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PULMONOLOGY / EXPERIMENTAL RESEARCH
Hyperbaric oxygen effects on the alveoli-capillary unit in a murine model of pulmonary arterial hypertension
1
Escuela Superior de Medicina, Instituto Politecnico Nacional, Mexico
2
Department of Pathological Anatomy, Hospital Regional de Alta Especialidad de Ixtapaluca, Mexico
3
Histology Department, Universidad Panamericana, Mexico
Submission date: 2020-04-06
Final revision date: 2020-08-05
Acceptance date: 2020-08-16
Online publication date: 2020-09-15
Publication date: 2026-06-30
Corresponding author
Arch Med Sci 2026;22(3):1882-1892
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Pulmonary hypertension (PH) is an increase in the normal value of systolic pressure of the pulmonary artery, frequently due to congenital heart diseases being its treatment the correction of this defects; alternatively, hyperbaric oxygen (HBO) has shown beneficial effects facilitating neovascularisation and decreased vascular resistance. An experimental study was designed to determine the effect of HBO on the alveoli-capillary unit in a murine model of irreversible pulmonary hypertension (IPAH) induced with monocrotaline.
Material and methods:
Four groups of 10 Wistar rats each were considered: A (control), B (HBO), C (IPAH), and D (IPAH+HBO). HBO was administered at 2 atm, 1 h daily, for 15 days. At the end of this time, systolic pulmonary artery pressure (PAP) was measured, followed by histologically quantification of the number of cells, vascular buttons, and neoformation vessels employing the immunochemistry detection of hypoxia-induced factor-1 (HIF-1), vascular endothelial growth factor (VEGF), and CD34, respectively.
Results:
Histologically, this matches with an increase of the average number of positive HIF-1 cells, and an increase in VEGF-positive vascular buttons in group D rats compared with those of group C. The number of CD34-positive neovessels was similar in groups C and D, but in the latter group the number of capillary vessels was more significant.
Conclusions:
This suggests that angiogenesis and vasculogenesis were induced by HIF-1, and it has been achieved due to an early effect of HBO therapy. Presumably, neovessels were formed between days 5 and 10 following HBO therapy, but more experimental studies are required to test this hypothesis.
Pulmonary hypertension (PH) is an increase in the normal value of systolic pressure of the pulmonary artery, frequently due to congenital heart diseases being its treatment the correction of this defects; alternatively, hyperbaric oxygen (HBO) has shown beneficial effects facilitating neovascularisation and decreased vascular resistance. An experimental study was designed to determine the effect of HBO on the alveoli-capillary unit in a murine model of irreversible pulmonary hypertension (IPAH) induced with monocrotaline.
Material and methods:
Four groups of 10 Wistar rats each were considered: A (control), B (HBO), C (IPAH), and D (IPAH+HBO). HBO was administered at 2 atm, 1 h daily, for 15 days. At the end of this time, systolic pulmonary artery pressure (PAP) was measured, followed by histologically quantification of the number of cells, vascular buttons, and neoformation vessels employing the immunochemistry detection of hypoxia-induced factor-1 (HIF-1), vascular endothelial growth factor (VEGF), and CD34, respectively.
Results:
Histologically, this matches with an increase of the average number of positive HIF-1 cells, and an increase in VEGF-positive vascular buttons in group D rats compared with those of group C. The number of CD34-positive neovessels was similar in groups C and D, but in the latter group the number of capillary vessels was more significant.
Conclusions:
This suggests that angiogenesis and vasculogenesis were induced by HIF-1, and it has been achieved due to an early effect of HBO therapy. Presumably, neovessels were formed between days 5 and 10 following HBO therapy, but more experimental studies are required to test this hypothesis.
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