Cardiovascular Reflexes from Ventricular and Coronary Receptors

Hainsworth, R.

doi:10.1007/978-1-4615-1895-2_15

Cited by 22 publications

(22 citation statements)

References 47 publications

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“…Postnatally, stimulation of ventricular stretch receptors with acute distention or preload reduction can produce reflex bradycardia and hypotension due to a combination of vagal efferent activity and withdrawal of sympathetic outflow, the so-called Bezold-Jarisch reflex (19). Little is known about 328 ventricular stretch responses in the human fetus.…”

Section: Discussionmentioning

confidence: 99%

Pathophysiology, Management, and Outcomes of Fetal Hemodynamic Instability During Prenatal Cardiac Intervention

et al. 2007

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Prenatal cardiac intervention (PCI) may favorably alter the in utero course of some congenital heart defects. In our preliminary experience with PCI, fetal hemodynamic instability (FHI) characterized by bradycardia and ventricular dysfunction was common. This study evaluated the pathophysiology, management, and short-term outcomes of FHI during PCI for aortic stenosis with evolving hypoplastic left heart syndrome (HLHS), HLHS with restrictive atrial septum, pulmonary atresia with intact ventricular septum, and hydrops due to structural heart disease. From 2000 to 2006, 83 fetuses underwent PCI, with ventricular access in 63, atrial access in 17, and both in three. FHI occurred in 37 fetuses (45%). FHI was associated with transventricular PCI (all but one case of FHI; p Ͻ 0.001) and large hemopericardium (n ϭ 9; p ϭ 0.07). Prolonged FHI was associated with severe ventricular distortion during ventricular puncture (p ϭ 0.06). FHI was treated with resuscitation medications in 31 of 37 fetuses and resolved in all 37. Five fetuses died within 1 d of PCI: four had FHI and one had a massive hemopericardium. FHI is common and clinically important during transventricular PCI and may be caused by a ventricular reflex or reduced cardiac output from cardiac distortion during ventricular puncture. Hemopericardium may be causative in a subset of fetuses. I n some forms of congenital heart disease, relatively simple obstructive anomalies causing physiologic changes in utero may lead to more serious abnormalities of cardiovascular growth and development. For example, severe left ventricular (LV) outflow obstruction in the early fetus may produce myocardial and hemodynamic abnormalities resulting in growth arrest of the entire left heart complex, culminating in HLHS. Similarly, in fetuses with established HLHS, closure of the foramen ovale may cause left atrial hypertension, with subsequent abnormalities of lung parenchymal and vascular development that contribute to high mortality after birth (1,2). Although such processes have not been well defined, the hypothesis that flow disturbances early in gestation can lead to abnormal cardiac growth is supported by experimental animal data (3-5) and by documented progression of isolated LV or right ventricular (RV) outflow obstruction to ventricular hypoplasia in human fetuses (6,7).In fetuses with such congenital heart defects, PCI may limit the secondary abnormalities of growth or development that result from primary structural anomalies by restoring more normal hemodynamic conditions. Since 2000, we have offered PCI for selected fetuses with (1) severe aortic stenosis (AS) with evolving HLHS, (2) critically restrictive or intact atrial septum and established HLHS, (3) pulmonary atresia with evolving hypoplastic right heart syndrome (HRHS), and (4) hydrops fetalis due to structural heart disease (8 -10).Almost immediately, we observed that FHI characterized by bradycardia and ventricular dysfunction was common during PCI. Although cases of fetal cardiac arrest or bradycardi...

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Section: Discussionmentioning

confidence: 99%

Pathophysiology, Management, and Outcomes of Fetal Hemodynamic Instability During Prenatal Cardiac Intervention

et al. 2007

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“…Rather, neurocardiogenic syncope has a more elusive pathophysiology [8], which may include C-fibremediated reflexes under some conditions such as haemorrhage, but also potential coronary receptor mediation [35], humoral mechanisms [36,37] and centrally mediated mechanisms [38]. Efforts to demonstrate an antecedent reduction in CNS blood flow have been largely unsuccessful, showing instead that cerebral hypoperfusion follows rather than precedes the fall in blood pressure with faint, and that cerebral autoregulation is normal [1,39].…”

Section: The Pathophysiology Of Episodic Neurocardiogenic Syncope Remmentioning

confidence: 97%

Contrasting neurovascular findings in chronic orthostatic intolerance and neurocardiogenic syncope

STEWART¹,

WELDON²

2003

Clinical Science

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Simple faint (neurocardiogenic syncope) and postural tachycardia syndrome (POTS) characterize acute and chronic orthostatic intolerance respectively. We explored the hypothesis that vascular function is similar in the two conditions. We studied 29 patients with POTS and compared them with 20 patients with neurocardiogenic syncope who were otherwise well, and with 15 healthy control subjects. We measured continuous heart rate, respiration and blood pressure, and used venous occlusion strain gauge plethysmography to measure calf and forearm blood flow, peripheral arterial resistance, peripheral venous resistance and venous pressure ( P (v)). Upright tilt was performed to 70 degrees for 10 min, during which calf blood flow and volume were measured. Calf P (v) was increased (to 27.2+/-2.0 mmHg) in a subgroup of POTS patients, who also had increased arterial resistance (57+/-6 mmHg.ml(-1).min(-1).100 ml(-1) tissue), increased venous resistance (2.4+/-0.3 mmHg.ml(-1).min(-1).100 ml(-1) tissue), and decreased peripheral flow (1.0+/-0.2 ml.min(-1).100 ml(-1) tissue) in the calf; other POTS patients with a normal P (v) had decreased arterial resistance (18+/-2 mmHg.ml(-1).min(-1).100 ml(-1) tissue) and increased blood flow (3.8+/-0.3 ml.min(-1).100 ml(-1) tissue). Syncope patients were not different from controls ( P (v)=11.4+/-0.5 mmHg; calf flow=3.1+/-0.2 ml.min(-1).100 ml(-1) tissue; arterial resistance=27+/-2 mmHg.ml(-1).min(-1).100 ml(-1) tissue; venous resistance=1.2+/-0.3 mmHg.ml(-1).min(-1).100 ml(-1) tissue). When upright, syncope patients and control subjects had similar increases in heart rate and calf volume, stable blood pressure, and decreases in blood flow. POTS patients had markedly increased heart rate and calf blood flow, unstable blood pressure, and pooling in the lower extremities, regardless of subgroup. We conclude that peripheral vascular physiology in patients with POTS is abnormal, in contrast with normal peripheral vascular physiology in neurocardiogenic syncope.

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“…Vasosensory nerves might be silent nociceptors that may never be activated during a lifetime, but we hypothesize that they also play a physiological role in the local and re¯ex regulation of the cardiovascular and respiratory (CVR) systems. Whilst the sensory function of specialized arterial baro-and chemo-sensory aerents in cardiovascular regulation has been established (Heymans & Neil, 1958;Shepherd, 1981;Marshall, 1994;Hainsworth, 1995), that of other aerents remains uncertain, particularly sensors associated with peripheral blood vessels.…”

Section: Introductionmentioning

confidence: 99%

Anandamide induces cardiovascular and respiratory reflexesviavasosensory nerves in the anaesthetized rat

Smith

McQueen

2001

British J Pharmacology

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1 We tested the hypothesis that sensory nerves innervating blood vessels play a role in the local and systemic regulation of the cardiovascular and respiratory (CVR) systems. We measured CVR re¯exes evoked by administration of anandamide (86 ± 863 nmoles) and capsaicin (0.3 ± 10 nmoles) into the hindlimb vasculature of anaesthetized rats. 2 Anandamide and capsaicin each caused a rapid dose-dependent re¯ex fall in blood pressure and an increase in ventilation when injected intra-arterially into the hindlimb. 3 Action of both agonists at the vanilloid receptor (VR1) on perivascular sensory nerves was investigated using capsazepine (1 mg kg 71 i.a.) a competitive VR1 antagonist, ruthenium red (1 mg kg 71 i.a.), a non-competitive antagonist at VR1, or a desensitizing dose of capsaicin (200 nmoles i.a.). The cannabinoid receptor antagonist SR141716 (1 mg kg 71 i.a.) was used to determine agonist activity at the CB 1 receptor. 4 Capsazepine, ruthenium red, or acute VR1 desensitization by capsaicin-pretreatment, markedly attenuated the re¯ex CVR responses evoked by anandamide and capsaicin (P50.05; paired Student's t-test). Blockade of CB 1 had no signi®cant e ect on the responses to anandamide. 5 Local sectioning of the femoral and sciatic nerves attenuated CVR responses to anandamide and capsaicin (P50.05). Vagotomy or carotid sinus sectioning had no signi®cant e ect on anandamideor capsaicin-induced responses. 6 These data demonstrate that both the endogenous cannabinoid, anandamide, and the vanilloid, capsaicin, evoke CVR re¯exes when injected intra-arterially into the rat hindlimb. These responses appear to be mediated re¯exly via VR1 located on sensory nerve endings within the hindlimb vasculature.

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Cardiovascular Reflexes from Ventricular and Coronary Receptors

Cited by 22 publications

References 47 publications

Pathophysiology, Management, and Outcomes of Fetal Hemodynamic Instability During Prenatal Cardiac Intervention

Pathophysiology, Management, and Outcomes of Fetal Hemodynamic Instability During Prenatal Cardiac Intervention

Contrasting neurovascular findings in chronic orthostatic intolerance and neurocardiogenic syncope

Anandamide induces cardiovascular and respiratory reflexesviavasosensory nerves in the anaesthetized rat

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