2005 mice study adds more evidence that a myocarditis scarred heart (as in 'silent' myocarditis) due to the COVID gene injection vaccine may be strained & devastated by epinephrine (adrenaline)
by Paul Alexander
This study supports our argument (McCullough, Stock, I etc.) that we are looking at vaccine-induced myocardium scarring strained via exertional induced catecholamines e.g. epinephrine on damaged heart
A single dose of epinephrine 120 days after EMCV inoculation caused sudden death in 70% of infected mice; propranolol significantly reduced incidence of death to 33%.
Our argument on ‘DYING AT DAWN IN YOUR SLEEP’ and ‘DIED SUDDENLY’ is given support by this rodent study.
‘Researchers investigated the impact of the ‘β-adrenergic system on cytokines and neurohumoral factors and the sequelae of viral myocarditis. In an experimental model with virus-infected BALB/c mice, we studied the acute and chronic effects of epinephrine and propranolol on myocardial morphology, cytokine gene expression, and survival.
Mice were inoculated with the encephalomyocarditis virus (EMCV) or sham inoculated with saline and followed for 30 days.
Epinephrine increased the severity of inflammatory cell infiltration and myocardial necrosis induced by EMCV. Gene expression of TNF-α, IL-6, and IL-10 was markedly enhanced by epinephrine in EMCV-inoculated mice. Survival rate after 30 days was reduced to 40% in epinephrine-treated EMCV-inoculated mice compared with 70% in untreated EMCV-inoculated mice (P < 0.05).
Treatment with the β-blocker propranolol significantly decreased mortality, myocardial necrosis, and infiltration of inflammatory cells in EMCV-inoculated mice. Propranolol also suppressed gene expression of TNF-α, IL-6, and IL-10.
A single dose of epinephrine 120 days after EMCV inoculation caused sudden death in 70% of infected mice; propranolol significantly reduced incidence of death to 33%. These results indicate that acute and chronic stages of viral myocarditis are modulated by the β-adrenergic system and its interactions with proinflammatory cytokines.’