If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
Background: Cardiac sensory nerves that traverse anatomically defined sympathetic
pathways (“cardiac sympathetic afferents”) have been traditionally thought to convey
the sensation of pain during coronary ischemia. They also have been shown to mediate
sympatho-excitation. Previous studies from our laboratory have shown that the afferent
discharge and the reflex effects upon stimulation of these afferents with either bradykinin
or capsaicin evoke increased responses in the setting of chronic heart failure (CHF).
More recently, we demonstrated that cardiac sympathetic afferents also participate
in the cardiac remodeling process following a myocardial infarction (MI). Results:
Epicardial application of the ultra-potent capsaicin analog resiniferitoxin (RTX)
at the time of coronary ligation significantly reduced both cardiac and renal sympathetic
nerve activity as well as norepinephrine excretion 12 weeks after MI. Furthermore, several markers of the remodeling process were also abrogated
in RTX treated animals. This included collagen, fibronectin, and TGFβ receptor expression
in the remote left ventricular myocardium. RTX reduced tissue cytokine expression.
While cardiac systolic function was not improved there was a marked increase in diastolic
function as measured by pressure-volume loop analyses. Cardiac reserve (response to
isoproterenol) was also enhanced in the RTX treated group. Most importantly the 6 month survival curves were markedly enhanced for both epicardial and epidural application
of RTX. Conclusion: Cardiac sympathetic afferent ablation may have important therapeutic
benefits in the setting of CHF.
To read this article in full you will need to make a payment