Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale
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Temporal summation due to repeated pain stimulation of deep somatic structures is facilitated in chronic musculoskeletal pain. In this study, the relation between repeated pressure-induced pain and stress/strain distribution within the deep tissue was evaluated to understand whether tissue characteristics may change during repeated stimulation. This information is important for interpret the pain-evoked responses. ⋯ The peak principal strain in adipose tissue was 0.12; in muscle tissue, it was 0.108 during the first stimulus and increased by 16 % in the tenth stimulus. In a model of a one-stimulus paradigm, it was found that a VAS increase of 2.5 cm required a 47 % increase in muscle strain. These findings show that the increase in muscle strain during repeated pressure stimulations is not sufficient to explain the VAS increase; the temporal summation of deep-tissue pain evoked by repetitive pressure stimulations is not likely to be fully explained by peripheral tissue changes.
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Cerebral arteries subjected to different types of experimental stroke upregulate their expression of certain G-protein-coupled vasoconstrictor receptors, a phenomenon that worsens the ischemic brain damage. Upregulation of contractile endothelin B (ET(B)) and 5-hydroxytryptamine 1B (5-HT(1B)) receptors has been demonstrated after subarachnoid hemorrhage and global ischemic stroke, but the situation is less clear after focal ischemic stroke. Changes in smooth muscle calcium handling have been implicated in different vascular diseases but have not hitherto been investigated in cerebral arteries after stroke. ⋯ Expression and contractile functions of ET(B) and 5-HT(1B) receptors were strongly upregulated and slightly downregulated, respectively, 24 h after experimental stroke or organ culture. ET(B) receptor-mediated contraction was mediated by calcium from intracellular and extracellular sources, whereas 5-HT(1B) receptor-mediated contraction was solely dependent on extracellular calcium. Organ culture and stroke increased basal intracellular calcium levels in MCA smooth muscle cells and decreased the expression of inositol triphosphate receptor and transient receptor potential canonical calcium channels, but not voltage-operated calcium channels.