Abstract
Enhanced carotid body (CB) chemoreflex function is strongly related to cardiorespiratory disorders and disease progression in heart failure (HF). The mechanisms underlying CB sensitization during HF are not fully understood, however previous work indicates blood flow per se can affect CB function. Then, we hypothesized that the CB-mediated chemoreflex drive will be enhanced only in low output HF but not in high output HF. Myocardial infarcted rats and aorto-caval fistulated rats were used as a low output HF model (MI-CHF) and as a high output HF model (AV-CHF), respectively. Blood flow supply to the CB region was decreased only in MI-CHF rats compared to Sham and AV-CHF rats. MI-CHF rats exhibited a significantly enhanced hypoxic ventilatory response compared to AV-CHF rats. However, apnea/hypopnea incidence was similarly increased in both MI-CHF and AV-CHF rats compared to control. Kruppel-like factor 2 expression, a flow sensitive transcription factor, was reduced in the CBs of MI-CHF rats but not in AV-CHF rats. Our results indicate that in the setting of HF, potentiation of the CB chemoreflex is strongly associated with a reduction in cardiac output and may not be related to other pathophysiological consequences of HF.
Highlights
Heart failure (HF) is a global public health problem
Echocardiography measurements show that the left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were significantly reduced in MI-CHF rats vs. Sham
Left ventricular end systolic volume (LVESV) and left ventricular end diastolic volume (LVEDV) were significantly increased in MI and AV-CHF rats compared to Sham animals showing clear signs of ventricular dilatation
Summary
Heart failure (HF) is a global public health problem. Currently, it is estimated that 26 million people worldwide are living with this condition, affecting approximately 20% of the world population over 75 years of age, and resulting in more than 1 million hospitalizations annually in both the United States and Europe[1, 2]. Ding and colleagues (2011) showed for the first time that control rabbits subjected to chronic carotid artery occlusion using pneumatic cuff occluders resulted in chemoreflex activation and autonomic imbalance that was similar to that observed in HF animals[11]. Et al.[20] showed that in myocardial infarcted HF rats, CB KLF2 expression was significantly lower than in sham animals[20] This reduction in KLF2 may be mediated by the reduction of blood flow to the CB during low output heart failure (myocardial infarction-CHF [MI-CHF]). Together, these results strongly suggest that potentiation of the CB-mediated chemoreflex function may be related to changes in cardiac output. We aimed to determine whether alterations in cardiac output, in the setting of HF, induced CB chemoreflex potentiation and cardiac autonomic imbalance and if these alterations are associated with changes in KLF2 expression
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