Serotonin – One Possible Link between Oxygen Metabolism and the Regulation of Blood Flow in the Brain?

Abstract

Hyperoxemia is known to alter tissue oxygenation, which in the brain results in a scattered and an uneven distribution of cerebrocortical tissue oxygen pressures (PtO₂). This study examined the effect of ritanserin (a highly specific serotonin receptor antagonist, 5-HT₂) on the P_tO₂ distribution during hyperoxemia. The measurements of brain oxygenation were performed on the motor cortex in anesthetized pigs with a multiwire Clark-type microelectrode. Ritanserin was administered (0.035 mg/kg i.v.) during hyperoxemia (inspired oxygen fraction = 0.70). In 4 of 5 animals, the disturbed oxygenation that was registered during hyperoxemia was normalized after the ritanserin injection. These results indicate that serotonin may be involved in the regulation of brain oxygenation during hyperoxemia, and they also suggest that serotonin may be a link in the coupling between the oxygen metabolism and the regulation of blood flow in the brain.

The medical use of oxygen: a time for critical reappraisal

“…Secondly, erythrocytes themselves may sense the PO 2 , thereby regulating vascular tone by increasing or decreasing uptake or extrusion of intracellular ATP, which binds to endothelial purinergic P2Y receptors, stimulating local production of nitric oxide . Thirdly, hyperoxia may reduce the availability of the vasodilator prostaglandin PGI 2 , or enhance serotonin (5‐HT) effects on the 5‐HT 2 receptor . However, increased blood serotonin levels were not found in individuals exposed to high oxygen concentrations .…”

Acute hyperoxaemia‐induced effects on regional blood flow, oxygen consumption and central circulation in man

“…1972). However, the results from several more recent studies suggest that the vasoconstriction seen during hyperoxia/hyperoxaemia is mediated at the microvascular level, through the endothelium by either an increased release or effect of vasoconstrictors (oxygen radicals or serotonin, 5‐HT) (Rubanyi & Vanhoutte 1986, Gustafsson & Sjoberg 1996), or decreased effect of vasodilators (prostaglandin E2 and/or endothelium‐derived relaxing factor) (Messina et al. 1994).…”

Controle neurovascular em repouso e durante o exercí­cio em indiví­duos com diferentes ní­veis de pressão arterial: papel dos quimiorreceptores periféricos

“…Sinski e colaboradores (SINSKI et al, 2012) mostraram, assim como nós, que a desativação dos quimiorreceptores periféricos, nos pacientes hipertensos, não alterou os níveis da pressão arterial sistólica e diastólica, mesmo observando redução da atividade nervosa simpática muscular. Uma possível explicação para esse fenômeno é que a suplementação de oxigênio (hiperóxia) usada para desativar os quimiorreceptores periféricos possa causar uma vasoconstrição, a qual é mediada em nível microvascular no endotélio, devido à maior liberação ou efeito aumentado de vasoconstritores ou por redução dos vasodilatadores endoteliais (RUBANYI & VANHOUTTE, 1986;MESSINA et al, 1994;GUSTAFSSON & SJOBERG, 1996;ROUSSEAU et al, 2005). Assim, essa vasoconstrição causada pela hiperóxia compensaria parte do efeito simpato-inibitório observado pela desativação dos quimiorreceptores periféricos nos pacientes hipertensos.…”