Reflex Inhibition of Renal Sympathetic Nerve Activity during Myocardial Ischemia Mediated by Left Ventricular Receptors with Vagal Afferents in Dogs

Thames, Marc D.; Abboud, François M.

doi:10.1172/jci109315

Cited by 79 publications

(38 citation statements)

References 28 publications

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“…For example, we found no significant lateral zone of salvage when infarct size was reduced by coronary reperfusion. Under these circumstances infarcts are reduced by becoming subendocardial; however, some pharmacologic agents reduce infarct size along both the subepicardial and lateral edges of necrosis.31' 4 Our results suggest that CEI is a potent agent that limits infarct size after 6 hours of experimental coronary occlusion. Whether CEI reduces infarct size in animals with coronary artery occlusions of longer duration is not known.…”

Section: Area-at-risk Techniquementioning

confidence: 72%

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Limitation of experimental infarct size by an angiotensin-converting enzyme inhibitor.

Ertl¹,

Kloner²,

Alexander³

et al. 1982

Circulation

292

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SUMMARY The effects of angiotensin-converting enzyme inhibitor (CEI) SQ14225 on infarct size and regional myocardial blood flow were studied in 21 anesthetized dogs subjected to 6 hours of coronary occlusion. An area of myocardium at risk of necrosis was determined in vivo after 15 minutes of coronary occlusion but before CEI treatment (AR1) using an autoradiographic technique and after treatment after 6 hours of coronary occlusion (AR2) using a fluorescent dye technique. An MYOCARDIAL ISCHEMIA and, ultimately, infarction result from an imbalance between oxygen supply and oxygen demand. Coronary occlusion may induce hypotension, which results in baroreceptor activation and then systemic reflex vasoconstriction. -3 Systemic vasoconstriction may worsen the imbalance between myocardial oxygen supply and demand. Renal nerve activity,' a determinant of renin release,5 may be increased as well. Moreover, hypotension may activate intrarenal vascular pressoreceptors and may thus increase renin release directly.5 Because angiotensin II is a potent systemic and coronary vasoconstrictor, activation of the renin-angiotensin system may increase myocardial oxygen demand and decrease myocardial oxygen supply. Because interference with angiotensin II-production might exert a beneficial effect in myocardial ischemia and myocardial infarction, we studied the effects of the angiotensin-converting enzyme inhibitor (CEI) captopril (SQ14225) on infarct size after experimental coronary occlusion. To elucidate the mechanism of the salutary action of the drug, we also determined the effect of CEI on regional myocardial blood flow (RMBF) and measured plasma renin activity (PRA). Methods Twenty-one mongrel dogs of either sex weighing 16-28 kg that had been maintained on normal laboratory chow and had free access to water were anesthetized with i.v. thiamylal sodium (10 mg/kg), intubated and ventilated with room air using a Harvard respirator pump. Anesthesia was maintained by additional thiamylal sodium when needed. Lead aVF of the ECG was monitored. Saline was infused at a rate of 2 ml/min throughout the experiment to minimize hypovolemia and renin release. The chest was opened in the fifth left intercostal space and the heart was suspended in a pericardial cradle. The left anterior descending coronary artery was freed up approximately 2 cm from its origin just distal to the first major diagonal branch. Polyethylene catheters were placed in the femoral artery and vein and in the left atrial appendage. Arterial and left atrial pressures were measured by Statham P23Db pressure transducers.Infarct size after coronary occlusion depends on both the quantity of myocardium perfused by the occluded coronary vessel and the quantity of collateral flow to the jeopardized tissue.7'9 The variations in infarct size after coronary occlusion can be limited when these factors are taken into account by determining the area of myocardium at risk of developing necrosis and expressing infarct size as a percentage of the area at risk. In the present study, ...

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Section: Area-at-risk Techniquementioning

confidence: 72%

“…In group A, infarct size as a fraction of the area at risk was not significantly different 2.0 ± 0. 4 2.9 ± 0.7* Values are given in ng/ml/hour. *Higher than at 1 minute before occlusion (p < 0.025).…”

Section: Hemodynamic Datamentioning

confidence: 99%

Limitation of experimental infarct size by an angiotensin-converting enzyme inhibitor.

Ertl¹,

Kloner²,

Alexander³

et al. 1982

Circulation

292

View full text Add to dashboard Cite

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“…[3][4][5][6][12][13][14][15][16] These uniform findings of sympathetic activation directed to tissues governed by the baroreflexes have prompted the concept that impaired baroreflex restraint underlies sympathetic activation. It is unknown if increased sympathetic neural outflow in heart failure is limited to regions governed by the baroreflexes or is generalized to all tissues -a distinction with mechanistic implications.…”

Section: Methods and Resultsmentioning

confidence: 99%

Independent control of skin and muscle sympathetic nerve activity in patients with heart failure.

et al. 1994

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BACKGROUND Sympathetic excitation characterizes heart failure, but the underlying mechanisms remain unknown. Abnormal baroreflex restraint of sympathetic neural outflow has been proposed, since baroreflexes are known to be abnormal in heart failure. The purpose of this study was to determine if sympathetic activation in humans with heart failure is limited to regions governed by the baroreflexes or is generalized to other regions free from baroreflex control. METHODS AND RESULTS We report the first direct recordings of skin sympathetic nerve activity (free from baroreflex control) in humans with heart failure and compare simultaneous skin and muscle (baroreflex-dependent) sympathetic peroneal nerve activity in six patients with severe heart failure (mean left ventricular ejection fraction, 0.19 +/- 0.06) and in six age-matched normal control subjects. Although muscle sympathetic nerve activity was markedly increased in heart failure patients (heart failure versus controls, 69 +/- 3 versus 21 +/- 2 bursts per minute; P < .001), skin sympathetic nerve activity was not increased (heart failure versus controls, 12 +/- 1 versus 15 +/- 1 bursts per minute; P = NS). CONCLUSIONS The finding that skin sympathetic nerve activity in contrast to muscle sympathetic nerve activity is not increased in heart failure supports the concept that an altered reflex system, such as the baroreflexes, with nonuniform effects on muscle and skin sympathetic nerve activity, underlies sympatho-excitation in heart failure.

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“…These results suggest that cardiogenic hypotension due to the CxCAO results in an increase in vagal afferent activity that causes an inhibition of the reflexly activated SNA by arterial baroreceptors and by cardiac sympathetic afferent nerves. It was reported recently that the reflex inhibitory sympathetic responses to left coronary artery occlusion were mediated through the inhibitory cardiac receptors with vagal afferents, which were activated during myocardial ischemia (FELDER and THAMES, 1979;KEZDI et al, 1974;THAMES and ABBOUD, 1979;UCHIDA and SAKAMOTO, 1974). The cardiac receptors with vagal afferents were influencial in limiting the arterial baroreceptor-mediated increase in efferent cardiac sympathetic nerve activity resulting from acute coronary artery occlusion (FELDER and THAMES, 1979).…”

Section: Discussionmentioning

confidence: 99%

Neural control of sympathetic nerve response to cardiogenic hypotension in anesthetized cat.

Koyama

1985

Jpn.J.Physiol

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The present study was designed to determine effect of the preganglionic splanchnic nerve activity (SNA) on the brief hypotension accompanied with the occlusion of left circumflex coronary artery (CxCAO) in chloralose anesthetized cats. Following CxCAO in animals with neuraxis intact, no significant alterations of SNA occurred despite the significant fall in mean blood pressure (MBP). A significant fall in MBP also occurred in vagotomized animals with arterial baroreceptors intact, but SNA was significantly augmented from 12.9±2.7 impulses/sec before CxCAO to 24.4±4.3 impulses/sec 60 sec after the occlusion. In vagotomized animals, in which their carotid sinuses were isolated and perfused with the constant pressure at a level equal to systemic blood pressure (112±6 mmHg) and with higher pressure (167±7 mmHg), SNA was not altered significantly during the hypotension due to CxCAO. When the carotid sinuses were perfused with lower pressure (53±8 mmHg), a significant increase in SNA occurred simultaneously with the decrease in MBP after CxCAO. The peak decreases in blood pressure during the coronary occlusion were significantly greater in the vagotomized group (-46±5 mmHg) and in the Low-CSP group (-50 ± 5 mmHg) than in other groups. Onset of this excitatory efferent sympathetic response to the hypotension due to the coronary occlusion in the vagotomized and Low-CSP groups was delayed significantly despite a significant fall in arterial blood pressure. These results show that vagal afferents from the heart may play a role of inhibiting the sympathetic augmentation mediated by arterial baroreceptors during cardiogenic hypotension. An excessive activation of cardiac receptors with sympathetic afferents may be induced by the profound fall in blood pressure, resulting in further impairment of cardiac function due to progressive myocardial ischemia under the condition of high sympathetic tone activated by baroreceptor reflex.

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Reflex Inhibition of Renal Sympathetic Nerve Activity during Myocardial Ischemia Mediated by Left Ventricular Receptors with Vagal Afferents in Dogs

Cited by 79 publications

References 28 publications

Limitation of experimental infarct size by an angiotensin-converting enzyme inhibitor.

Limitation of experimental infarct size by an angiotensin-converting enzyme inhibitor.

Independent control of skin and muscle sympathetic nerve activity in patients with heart failure.

Neural control of sympathetic nerve response to cardiogenic hypotension in anesthetized cat.

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