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Propranolol impairs the closure of pressure ulcers in mice
Thatiana L Assis de Brito1, Andréa Monte-Alto-Costa1, Bruna Romana-Souza1
1Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Aims:
β-Adrenoceptors modulate acute wound healing; however, few studies have shown the effects of β-adrenoceptor blockade on chronic wounds. Therefore, this study investigated the effect of β1-/β2-adrenoceptor blockade in wound healing of pressure ulcers.
Main Methods:
Male mice were daily treated with propranolol (β1-/β2-adrenoceptor antagonist) until euthanasia. One day after the beginning of treatment, two cycles of ischemia-reperfusion by external application of two magnetic plates were performed in skin to induce pressure ulcer formation.
Key Findings:
Propranolol administration reduced keratinocyte migration, transforming growth factor-β protein expression, re-epithelialization, and necrotic tissue loss. Neutrophil number and neutrophil elastase protein expression were increased in propranolol-treated group when compared with control group. Propranolol administration delayed macrophage mobilization and metalloproteinase-12 protein expression and reduced monocyte chemoattractant protein-1 protein expression. Myofibroblastic differentiation, angiogenesis, and wound closure were delayed in the propranolol-treated animals. Propranolol administration increased neo-epidermis thickness, reduced collagen deposition, and enhanced tenascin-C expression resulting in the formation of an immature and disorganized collagenous scar.
Significance:
β1-/β2-Adrenoceptor blockade delays wound healing of ischemia-reperfusion skin injury through the impairment of the re-epithelialization and necrotic tissue loss which compromise wound inflammation, dermal reconstruction, and scar formation.
Insights
Beta-blocker propranolol impairs chronic wound healing by delaying re-epithelialization and dermal repair. This study shows beta1-/beta2-adrenoceptor blockade negatively impacts pressure ulcer healing in mice.
Area of Science:
- Dermatology
- Pharmacology
- Wound Healing Research
Background:
- Beta-adrenoceptors influence acute wound healing.
- Limited research exists on beta-adrenoceptor blockade's impact on chronic wounds.
- Pressure ulcers represent a significant clinical challenge in chronic wound care.
Purpose of the Study:
- To investigate the effect of beta1-/beta2-adrenoceptor blockade on pressure ulcer healing.
- To determine the role of propranolol in the complex processes of wound repair.
Main Methods:
- Male mice received daily propranolol treatment (beta1-/beta2-adrenoceptor antagonist).
- Pressure ulcers were induced via ischemia-reperfusion injury.
- Wound healing parameters were assessed throughout the study period.
Main Results:
- Propranolol reduced keratinocyte migration, re-epithelialization, and necrotic tissue loss.
- Neutrophil infiltration and elastase expression increased with propranolol treatment.
- Macrophage mobilization, angiogenesis, and wound closure were delayed.
- Immature scar formation with disorganized collagen was observed.
Conclusions:
- Beta1-/beta2-adrenoceptor blockade by propranolol delays pressure ulcer healing.
- Impaired re-epithelialization and necrotic tissue loss compromise inflammation and dermal repair.
- The study highlights the detrimental effects on scar formation and overall wound reconstruction.
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