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. 2014 Jul-Sep;12(3):382–383. doi: 10.1590/S1679-45082014AI2681
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Histopathological characteristics of pulmonary emphysema in experimental model

Antonio Di Petta 1
PMCID: PMC4872956  PMID: 25184805

Historically pulmonary emphysema was described in 1834 by Laennec on the basis of observations made on the cut surface of postmortem human lungs being the lesion attributed to the atrophy of lung tissue from pulmonary hyperinflation.(1) Hence, emphysema was redefined as a “abnormal and permanent dilation of distal air spaces of terminal bronchiole”.(2) In addition, evidences of destruction of alveolar wall and fibrosis must not be ignored in this disease pathogenesis.(3)

These anatomopathological changes result in loss of respiratory surface and blood irrigation, decrease of elastic recognition and pulmonary hyperexpansion, and it could also affect part of acinus or its structure.(4)

Pulmonary emphysema is caused by enzymatic imbalance between proteases and anti-proteases that results in destruction of the alveolar wall due to proteolytic enzymes action, which affects the extracellular matrix (ECM)(5) and its component integrity especially the elastic fibres.(6)

Experimental model of pulmonary emphysema is based on nebulization or instillation of proteolytic enzyme, such as panain (Carica papaya),(7) porcine pancreatic elastase,(4) and human neutrophil elastase.(8) This proteolytic process, associated with uniform destruction of ECM of pulmonary acinus, ends up in morphohistological and physiological changes in lungs that resemble those changes find in emphysema in humans.(9,10)

Dilatation of distal air spaces of terminal bronchiole (Figure 1) and reduction of area occupied by elastic fibres (Figure 2) evidenced histologically the pulmonary emphysema in experimental models that use porcine pancreatic elastase.

Figure 1. Photomicrographs of lung parenchyma (hematoxylin-eosin) x 100 increased. (A) Naïve lung and (B) emphysematous lung showing hyperdistension of alveolar ducts associated with the rupture of alveolar septa.

Figure 1

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Figure 2. Photomicrographs of lung parenchyma (Verhoeff), x 400 increased. Lung naïve showing integrity of elastic component of alveolar wall, opposing to areas revealed throughout septa associated with thickening of elastic fibres in alveolar wall and decreasing of proportion of elastic fibres in emphysematous lung (B).

Figure 2

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REFERENCES

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Einstein (Sao Paulo). 2014 Jul-Sep;12(3):382–383. [Article in Portuguese]

Características histopatológicas do enfisema pulmonar em modelo experimental

Antonio Di Petta 1

Historicamente, Laennec (1834) descreveu o enfisema pulmonar a partir de observações em cortes necroscópicos superficiais de pulmões humanos, atribuindo a lesão à atrofia do tecido pulmonar resultante da hiperinsuflação pulmonar.(1) O enfisema foi, então, redefinido como uma “dilatação anormal e permanente dos espaços aéreos distais do bronquíolo terminal”.(2) Além do mais, a evidência da destruição da parede alveolar e de fibrose não deve ser ignorada na patogenia da doença.(3)

Essas alterações anatomopatológicas resultam na perda da superfície respiratória e de irrigação sanguínea, na diminuição do recolhimento elástico e na hiperexpansão pulmonar, podendo atingir parte do ácino ou toda sua estrutura.(4)

O enfisema pulmonar é obviamente uma doença causada pelo desequilíbrio enzimático existente entre proteases e antiproteases, resultando na destruição da parede alveolar ocasionada pela ação de enzimas proteolíticas, que degradam a matriz extracelular (MEC)(5) e afetam a integridade de seus componentes, particularmente as fibras elástica.(6)

Modelos experimentais de enfisema pulmonar baseiam-se na nebulização ou instilação de enzimas proteolíticas, como papaína (Carica papaya),(7) elastase pancreática de porco,(4) e elastase neutrofílica humana.(8) Esse processo proteolítico, associado à destruição uniforme da MEC do ácino pulmonar, resulta em alterações morfo-histológicas e fisiológicas dos pulmões equivalentes às alterações encontradas no enfisema em seres humanos.(9,10)

A dilatação dos espaços aéreos distais do bronquíolo terminal (Figura 1) e a redução da área ocupada pelas fibras elásticas (Figura 2) evidenciam histologicamente o enfisema pulmonar em modelos experimentais instilados por elastase pancreática de porco.

Figura 1. Fotomicrografias do parênquima pulmonar (hematoxilina-eosina), aumento x100. (A) Pulmão naive e (B) pulmão enfisematoso, demonstrando hiperdistensão dos ductos alveolares com ruptura dos septos alveolares.

Figura 1

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Figura 2. Fotomicrografias do parênquima pulmonar (Verhoeff), aumento de 400x. (A) Pulmão naive demonstrando integridade dos componentes elásticos da parede alveolar, contrastando com áreas desnudas ao longo dos septos associadas ao adensamento de fibras elásticas na parede alveolar e diminuição da concentração de fibras elásticas no pulmão enfisematoso (B).

Figura 2

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