Volume expansion fails to normally activate neural pathways in the brain of conscious rabbits with heart failure

Akama, Hiroyoshi; McGrath, Barry P; Badoer, Emilio

doi:10.1016/s0165-1838(98)00124-6

Cited by 13 publications

(11 citation statements)

References 24 publications

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“…An explanation for a generalized desensitization is that it is due mainly to the reduced sensitivity of atrial vagal afferents, which were shown to become less sensitive in dogs with chronic high-output HF (40). Further evidence that the afferent pathway responding to volume is abnormal in HF was the lack of activation of neural pathways in the brain that were normally activated by volume expansion (2).…”

Section: Discussionmentioning

confidence: 99%

Responses of cardiac sympathetic nerve activity to changes in circulating volume differ in normal and heart failure sheep

Ramchandra

Hood

Watson

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Factors controlling cardiac sympathetic nerve activity (CSNA) in the normal state and those causing the large increase in activity in heart failure (HF) remain unclear. We hypothesized from previous clinical findings that activation of cardiac mechanoreceptors by the increased blood volume in HF may stimulate sympathetic nerve activity (SNA), particularly to the heart via cardiocardiac reflexes. To investigate the effect of volume expansion and depletion on CSNA we have made multiunit recordings of CSNA in conscious normal sheep and sheep paced into HF. In HF sheep (n = 9) compared with normal sheep (n = 9), resting levels of CSNA were significantly higher (34 +/- 5 vs. 93 +/- 2 bursts/100 heart beats, P < 0.05), mean arterial pressure was lower (76 +/- 3 vs. 87 +/- 2 mmHg; P < 0.05), and central venous pressure (CVP) was greater (3.0 +/- 1.0 vs. 0.0 +/- 1.0 mmHg; P < 0.05). In normal sheep (n = 6), hemorrhage (400 ml over 30 min) was associated with a significant increase in CSNA (179 +/- 16%) with a decrease in CVP (2.7 +/- 0.7 mmHg). Volume expansion (400 ml Gelofusine over 30 min) significantly decreased CSNA (35 +/- 12%) and increased CVP (4.7 +/- 1.0 mmHg). In HF sheep (n = 6) the responses of CSNA to both volume expansion and hemorrhage were severely blunted with no significant changes in CSNA or heart rate with either stimulus. In summary, these studies in a large conscious mammal demonstrate that in the normal state directly recorded CSNA increased with volume depletion and decreased with volume loading. In contrast, both of these responses were severely blunted in HF with no significant changes in CSNA during either hemorrhage or volume expansion.

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Section: Discussionmentioning

confidence: 99%

Responses of cardiac sympathetic nerve activity to changes in circulating volume differ in normal and heart failure sheep

Ramchandra

Hood

Watson

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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show abstract

“…One possibility is a cardiac sympathoexcitatory reflex driven by raised cardiac filling pressures 52 . Although it is established that this reflex is desensitized in HF, 41,50,53 there is clinical evidence that an excitatory cardiac reflex responding to increased volume may contribute tonically to the raised CSNA in this condition. In support of this, among patients with HF there is a positive correlation between cardiac NA spillover and their pulmonary artery and pulmonary wedge pressures 37 .…”

Section: Mechanisms Of Sympathetic Overactivity In Hfmentioning

confidence: 99%

Mechanisms of Sympathetic Activation in Heart Failure

Watson

Hood

May

2006

Clin Exp Pharma Physio

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1. Heart Failure (HF) is a serious, debilitating condition with poor survival rates and an increasing level of prevalence. A characteristic of HF is a compensatory neurohumoral activation that increases with the severity of the condition. 2. The increase in sympathetic activity may be beneficial initially, providing inotropic support to the heart and peripheral vasoconstriction, but in the longer term it promotes disease progression and worsens prognosis. This is particularly true for the increase in cardiac sympathetic nerve activity, as shown by the strong inverse correlation between cardiac noradrenaline spillover and prognosis and by the beneficial effect of beta-adrenoceptor antagonists. 3. Possible causes for the raised level of sympathetic activity in HF include altered neural reflexes, such as those from baroreceptors and chemoreceptors, raised levels of hormones, such as angiotensin II, acting on circumventricular organs, and changes in central mechanisms that may amplify the responses to these inputs. 4. The control of sympathetic activity to different organs is regionally heterogeneous, as demonstrated by a lack of concordance in burst patterns, different responses to reflexes, opposite responses of cardiac and renal sympathetic nerves to central angiotensin and organ-specific increases in sympathetic activity in HF. These observations indicate that, in HF, it is essential to study the factors causing sympathetic activation in individual outflows, in particular those that powerfully, and perhaps preferentially, increase cardiac sympathetic nerve activity.

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“…We have recently used the technique of immunohistochemical detection of Fos to determine the distribution of neurons activated following disturbances in body fluid balance 11–15 . We have also combined this technique with neuroanatomical tract tracing techniques to examine specific neuronal cell groups within the PVN to gain an insight into the potential functional role of those cell groups in the responses elicited by perturbations in body fluid homeostasis.…”

Section: Functional Studies Of Neuronal Groups Within the Pvnmentioning

confidence: 99%

Proceedings of the Australian Physiological and Pharmacological Society Symposium: The Hypothalamus HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND CARDIOVASCULAR REGULATION

Badoer

2001

Clin Exp Pharma Physio

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192

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1. The hypothalamic paraventricular nucleus (PVN) is an important integrative site within the brain composed of magnocellular and parvocellular neurons. It is known to influence sympathetic nerve activity. 2. The parvocellular PVN contains neurons that project to the intermediolateral cell column of the thoraco-lumbar spinal cord (IML). This defines the PVN as an autonomic 'premotor nucleus', one of only five present within the brain. 3. Another projection arising from the PVN is a prominent innervation of the pressor region of the rostral ventrolateral medulla (RVLM), also a premotor nucleus. The distribution of the PVN neurons projecting to the RVLM is similar to that of the PVN neurons that project to the IML. 4. It has been found that up to 30% of spinally projecting neurons in the PVN also send collaterals to the RVLM. Thus, there are neurons in the PVN that can: (i) directly influence sympathetic nerve activity (via PVN-IML connections); (ii) indirectly influence sympathetic nerve activity (via PVN-RVLM connections); and (iii) both directly and indirectly influence sympathetic nerve activity (via neurons with collaterals to the IML and RVLM). 5. In the rat, results of studies using the protein Fos to identify activated neurons in the brain suggest that neurons in the PVN with projections to the IML or RVLM may be activated by decreases in blood volume. 6. In conclusion, the PVN can influence sympathetic nerve activity. Within the PVN are neurons with anatomical connections that enable them to affect sympathetic nerve activity either directly, indirectly or via both mechanisms (via collaterals). Studies that have examined the role of specific subgroups within the PVN suggest that PVN neurons with connections to the IML or to the RVLM may play a role in the reflex changes in sympathetic nerve activity that are involved in blood volume regulation.

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Volume expansion fails to normally activate neural pathways in the brain of conscious rabbits with heart failure

Cited by 13 publications

References 24 publications

Responses of cardiac sympathetic nerve activity to changes in circulating volume differ in normal and heart failure sheep

Responses of cardiac sympathetic nerve activity to changes in circulating volume differ in normal and heart failure sheep

Mechanisms of Sympathetic Activation in Heart Failure

Proceedings of the Australian Physiological and Pharmacological Society Symposium: The Hypothalamus HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND CARDIOVASCULAR REGULATION

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