Abstract
Several years ago, we observed the stress induced malignant hyperthermia (MH) syndrome in our malignant hyperthermia susceptible (MHS) pigs after transport. We were astounded by the cardiac palpitations that were readily apparent in the arterial supply to the ears and the carotid or jugular throbbing visible in the neck region whenever spontaneous MH developed. In white MHS pigs, we could observe the cyanotic appearance of the ears, nose, and skin. It became apparent from our calorimeter studies that an intense peripheral vasoconstriction was the lethal part of the acute MH syndrome.1—4 Our previous studies further documented the acute hemodynamic shutdown that produced cardiovascular collapse in inbred MH pigs.1,2 We have pursued the hemodynamic studies in order to document further the hemodynamic response to developing MH in a larger population of MHS pigs of both inbred and outcross breeding patterns.
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