We have previously shown that unsaturated phosphatidylserines inhibit mitogen‐induced T cell activation. We now report that the inhibitory action requires a protein present in bovine and human serum. Partial purification and phospholipase assay show that this protein has phospholipase A activity on phosphatidylserine but not phosphatidylethanolamine, phosphatidylcholine and phosphatidylinositol. In short incubations (1–3 h) 2‐acyl lysophosphatidylserine is produced but in longer incubations the cis‐unsaturated fatty acid is also released. Experiments on peripheral blood mononuclear cells indicate that the unsaturated fatty acid becomes the main responsible for the PS‐induced inhibition and that 2‐acyl lysophosphatidylserine enhances the inhibitory effect of fatty acid.
To further investigate the role of somatic nociceptive afferents in the neural control of breathing, we studied the respiratory effects of their activation by means of either electrical stimulation or ischemic pain in 14 healthy volunteers. Painful electrical cutaneous stimulation increased respiratory frequency (f), mean inspiratory flow (VT/TI), and rate of rise (XP/TI) of integrated electromyographic activity of diaphragm (IEMGdi). Painful muscular electrical stimulation caused similar but larger changes accompanied by increases in tidal volume (VT), peak XP of IEMGdi, and ventilation (VE); it also entrained respiratory rhythm. Ischemic pain, which was characterized by a progressively increasing intensity, caused augmentation in respiratory activity that displayed an increasing trend: VE, f, VT, XP, VT/TI, and XP/TI increased. In the light of available literature, it seems conceivable to suggest that respiratory responses to painful electrical stimulation are mediated through the activation of cutaneous (A delta) and muscular (group III) fine-myelinated afferents, and responses to ischemic pain are mediated by the activation of both fine myelinated (group III) and unmyelinated (group IV) muscular afferents. The input conveyed by these afferents may constitute an effective stimulus to respiration in humans.
The effects of vibratory stimulation on muscular pain threshold were investigated in 28 healthy subjects. Pain sensation was evaluated by the subjects' verbal reports in response to electrical stimulation of the vastus medialis muscle. Concomitant variations of blink response evoked as a component of the startle reaction were also studied. In all the subjects tested, high frequency vibration (110 Hz) induced a marked and long lasting elevation of the muscular pain threshold but only when vibration was applied to the skin overlying the ipsilateral quadriceps tendon or neighbouring areas and not when applied to remote ipsi- or contralateral regions. This effect was prevented either when tonic vibration reflex (TVR) of the quadriceps muscle was elicited or the skin underlying the vibrator was anaesthetized. Vibratory stimulation at low frequency (30 Hz) failed to produce any consistent effect on muscular pain threshold. Variations in threshold for blink response, as a rule, closely followed those of muscular pain threshold. However, a facilitation of the blink response, not accompanied by changes in pain sensation, was observed during the first period of both high and low frequency vibratory stimulation. The effectiveness of high frequency vibration in raising the muscular pain threshold is coherent with previous results showing that vibration is able to affect pain sensation. Present results suggest a role for rapidly adapting receptors (RA) and/or pacinian corpuscles (PC) in this effect and support the hypothesis of an inhibition of nociceptive messages, possibly at spinal segmental levels, by volleys in large myelinated afferent fibres.
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