Isoproterenol-induced myocardial necrosis triggers a transient accumulation of the stress protein SP71 in rat tissues, suggesting a cellular response to stress and tissue repair.
Does not inform clinical practice; leaves open SP71's role in human cardiac stress responses.
Large doses of isoproterenol, which produced macroscopically visible myocardial necrosis, induced the synthesis and accumulation of a 71,000 dalton protein (SP71) in the heart, aorta, and salivary gland of adult male rats. This protein was identical to a protein that has previously been found to be synthesised in the heart in response to heat shock and tissue slicing. Detectable amounts of SP71 were no longer seen five days after the isoproterenol injection, suggesting that this protein accumulates as part of a cellular response to stress and then degrades during tissue repair.
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White et al. (1986) studied this question.
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