamento de Patologia</institution>
          <addr-line>
            <named-content content-type="city">Buenos Aires</named-content>
          </addr-line>
          <country country="AR">Argentina</country>
          <institution content-type="original">Instituto de Fisiopatologia Cardiovascular, Departamento de Patologia, Faculdade de Medicina, Universidade de Buenos Aires, Buenos Aires &#8211; Argentina</institution>
        </aff>
      </contrib-group>
      <author-notes>
        <corresp id="c1"><bold>Correspond&#234;ncia: Ricardo J. Gelpi</bold> &#8226; J. E. Uriburu 950, 2&#186; andar. <postal-code>1114</postal-code> Buenos Aires - Argentina. E-mail: <email>rgelpi@fmed.uba.ar</email> </corresp>
      </author-notes>
      <pub-date date-type="pub" publication-format="electronic">
        <day>03</day>
        <month>12</month>
        <year>2021</year>
      </pub-date>
      <pub-date date-type="collection" publication-format="electronic">
        <month>12</month>
        <year>2021</year>
      </pub-date>
      <volume>117</volume>
      <issue>6</issue>
      <fpage>1113</fpage>
      <lpage>1114</lpage>
      <permissions>
        <license license-type="open-access" xlink:href="https://creativecommons.org/licenses/by/4.0/" xml:lang="en">
          <license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License</license-p>
        </license>
      </permissions>
      <kwd-group xml:lang="pt">
        <title>Palavras-chave</title>
        <kwd>Doen&#231;a Cardiopulmonar</kwd>
        <kwd>Hipertens&#227;o Pulmonar</kwd>
        <kwd>Transplante de Pulm&#227;o</kwd>
        <kwd>Ratos</kwd>
        <kwd>Monocrotalina</kwd>
        <kwd>Insufici&#234;ncia Card&#237;aca</kwd>
        <kwd>Estresse Oxidativo</kwd>
        <kwd>Cardiomegalia</kwd>
        <kwd>&#211;leo de Copaiba</kwd>
        <kwd>Fitoterapia</kwd>
        <kwd>Fabaceae</kwd>
      </kwd-group>
      <counts>
        <fig-count count="0"/>
        <table-count count="0"/>
        <equation-count count="0"/>
        <ref-count count="9"/>
        <page-count count="2"/>
      </counts>
    </article-meta>
  </front>
  <body>
    <p>Neste n&#250;mero da revista Arquivos Brasileiros de Cardiologia, foi publicada uma pesquisa importante e original sobre ratos.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> O trabalho &#233; importante porque a hipertens&#227;o pulmonar representa uma patologia grave, de dif&#237;cil tratamento e cuja &#250;nica forma de aliviar o paciente &#233; o transplante de pulm&#227;o com as dificuldades e limita&#231;&#245;es que esse dif&#237;cil tratamento apresenta. O trabalho tamb&#233;m &#233; original porque muito se publicou sobre os efeitos ben&#233;ficos do &#243;leo de copa&#237;ba, por exemplo, sua a&#231;&#227;o antiinflamat&#243;ria, seu efeito analg&#233;sico, bem como sua capacidade de prevenir infec&#231;&#245;es e melhorar o processo de cicatriza&#231;&#227;o. No entanto, o efeito ben&#233;fico do &#243;leo de copa&#237;ba na hipertens&#227;o pulmonar n&#227;o foi descrito. Nesse sentido, o grupo liderado por Adriane Bell&#243; Klein, vem trabalhando h&#225; v&#225;rios anos com o grande problema da hipertens&#227;o pulmonar em geral<sup><xref ref-type="bibr" rid="B2">2</xref>-<xref ref-type="bibr" rid="B4">4</xref></sup> e os efeitos do &#243;leo de copa&#237;ba nesta patologia,<sup><xref ref-type="bibr" rid="B5">5</xref>,<xref ref-type="bibr" rid="B6">6</xref></sup> o que tornou este grupo de pesquisa uma refer&#234;ncia internacional neste tema.</p>
    <p>&#201; importante mencionar que a hipertens&#227;o pulmonar induzida em ratos por monocrotalina produz les&#245;es vasculares muito semelhantes &#224;s encontradas em pacientes com essa patologia.<sup><xref ref-type="bibr" rid="B7">7</xref>,<xref ref-type="bibr" rid="B8">8</xref></sup> Em ess&#234;ncia, o que mostra o trabalho publicado neste n&#250;mero da revista Arquivos Brasileiros de Cardiologia,<sup><xref ref-type="bibr" rid="B1">1</xref></sup> &#233; que a administra&#231;&#227;o de aceite de copa&#237;ba a um grupo de ratas com hipertens&#227;o pulmonar induzida por monocrotalina, produz um claro efeito ben&#233;fico, por m&#233;dio da diminui&#231;&#227;o dos indicadores em sangre perif&#233;rica de stress oxidativo, uma redu&#231;&#227;o da resist&#234;ncia vascular pulmonar, e um remodelamento favor&#225;vel do ventr&#237;culo direito, com redu&#231;&#227;o da hipertrofia, o que se traduz numa melhor fun&#231;&#227;o sist&#243;lica desse ventr&#237;culo. Este achado &#233; muito importante porque &#233; bem conhecido que a hipertrofia mioc&#225;rdica &#233; uma das principais causas de insufici&#234;ncia card&#237;aca e morte s&#250;bita. A rela&#231;&#227;o positiva entre o grau de hipertrofia e a diminui&#231;&#227;o do estresse oxidativo apresentada pelos autores &#233; claramente comprovada neste trabalho pelo alto valor de r obtido quando essas duas vari&#225;veis foram correlacionadas. No entanto, e al&#233;m desta importante correla&#231;&#227;o, estudos futuros devem determinar se o efeito ben&#233;fico no ventr&#237;culo direito se deve &#224; redu&#231;&#227;o do estresse oxidativo ou se h&#225; tamb&#233;m um efeito direto do &#243;leo de copa&#237;ba nas fibras mioc&#225;rdicas. Talvez experimentos que pudessem ser feitos em cora&#231;&#245;es isolados tornassem poss&#237;vel detectar ou n&#227;o um efeito direto desse agente natural. Nesse sentido, &#233; importante mencionar que os autores deste estudo tamb&#233;m publicaram um interessante trabalho anteriormente<sup><xref ref-type="bibr" rid="B5">5</xref></sup> onde mostraram que a administra&#231;&#227;o do &#243;leo de copa&#237;ba diminuiu os sinais de apoptose no ventr&#237;culo direito hipertr&#243;fico e atribu&#237;ram o melhor remodelamento a uma poss&#237;vel diminui&#231;&#227;o da j&#225; mencionada apoptose, obviamente esse mesmo mecanismo poderia estar agindo no trabalho que estamos discutindo agora. Por&#233;m, aqui &#233; importante fazer alguns esclarecimentos que podem nos permitir entender melhor o que est&#225; acontecendo nesses cora&#231;&#245;es com hipertrofia secund&#225;ria &#224; hipertens&#227;o pulmonar.</p>
    <p>Em trabalho anterior, mostramos<sup><xref ref-type="bibr" rid="B9">9</xref></sup> que a apoptose que se desenvolve durante a hipertrofia n&#227;o se correlaciona com a fun&#231;&#227;o ventricular, ou seja, a apoptose n&#227;o &#233; necessariamente respons&#225;vel pela diminui&#231;&#227;o da fun&#231;&#227;o ventricular como foi sugerido anteriormente, al&#233;m disso, e ainda mais importante, a apoptose card&#237;aca n&#227;o &#233; apenas de mi&#243;citos, mas a grande maioria &#233; devida a c&#233;lulas n&#227;o mi&#243;citos, o que inclui c&#233;lulas endoteliais, fibroblastos ou macr&#243;fagos. Portanto, pode acontecer que a diminui&#231;&#227;o da apoptose por &#243;leo de copa&#237;ba nesses cora&#231;&#245;es com hipertrofia secund&#225;ria &#224; hipertens&#227;o pulmonar n&#227;o seja principalmente nas c&#233;lulas mioc&#225;rdicas e, portanto, essa diminui&#231;&#227;o da apoptose n&#227;o afeta a fun&#231;&#227;o ventricular, n&#227;o estando envolvida no efeito ben&#233;fico do &#243;leo de copa&#237;ba. Embora as vari&#225;veis relacionadas &#224; apoptose n&#227;o tenham sido medidas no presente trabalho, o fato de os mesmos autores terem sugerido em um trabalho anterior que esse mecanismo poderia ter sido inclu&#237;do no efeito ben&#233;fico do &#243;leo de copa&#237;ba, acho que justifica esse coment&#225;rio sobre a apoptose. Ou seja, estamos comentando neste editorial um excelente trabalho experimental, bem desenhado, com resultados claros, importantes e originais, mostrando fortes evid&#234;ncias experimentais de um efeito ben&#233;fico do &#243;leo de copa&#237;ba na inibi&#231;&#227;o do estresse oxidativo. Talvez em trabalhos futuros outros mecanismos envolvidos possam ser descritos, que poderiam incluir, al&#233;m do efeito do estresse oxidativo, uma a&#231;&#227;o direta sobre a fibra mioc&#225;rdica ou um estudo mais detalhado da apoptose.</p>
  </body>
  <back>
    <fn-group>
      <fn fn-type="other" id="fn1">
        <p>Minieditorial referente ao artigo: Efeitos do &#211;leo de Copa&#237;ba em Marcadores Perif&#233;ricos de Estresse Oxidativo em um Modelo de Cor Pulmonale em Ratos</p>
      </fn>
    </fn-group>
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              <given-names>S</given-names>
            </name>
            <name>
              <surname>Vatner</surname>
              <given-names>DE</given-names>
            </name>
            <name>
              <surname>Vatner</surname>
              <given-names>SF</given-names>
            </name>
          </person-group>
          <article-title>Apoptosis in severe, compensated pressure overload predominates in nonmyocytes and is related to the hypertrophy but not function</article-title>
          <source>Am J Physiol Heart Circ Physiol</source>
          <year>2011</year>
          <volume>300</volume>
          <issue>3</issue>
          <fpage>H1062</fpage>
          <lpage>H1068</lpage>
        </element-citation>
        <mixed-citation>9 Gelpi RJ, Park M, Gao S, Dhar S, Vatner DE, Vatner SF. Apoptosis in severe, compensated pressure overload predominates in nonmyocytes and is related to the hypertrophy but not function. Am J Physiol Heart Circ Physiol. 2011;300(3):H1062-8.</mixed-citation>
      </ref>
    </ref-list>
  </back>
  <sub-article article-type="translation" id="S01" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Short Editorial</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>A New Therapeutic Alternative for the Treatment of Pulmonary Hypertension?</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="editor">
          <contrib-id contrib-id-type="orcid">0000-0001-6491-9209</contrib-id>
          <name>
            <surname>Gelpi</surname>
            <given-names>Ricardo J</given-names>
          </name>
          <xref ref-type="aff" rid="aff2">
            <sup>1</sup>
          </xref>
          <xref ref-type="corresp" rid="c2"/>
        </contrib>
        <aff id="aff2">
          <label>1</label>
          <addr-line>
            <named-content content-type="city">Buenos Aires</named-content>
          </addr-line>
          <country country="AR">Argentina</country>
          <institution content-type="original">Institute of Cardiovascular Physiopathology, Department of Pathology, Faculty of Medicine, University of Buenos Aires, Buenos Aires - Argentina</institution>
        </aff>
      </contrib-group>
      <author-notes>
        <corresp id="c2"><bold>Mailing Address: Ricardo J. Gelpi</bold> &#8226; J. E. Uriburu 950, 2nd floor. <postal-code>1114</postal-code> Buenos Aires - Argentina. E-mail: <email>rgelpi@fmed.uba.ar</email> </corresp>
      </author-notes>
      <kwd-group xml:lang="en">
        <title>Keywords</title>
        <kwd>Cor Pulmonale</kwd>
        <kwd>Hypertension,Pulmonary</kwd>
        <kwd>Lung Transplantation</kwd>
        <kwd>Rats</kwd>
        <kwd>Monocrotaline</kwd>
        <kwd>Heart Failure</kwd>
        <kwd>Oxidative Stress</kwd>
        <kwd>Cardiomegaly</kwd>
        <kwd>Copaiba Oil</kwd>
        <kwd>Phytotherapy</kwd>
        <kwd>Fabaceae</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>In this issue of the journal <italic>Arquivos Brasileiros de Cardiologia,</italic> important and original research work on rats is published.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> The work is important because pulmonary hypertension represents a serious pathology that is very difficult to treat. The only way to relieve patients is lung transplantation, but are very well known the difficulties and limitations of this treatment. The work is also original because a lot has been published about the beneficial effects of copaiba oil, such as its anti-inflammatory action, analgesic effect, and ability to prevent infections and improve the healing process. However, the beneficial effect of copaiba oil on pulmonary hypertension had not been described. In this sense, the group led by Adriane Bell&#243; Klein has been working for several years on this important issue of pulmonary hypertension in general,<sup><xref ref-type="bibr" rid="B2">2</xref>-<xref ref-type="bibr" rid="B4">4</xref></sup> and the effects of copaiba oil on this particular pathology,<sup><xref ref-type="bibr" rid="B5">5</xref>,<xref ref-type="bibr" rid="B6">6</xref></sup> which has made this research group an international benchmark on this theme.</p>
      <p>It is important to mention that pulmonary hypertension induced in rats by monocrotaline produces vascular lesions very similar to those found in patients with this pathology.<sup><xref ref-type="bibr" rid="B7">7</xref>,<xref ref-type="bibr" rid="B8">8</xref></sup> In essence, what the work published in this issue of the journal <italic>Arquivos Brasileiros de Cardiologia</italic><sup><xref ref-type="bibr" rid="B1">1</xref></sup> shows is that the administration of copaiba oil to a group of rats with pulmonary hypertension induced by monocrotaline produces a clear beneficial effect, through the decrease in peripheral blood indicators of oxidative stress, a reduction in pulmonary vascular resistance, and a favorable remodeling of the right ventricle, with a reduction in hypertrophy, which translates into a better systolic function of that ventricle. This finding is very important because it is well known that myocardial hypertrophy is one of the most important causes of heart failure and sudden death. The positive relationship between the degree of hypertrophy and the decrease in oxidative stress shown by the authors is clearly proven in this work by the high r-value obtained when these two variables were correlated. However, and beyond this important correlation, future studies should determine if the beneficial effect on the right ventricle is due to the reduction of oxidative stress or if there is also a direct effect of copaiba oil on myocardial fibers. Perhaps experiments that could be carried out on isolated hearts would make it possible to detect or not a direct impact of this natural agent. In this sense, it is important to mention that the authors of this study also published an interesting work previously<sup><xref ref-type="bibr" rid="B5">5</xref></sup> where they showed that the administration of copaiba oil decreased apoptosis signals in the hypertrophic right ventricle and attributed the better remodeling to a possible decrease in the apoptosis mentioned above; obviously this same mechanism could be acting in the work that we are commenting now. Nevertheless, here it is important to make some clarifications that may allow a better understanding of what is happening in these hearts with hypertrophy secondary to pulmonary hypertension.</p>
      <p>In previous work, we have shown<sup><xref ref-type="bibr" rid="B9">9</xref></sup> that apoptosis that develops during hypertrophy does not correlate with ventricular function. That is, apoptosis is not necessarily responsible for the decrease in ventricular function as has been previously suggested, and in addition, and even more important, cardiac apoptosis is not only of myocytes, but the vast majority is due to nonmyocyte cells, which includes endothelial cells, fibroblasts, or macrophages. Therefore, it could be that the decrease in apoptosis due to copaiba oil in these hearts with hypertrophy secondary to pulmonary hypertension is not mainly in myocardial cells and therefore, this decrease in apoptosis does not affect ventricular function, not being involved in the beneficial effect of copaiba oil. Although variables related to apoptosis were not measured in the present work, the fact that the same authors have suggested in a previous work that this mechanism could have been included in the beneficial effect of copaiba oil, I think, justifies this comment on apoptosis. In other words, we are commenting in this editorial an excellent experimental work, well designed, with clear, important and original results, showing strong experimental evidence of a beneficial effect of copaiba oil in inhibiting oxidative stress. Perhaps in future works, other mechanisms involved could be described, which could include, in addition to the effect of oxidative stress, direct action on the myocardial fiber or a more detailed study of apoptosis.</p>
    </body>
    <back>
      <fn-group>
        <fn fn-type="other" id="fn2">
          <p>Short Editorial related to the article: Effects of Copaiba Oil in Peripheral Markers of Oxidative Stress in a Model of Cor Pulmonale in Rats</p>
        </fn>
      </fn-group>
    </back>
  </sub-article>
</article>
