The frequency of gastric slow waves is dependent on metabolic activity, whereas temperature-dependent changes in other parameters are largely driven by non-metabolic mechanisms.
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Hypothesis-generating for metabolic control of gastric slow waves; leaves open human relevance pending further study.
The effects of changes in temperature on slow waves were investigated in smooth muscle tissues isolated from the guinea-pig gastric antrum. Within the range 24 degrees C to 42 degrees C, elevation of temperature increased the frequency and maximum rate of rise of the upstroke phase (dV/dt) of slow waves and decreased their duration, with no alteration to amplitude or resting membrane potential. These observations also applied to follower potentials and pacemaker potentials recorded from longitudinal muscle and myenteric interstitial cells, respectively. Slow waves were comprised of 1st and 2nd components, and the latency for generating the 2nd component was decreased exponentially by elevating temperature, reaching a stable value of about 1 s above 32 degrees C. The temperature coefficient was >2 for the frequency, dV/dt and latency of the 2nd component, about 1.7 for the duration and about 1 for amplitude. Potassium cyanide (KCN), an inhibitor of mitochondrial metabolic activity, reduced the frequency and duration of slow waves, with no alteration to other parameters (amplitude, dV/dt, latency). In the presence of 30 microM KCN, the temperature-dependency of the frequency of slow waves was diminished or abolished, while other parameters of slow waves remained unaltered. These results indicate that in slow waves the frequency may be related to metabolic activities, while the temperature-dependent changes in the dV/dt, latency for the 2nd component and duration of slow waves are produced largely by mechanisms other than metabolic activity.
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Nakamura et al. (2006) studied this question.
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