RESUMO

Sex differences related with pain have been studied and evidences suggesting influence of sex steroid hormones on the thresholds of pain. Experimental nociception has been test using formalin as a model of nociceptive stimulus. Association of stress, pain and metabolic and hormonal changes has not been explored. The aim of this study was to compare metabolic and hormonal changes between male rats and female rats in proestrus and estrus cycle after painful stimulus by formalin into the masseter muscle. Male and female Wistar rats (200-250 g b.w.) were submitted to an injection of formalin (F, 1.5%) or saline (S, 9.9%) into the masseter muscle and after 0 (N, control group without injection), 5, 15, 30 or 60 minutes they were decapitate and blood was collected to measure biochemical parameters. Plasma estradiol concentration (pg dL-1) was significantly higher in proestrus (106.3 ± 4.3, n = 45, p 0.05) group compared to the estrous group (89.4 ± 3.5, n = 43). Blood plasma concentration of glucose (mg dL-1) was increased after 5 and 15 minutes of injection of formalin or saline in the animals, but in the estrus group the increase was bigger than in the others. Free fatty acids levels increased in the estrous group after 5, 15 and 30 minutes and also the corticosterone levels and these concentrations wer significantly different (p 0.05) from either male or female animals i

RESUMO

Sex differences related with pain have been studied and evidences suggesting influence of sex steroid hormones on the thresholds of pain. Experimental nociception has been test using formalin as a model of nociceptive stimulus. Association of stress, pain and metabolic and hormonal changes has not been explored. The aim of this study was to compare metabolic and hormonal changes between male rats and female rats in proestrus and estrus cycle after painful stimulus by formalin into the masseter muscle. Male and female Wistar rats (200-250 g b.w.) were submitted to an injection of formalin (F, 1.5%) or saline (S, 9.9%) into the masseter muscle and after 0 (N, control group without injection), 5, 15, 30 or 60 minutes they were decapitate and blood was collected to measure biochemical parameters. Plasma estradiol concentration (pg dL-1) was significantly higher in proestrus (106.3 ± 4.3, n = 45, p 0.05) group compared to the estrous group (89.4 ± 3.5, n = 43). Blood plasma concentration of glucose (mg dL-1) was increased after 5 and 15 minutes of injection of formalin or saline in the animals, but in the estrus group the increase was bigger than in the others. Free fatty acids levels increased in the estrous group after 5, 15 and 30 minutes and also the corticosterone levels and these concentrations wer significantly different (p 0.05) from either male or female animals i

RESUMO

Several identifyed substances are involved with liver proliferative process, somatomedines (growth factors) among them. The most of them show different actions, stimulating or inhibiting cell division, depending on their concentrations. The following factors play important role on the liver: HGF; EGF; TGF-alpha; TGF b ; Interleucin-6; IGF; FGF; VEGF; KGF; HSS e ALR. The combined action of HGF, TGF-alpha, IL-6, TNF-alpha, norepinephrin and EGF, allows insulin, glucagon and also EGF to express their effects. HGF seems to be essential and constitutes, maybe, the main trigger of this process, generating endocrine signal wich strongly ativates mitogenesis in the hepatocytes primmed by EGF, IL-6, insulin, remainig matrix matriz and others, leading to DNA synthesis. EGF probably participates of initial events imediately after partial hepatectomy. Besides their actions upon the liver, FGF, VEGF and KGF propably play role in the tissue recovering processes.

Várias substâncias identificáveis estão implicadas no processo de crescimento hepático, entre elas os fatores de crescimento. A maioria deles possui diferentes ações, estimulando a proliferação de células, ou mesmo inibindo na dependência de suas concentrações. Dentre os fatores de crescimento, ou somatomedinas, com ação sobre o fígado pode-se destacar: HGF; EGF; TGF-alpha; TGF b ; Interleucina 6; IGF; FGF; VEGF; KGF; HSS e ALR. A ação conjunta dos hormônios HGF, TGF-alpha, IL-6, TNF-alpha, norepinefrina, EGF, permite que insulina, glucagon e o próprio EGF manifestem seus efeitos. O HGF tem papel vital, talvez o principal "gatilho" deste processo, gerando um sinal endócrino que ativa fortemente a mitogênese nos hepatócitos já "preparados" pelo EGF, IL-6, insulina, matriz remanescente e outros, levando à síntese de DNA. Admite-se que o EGF também participe dos eventos iniciais do processo logo após a hepatectomia e que FGF, VEGF e KGF também participem dos eventos ligados à recomposição de outros tecidos.

RESUMO

Regarding the cell proliferative process, hormones can show different actions when reach tissue receptors. HGF, TGF-alpha, IL-6, TNF-alpha, norepinefrin, EGF and insulin are known to be the main factors connected to liver growth. GH enhances DNA synthesis and gene expression of HGF as well as stimulates liver to produce growth factors. Thyroid hormones improve hepatocytes proliferative capacity. Insulin isnt a primary mitogenic but enhances regenerative stimulation started by epinephrine and norepinephrine. Norepinephrine amplifies mitogenic signals of EGF and HGF. Moreover induces EGF secretion and antagonizes inhibitory efects of TGF-beta 1. Glucagon doesnt produce effects alone but, probably participates of DNA synthesis and homeostasic process by wich glicemia is kept steady during regeneration. Finaly, there are clues that gastrin may promote hepatotrophic effects.

No complexo processo de proliferação celular, os hormônios agem de diferentes maneiras ao atingirem seus receptores nos tecidos-alvo. Os principais fatores ligados ao crescimento hepático são HGF, TGF-alpha, IL-6, TNF-alpha, norepinefrina, EGF e insulina. O GH estimula tanto o fígado a produzir fatores de crescimento, como a expressão genética do HGF e a síntese de DNA. Hormônios tireoideanos aumentam a capacidade proliferativa dos hepatócitos. A insulina age sinergicamente com GH e glucagon. Não tem potencial mitogênico primário mas intensifica o estímulo regenerativo iniciado pela epinefrina e norepinefrina. Esta amplifica os sinais mitogênicos do EGF e HGF, induz a secreção de EGF e antagoniza os efeitos inibitórios do TGF-beta 1. O glucagon isoladamente não produz efeitos mas provavelmente participa na síntese de DNA e da resposta homeostásica pela qual a glicemia é mantida estável durante a regeneração. Também há indícios de ação hepatotrófica da gastrina.