Abstract
To investigate the subcutaneous injection of carbon dioxide (CO2) on neuropeptides Calcitonin Gene-Related Peptide (CGRP) and Substance P (SP) secretion in rat skin. Fifty-six Wistar-EPM rats were distributed in two groups: one for CGRP analysis, the other for SP analysis. Each group was subdivided into four subgroups: control (Cont), control with needle (ContNd), CO2 injection (CO2Inj) and atmospheric air injection (AirInj) - with seven animals each. Sample analyses of partial skin were conducted by Western Blotting (WB). In SP group, there was a decrease in the amount of neuropeptides in subgroups CO2Inj and AirInj. Similarly, in CGRP group, there was a decrease in the amount of pro-CGRP neuropeptides (15 kDa) in subgroups CO2Inj and AirInj; Nevertheless, there was no decrease in the amount of CGRP (5 kDa) in any subgroups. Subcutaneous injection of CO2 and atmospheric air decreased the amount of Substance P and pro-Calcitonin Gene-Related Peptide (15 kDa) neuropeptides in rat skin.
Highlights
Carboxytherapy is a technique originated in 1930 in which carbon dioxide (CO2) is injected through a needle into the subcutaneous tissue
All the animals were submitted to trichotomy, with a 1 hour wait before conducting the procedures The animals were distributed into the following subgroups: Subgroup 1 Control (Cont), no needle perforation; Subgroup 2 - Control with Needle (ContNd), with hypodermic needle perforation; Subgroup 3 – CO2 Injection (CO2Inj), with carbon dioxide injection; Subgroup 4 - Atmospheric Air Injection (AirInj), with atmospheric air injection
Due to the importance of calcitonin gene-related peptide (CGRP) and SP neuropeptides in the skin, this study aimed at investigating the influence of carbon dioxide (CO2) on the release of these neuropeptides, which helps clarify the mechanisms leading to the increase in vascular perfusion by CO2
Summary
Carboxytherapy is a technique originated in 1930 in which carbon dioxide (CO2) is injected through a needle into the subcutaneous tissue. Lesions caused by the gas trigger a local inflammatory process which results in tissue healing, represented by angiogenesis and fibrogenesis. These effects may occur due to an increase in capillary blood flow triggered by hypercapnia, by a decreased consumption of cutaneous oxygen or by a rightward shift of the oxygen (O2) dissociation curve (Bohr effect)[1]. It is known that intranasal CO2 may inhibit trigeminal neuronal activation (in rats) and suppress in vitro calcitonin gene-related peptide (CGRP) release[2] Based on this assumption, the efficiency of intranasal noninhaled CO2 was investigated in the treatment of seasonal allergic rhinitis (SAR)[3]. Activation of trigeminal nerves causes local release of neuropeptides, including CGRP4
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