Rate-dependent changes in cell shortening, intracellular Ca(2+) levels and membrane potential in single, isolated rainbow trout (Oncorhynchus mykiss) ventricular myocytes.

The effects of increasing stimulation frequency (from 0.2 to 1.4 Hz) on the contractility, intracellular Ca(2+) concentration ([Ca(2+)](i)) and membrane potential of single ventricular myocytes isolated from the heart of rainbow trout (Oncorhynchus mykiss) were measured. Cell shortening, expressed as a percentage of resting cell length, was our index of contractility. The fluorescent Ca(2+) indicator Fura-2 was used to monitor changes in [Ca(2+)](i). Action potentials and L-type Ca(2+) currents (I(Ca)) were recorded using the whole-cell patch-clamp technique. Experiments were performed at 15 degrees C. Increasing the stimulation frequency caused a significant increase in diastolic [Ca(2+)](i) and a significant decrease in diastolic cell length and membrane potential. During systole, there was a significant fall in the amplitude of the [Ca(2+)](i) transient, cell shortening and action potential with a decrease in the duration of the action potential at both 20 % and 90 % repolarisation. Caffeine was used to assess the Ca(2+) content of the sarcoplasmic reticulum. We observed that sarcoplasmic reticulum Ca(2+) load was greater at 1.0 Hz than at 0.6 Hz, despite a smaller electrically evoked [Ca(2+)](i) transient. The amplitude of I(Ca) was found to decrease with increased stimulation frequency. At 0.6 Hz, electrically evoked [Ca(2+)](i) transients in the presence of 10 mmol l(-)(1) caffeine or 10 micromol l(-)(1) ryanodine and 2 micromol l(-)(1) thapsigargin were reduced by approximately 15 %. We have described the changes in contractility, [Ca(2+)](i) and action potential configuration in a fish cardiac muscle system. Under the conditions tested (0.6 Hz, 15 degrees C), we conclude that the sarcoplasmic reticulum contributes at least 15 % of the Ca(2+) associated with the [Ca(2+)](i) transient. The rate-dependent decrease in contraction amplitude appears to be associated with the fall in the amplitude of the [Ca(2+)](i) transient. This, in turn, may be influenced by changes in the action potential configuration via mechanisms such as altered Ca(2+) efflux and Ca(2+) influx. In support of our conclusions, we present evidence that there is a rate-dependent decrease in Ca(2+) influx via I(Ca) but that the Ca(2+) load of the sarcoplasmic reticulum is not reduced at increased contraction frequencies.

The effect of Trichinella spiralis infection on the mechanical properties of the mammalian diaphragm.

Trichinella spiralis larvae infect and develop within skeletal muscle cells causing major changes to their mechanical properties. The aim of this investigation was to determine the effects of T. spiralis on the power output and fatigue resistance of the mammalian diaphragm under conditions simulating in vivo operation and to relate these to respiratory performance. Infection with T. spiralis leads to major reductions in mechanical stress, work, power output and fatigue resistance. These changes are associated with the number of larvae present in the muscle and the duration of infection. However, the initial decline in mechanical performance occurs during the onset of infection when there are few larvae observed within the muscle cells, indicating that T. spiralis may affect the properties of muscle before encapsulation. This may correspond to the host's inflammatory response and the effects of larval excretory/secretory products. The decline in mechanical performance will have a profound effect on respiration both at rest and during exertion. This must influence the behaviour of the host and increase its chance of capture by predators, which is likely to benefit the parasite by facilitating its transmission.