Cardiac responses elicited by stimulation of loci within stellate ganglia of developing swine

Gootman, Phyllis M.; Gandhi, M.; Coren, Charles; Kaplan, Norman M.; Pisana, Frances M.; Buckley, Barbara; Armour, J. Andrew; Gootman, Norman

doi:10.1016/0165-1838(92)90030-k

Cited by 22 publications

(20 citation statements)

References 7 publications

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“…This is consistent with the finding from Yu & Lumbers (2002) that baroreceptor‐mediated changes in heart rate variability in the sheep also mature in late gestation and early neonatal life, and that vagal activity matures earlier than cardiac sympathetic activity. Further supporting the continuing maturation of the SNA around birth, in neonatal piglets the capacity of stellate ganglion neurons to modulate heart rate and inotropic responses increases during the first 4 weeks of postnatal life (Gootman et al 1992). This increase appeared to be related to increasing innervation of the stellate ganglion with the cardiac SNS.…”

Section: Discussionmentioning

confidence: 90%

Maturation-related changes in the pattern of renal sympathetic nerve activity from fetal life to adulthood

Booth

Bennet

Guild

et al. 2010

Experimental Physiology

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Sympathetic nerve activity (SNA) has two main properties, the presence of co-ordinated bursts of activity, indicative of many nerve fibres firing at a similar time, and entrainment of the bursts to the cardiac cycle, due to inhibitory input from baroreceptors to a network of cell groups within the CNS. Although this patterning is used as a 'gold standard' for the identification of successful nerve recordings, the maturation of these basic features of SNA from fetal life to adulthood has not been investigated. Using a telemetry-based nerve amplifier, renal SNA (RSNA) was recorded in preterm (99 ± 1 days gestation; term 147 days) and near-term fetal sheep (119 ± 0 days gestation), without anaesthesia or paralysis, and contrasted with RSNA recorded in adult sheep. All three age groups showed a classic bursting pattern of RSNA and co-ordination of bursts with the cardiac cycle. However, the delay between diastole and the next peak in RSNA was longest in preterm fetuses (319 ± 1 ms), compared with near-term fetuses (250 ± 13 ms), and shortest in the adult sheep (174 ± 38 ms). This was independent of the maturational decrease in heart rate. The near-term fetuses showed a marked but sleep-statedependent increase in resting RSNA compared with preterm fetuses. Although entrainment with the pressure pulse suggests that the intricate circuitry within the CNS is developed in the preterm fetus, the decrease in the length of the delay suggests continuing maturation of this key feature of RSNA in the last third of gestation and after birth. The sympathetic nervous system (SNS) plays a vital role in cardiovascular, metabolic and thermoregulatory homeostasis. Direct recording of sympathetic nerve activity (SNA) allows continuous assessment of changes in the SNS in response to various stimuli. Since the early recordings of SNA, a number of distinct features have been identified. Firstly, SNA has a co-ordinated bursting pattern as a result of synchronized firing of many individual neurons at approximately the same time and secondly, the bursts of nerve activity display a number of rhythmicities, in particular, synchronization with the heart rate (Adrian & Bronk, 1932;Bronk et al. 1936;Malpas, 1998Malpas, , 2010.Previous studies have quantified this cardiac-related rhythm as the delay between diastole and the following peak in SNA, reporting delays of 164 ± 7 ms in adult cats (cardiac SNA;Hedman et al. 1994) and 105 ± 7 ms in renal SNA (RSNA) in adult rabbits (Barrett et al. 2003). The presence of entrainment of RSNA to the cardiac cycle is indicative of the delicate control of efferent nerve activity and is often regarded as a 'gold standard' for the identification of successful nerve recordings. Indeed, in early descriptions of RSNA in near-term fetal sheep, the activity was described as being pulse synchronous; however, this relationship was not quantified (Smith et al. 1990;Segar et al. 1998).We have recently shown that preterm fetal sheep have co-ordinated bursts of RSNA that are entrained to the cardiac cycle ). However, the ...

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Section: Discussionmentioning

confidence: 90%

Maturation-related changes in the pattern of renal sympathetic nerve activity from fetal life to adulthood

Booth

Bennet

Guild

et al. 2010

Experimental Physiology

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“…The voltage output from the Doppler equipment was directed through a custom-built electrical circuit, which steered the roller pump to maintain LAD flow at 30% of baseline values. In animals subjected to sympathetic stimulation, the left stellate ganglion was dissected, and an electrode was inserted into the ganglion, as described by Gootman et al, 24 and connected to a nerve stimulator (Grass S9; pulses of 12 V, 10 Hz, and 5 ms).…”

Section: Animal Proceduresmentioning

confidence: 99%

Exogenous Angiotensin II Does Not Facilitate Norepinephrine Release in the Heart

et al. 2002

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Abstract-Studies on the effect of angiotensin II on norepinephrine release from sympathetic nerve terminals through stimulation of presynaptic angiotensin II type 1 receptors are equivocal. Furthermore, evidence that angiotensin II activates the cardiac sympathetic nervous system in vivo is scarce or indirect. In the intact porcine heart, we investigated whether angiotensin II increases norepinephrine concentrations in the myocardial interstitial fluid (NE MIF ) under basal conditions and during sympathetic activation and whether it enhances exocytotic and nonexocytotic ischemia-induced norepinephrine release. In 27 anesthetized pigs, NE MIF was measured in the left ventricular myocardium using the microdialysis technique. Key Words: norepinephrine Ⅲ angiotensin II Ⅲ renin-angiotensin system Ⅲ sympathetic nervous system A ctivation of the sympathetic nervous system simultaneously leads to activation of the renin-angiotensin system via stimulation of ␤-adrenergic receptors within the kidney, resulting in an increased renin release. There is also evidence, albeit conflicting, that the sympathetic nervous system is activated by the renin-angiotensin system. 1-13 This activation supposedly occurs through stimulation of angiotensin II receptors within the central nervous system and/or stimulation of presynaptic angiotensin II receptors located at sympathetic nerve terminals. When investigating the sympathetic nervous system and its interaction with the renin-angiotensin system, the heart is of particular interest. First of all, the mammalian heart has a dense sympathetic innervation. Second, all components of the renin-angiotensin system are present in the heart, and most angiotensin II in the heart is formed from locally synthesized angiotensin I. 14 Third, in conditions like hypertension, ischemia, and especially heart failure, the renin-angiotensin system and sympathetic nervous system are both activated, and this activation likely contributes to the deterioration of cardiac function. [15][16][17] Evidence that angiotensin II activates the cardiac sympathetic nervous system in vivo is scarce 4 or indirect. 7,18 In a recent study, Teisman et al 4 have shown with the use of the microdialysis technique that "pharmacological" (10 Ϫ6 mol/L) concentrations of locally applied angiotensin II were associated with an increase in norepinephrine concentrations in the myocardial interstitial fluid (NE MIF ) of the in vivo rat heart. In the present study, we determined whether "physiological" (10 Ϫ10 mol/L) to "pathophysiological" (10 Ϫ8 mol/L) concentrations of angiotensin II modulate NE MIF in the intact porcine heart. The pig is especially suitable as a model for studying the cardiac sympathetic nervous system because, unlike the rat, the prevailing parasympathetic control of cardiac function is very similar to that in man, which allows for a more reliable extrapolation of the experimental results to the reality of human patients.To exclude a masking effect of neuronal norepinephrine reuptake and negative feedback through pr...

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“…; Gootman et al. ). Instead, it could be due to increased levels of circulating catecholamines, or withdrawal of cardiac vagal tone as this pathway is mature prior to term (Lumbers et al.…”

Section: Discussionmentioning

confidence: 97%

“…; Gootman et al. ; Yu and Lumbers ), and thus these sympathetically mediated actions of Ang II could account for the positive correlation between blood pressure and Ang II levels and the negative correlation between skin blood flow and Ang II levels seen in term piglets only.…”

Section: Discussionmentioning

confidence: 98%

“…; Gootman et al. ; Yu and Lumbers ), the only vasoconstrictor action of Ang II would be a direct effect via the angiotensin type 1 receptor (AT 1 R), and even in the adult human this direct vasoconstrictor action of Ang II is weak (Scroop and Whelan ). But Ang II can also act via angiotensin type 2 receptors (AT 2 R) and have a vasodilator effect.…”

Section: Discussionmentioning

confidence: 99%

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Endogenous angiotensins and catecholamines do not reduce skin blood flow or prevent hypotension in preterm piglets

et al. 2014

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Endocrine control of cardiovascular function is probably immature in the preterm infant; thus, it may contribute to the relative ineffectiveness of current adrenergic treatments for preterm cardiovascular compromise. This study aimed to determine the cardiovascular and hormonal responses to stress in the preterm piglet. Piglets were delivered by cesarean section either preterm (97 of 115 days) or at term (113 days). An additional group of preterm piglets received maternal glucocorticoids as used clinically. Piglets were sedated and underwent hypoxia (4% FiO2 for 20 min) to stimulate a cardiovascular response. Arterial blood pressure, skin blood flow, heart rate and plasma levels of epinephrine, norepinephrine, angiotensin II (Ang II), angiotensin‐(1–7) (Ang‐(1‐7)), and cortisol were measured. Term piglets responded to hypoxia with vasoconstriction; preterm piglets had a lesser response. Preterm piglets had lower blood pressures throughout, with a delayed blood pressure response to the hypoxic stress compared with term piglets. This immature response occurred despite similar high levels of circulating catecholamines, and higher levels of Ang II compared with term animals. Prenatal exposure to glucocorticoids increased the ratio of Ang‐(1‐7):Ang II. Preterm piglets, in contrast to term piglets, had no increase in cortisol levels in response to hypoxia. Preterm piglets have immature physiological responses to a hypoxic stress but no deficit of circulating catecholamines. Reduced vasoconstriction in preterm piglets could result from vasodilator actions of Ang II. In glucocorticoid exposed preterm piglets, further inhibition of vasoconstriction may occur because of an increased conversion of Ang II to Ang‐(1‐7).

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Cardiac responses elicited by stimulation of loci within stellate ganglia of developing swine

Cited by 22 publications

References 7 publications

Maturation-related changes in the pattern of renal sympathetic nerve activity from fetal life to adulthood

Maturation-related changes in the pattern of renal sympathetic nerve activity from fetal life to adulthood

Exogenous Angiotensin II Does Not Facilitate Norepinephrine Release in the Heart

Endogenous angiotensins and catecholamines do not reduce skin blood flow or prevent hypotension in preterm piglets

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