Ca2+ signaling: Many enzymes in metabolism and signaling pathways are
responsive to Ca2+ concentrations. Calcium is sequestered within tissues
(e.g., within cisternae in the sarcoplasmic reticulum of muscle) and
released on signal increasing the Ca2+ concentration in the cytosolic
compartment and eliciting Ca2+-induced responses. Increased calcium
concentration stimulates the activity of muscle phosphorylase kinase
and activates pyruvate dehydrogenase phosphatase to increase the meta-
bolic flow of glucose to CO2 and H2O.
Ca2+ channel: A transport system allowing passage of the charged calcium
ion through a hydrophobic membrane.
Hyperthermia is a rare complication of anesthesia that is not completely
understood. Most of the evidence points to the ryanodine receptor (chromo-
some 19q13.1) as the defective gene product. This receptor is the Ca2+
release channel of muscle sarcoplasmic reticulum. Stimulation of this chan-
nel leads to excessive Ca2+ release from the cisternae of the sarcoplasmic
reticulum, and that Ca2+ prompts muscle contraction, an increase in body
temperature, tachycardia, and subsequent metabolic acidosis.
The scheme in Figure 18-1 summarizes the effects of Ca2+ release on
processes that bring about the complex of symptoms seen in malignant
Activation o f phosphorylasc kinase and glycogen breakdown
Increased actin/myosin-bascd muscle contraction
Increased utilization o f ATP
Increased glycolysis, TCA cycle, and ATP formation
Activation of uncoupling proteins by fatty acids mobilized
from storage depots
Figure 18-1. Direct and indirect effects of Ca2+ release in aberrant response to
anesthetics halothane and succinylcholine.
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