Abstract

ObjectiveTo investigate the effects of localized cooling and cooling rate on pressure-induced ischemia for people with and without neurological deficits.DesignA 2 × 3 mixed factorial design with two groups: (1) people with spinal cord injury (SCI) and (2) people without neurological deficits (control), and three test conditions: (1) pressure only, (2) pressure with fast cooling (−4°C/min), and (3) pressure with slow cooling (−0.33°C/min).SettingUniversity laboratory.ParticipantsFourteen controls and 14 individuals with SCI.InterventionsPressure on the sacrum was 0.4 kPa for 5 minutes, then 8 kPa for 20 minutes, and finally 0.4 kPa for 15 minutes. Fast and slow cooling to 25°C applied during 8 kPa of pressure.Outcome measuresReactive hyperemia and its spectral densities in the metabolic, neurogenic, and myogenic frequency ranges.ResultsIn controls, reactive hyperemia was greater in pressure only as compared with both cooling conditions. No change was noted in all spectral densities in both cooling conditions, and only neurogenic spectral density increased without cooling. In subjects with SCI, no difference was noted in reactive hyperemia among conditions. However, metabolic and myogenic spectral densities increased without cooling and all spectral densities increased with slow cooling. No change was noted in all spectral densities with fast cooling.ConclusionLocal cooling reduced the severity of ischemia in controls. This protective effect may be masked in subjects with SCI due to chronic microvascular changes; however, spectral analysis suggested local cooling may reduce metabolic vasodilation. These findings provide evidence towards the development of support surfaces with temperature control for weight-bearing soft tissues.

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