Evaluating the response of mild hypertensives to biofeedback-assisted relaxation using a mental stress test.

The objective of this study was to evaluate the long term effect of a program of biofeedback-assisted relaxation on hypertensive patients by mental stress test reactivity. Twenty mild hypertensive patients were subjected to a mental arithmetic stress test before and six months after completing biofeedback-assisted relaxation therapy. The therapy consisted of 10 sessions of biofeedback-assisted relaxation instruction and continuous home practise. The study group was compared to a control group. The biofeedback-assisted relaxation treatment produced a mild improvement in blood pressure control and decreased the dose of drugs used as well as a decrease in state-anxiety (p < 0.05). The stress-induced increases in systolic blood pressure, diastolic blood pressure, heart rate, galvanic skin response and skin temperature were all significantly attenuated six months after completion of biofeedback-assisted relaxation treatment.

Exposure to hyperbaric oxygen induces tumour necrosis factor-alpha (TNF-alpha) secretion from rat macrophages.

We investigated the secretion of TNF-alpha by monocytes and macrophages derived from the peripheral blood, spleen, and lungs after a single exposure to a therapeutic profile of hyperbaric oxygen (HBO). Rats were exposed for 90 min to either 100% oxygen at 0.28 MPa (2.8 atmospheres absolute) or air. Immediately after exposure, mononuclear cells were isolated from blood, spleen, and lungs and cultured for 18 h. The secretion of TNF-alpha from the cultured monocytes/macrophages was determined with and without stimulation with lipopolysaccharide (LPS). Exposure to hyperbaric oxygen induced a significant increase in the spontaneous ex vivo secretion of TNF-alpha (without LPS) by mononuclear cells from the blood, spleen, and lung (P < 0.05 from air controls). Stimulation with LPS after exposure to HBO induced a significant increase in TNF-alpha secretion by lung and spleen macrophages compared with air controls (P < 0.05). However, absolute TNF-alpha levels were not significantly higher than those achieved 'spontaneously' in macrophages exposed to HBO without LPS. Stimulation with LPS induced a marked increase in secretion of TNF-alpha from blood monocytes after exposure to air, but not after exposure to HBO. These results provide evidence in support of a role played by TNF-alpha in mediating HBO effects on different tissues and their immune responses.

Middle ear muscle activity during vocalization in normal speakers and stutterers.

Although it has been established that the middle ear muscles contract prior to vocalization, it is not known which muscle is mainly responsible for this activity. Also, there have been contradictory reports about whether this activity in stutterers differs from that of normal speakers. To tackle these questions, extratympanic pressure measurements prior to vocalization are reported for normal speakers and stutterers. This measure allows activity deriving from the two middle ear muscles to be differentiated and for the temporal course to be followed more accurately than by impedance measurement. To establish which muscle is primarily responsible for the pre-vocalization activity, the measured pressure changes prior to vocalization are compared with activity measured in tasks known to involve the stapedius or tensor tympani alone. These data show that in normal speakers and stutterers, the activity that is measured prior to vocalization resembles that of the tensor tympani. Contrary to other reports, there is no difference between normal speakers and stutterers in the time course of this activity.