Sympathetic Nervous System
Activation of the sympathetic nervous system occurs early during
MH. Fight, fright, or flight can initiate an MH episode in susceptible swine without
anesthetic agents.[9]
This is rarely observed in
humans (see "Awake Triggering: Exercise and Heat Stroke"). During MH, circulating
levels of epinephrine and norepinephrine increase markedly (e.g., from less than
1 ng/mL to 30 ng/mL). Sympathetic responses appear to be secondary in porcine MH,
although the physiologic effects of sympathetic excitation can magnify the changes
of an MH episode. For example, metabolic responses precede altered sympathetic activity
[46]
; the MH response is unaltered despite acute
sympathetic denervation (total spinal anesthesia)[69]
;
infusion of norepinephrine to blood levels greater than those associated with MH
does not trigger MH[70]
[71]
;
and norepinephrine does not potentiate halothane-induced porcine MH, although triggering
is delayed when blood flow to muscle is reduced.[71]
β-Agonist effects result in pronounced myocardial stimulation.[62]
Administration of α-agonists and β-agonists does not result in increased
metabolism in susceptible porcine muscle.[70]
[72]
Sympathetic antagonists may protect from or ameliorate episodes
of MH by lowering body temperature and modifying acid-base changes.[73]
The β-antagonists appear to increase heat loss and potentially increase muscle
perfusion. β-Antagonists attenuate metabolism and fever during MH but do not
improve survival.[73]
They block myocardial stimulation
of porcine MH, but this stimulation is secondary to β-agonist effects without
evidence for myocardial MH.[62]
There is no direct
evidence that the sympathetic nervous system initiates MH.[46]
