Peripheral chemoreceptors in health and disease

2004 ◽  
Vol 96 (1) ◽  
pp. 359-366 ◽  
Author(s):  
Nanduri R. Prabhakar ◽  
Ying-Jie Peng
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Defense Mechanism ◽  
Experimental Models ◽  
Cellular Mechanisms ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Oxygen Homeostasis ◽  
Arterial Blood ◽  
Carotid Bodies

Peripheral chemoreceptors (carotid and aortic bodies) detect changes in arterial blood oxygen and initiate reflexes that are important for maintaining homeostasis during hypoxemia. This mini-review summarizes the importance of peripheral chemoreceptor reflexes in various physiological and pathophysiological conditions. Carotid bodies are important for eliciting hypoxic ventilatory stimulation in humans and in experimental animals. In the absence of carotid bodies, compensatory upregulation of aortic bodies as well as other chemoreceptors contributes to the hypoxic ventilatory response. Peripheral chemoreceptors are critical for ventilatory acclimatization at high altitude. They also contribute in part to the exercise-induced hyperventilation, especially with submaximal and heavy exercise. During pregnancy, hypoxic ventilatory sensitivity increases, perhaps due to the actions of estrogen and progesterone on chemoreceptors. Augmented peripheral chemoreceptors have been implicated in early stages of recurrent apneas, congestive heart failure, and certain forms of hypertension. It is likely that chemoreceptors tend to maintain oxygen homeostasis and act as a defense mechanism to prevent the progression of the morbidity associated with these diseases. Experimental models of recurrent apneas, congestive heart failure, and hypertension offer excellent opportunities to unravel the cellular mechanisms associated with altered chemoreceptor function.

Pulmonary Edema I: Cardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Pulmonary Edema ◽  
Clinical Characteristics ◽  
Distress Syndrome ◽  
Capillary Permeability ◽  
Treatment Options ◽  
Experimental Models ◽  
Lung Mechanics ◽  
Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 24 references. Key words: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

Congestive Heart Failure in Copper-Deficient Mice

2003 ◽  
Vol 228 (7) ◽  
pp. 811-817 ◽  
Author(s):  
Laila Elsherif ◽  
Raymond V. Ortines ◽  
Jack T. Saari ◽  
Y. James Kang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Experimental Models ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Total Period

Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 weeks (pre- and postweanling). At week 4, the functional parameters of the heart were analyzed using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no significant change in heart rate, and more importantly contractility as measured by the maximal rate of left ventricular pressure rise (+dP/dt) and decline (−dP/dt) were significantly depressed in the CuD mice. However, left ventricle end diastolic pressure was elevated, and relaxation was impaired in the CuD animals; the duration of relaxation was prolonged. In addition to significant changes in the basal level of cardiac function, CuD hearts had a blunted response to the stimulation of the β-adrenergic agonist isoproterenol. Furthermore, morphological analysis revealed increased collagen accumulation in the CuD hearts along with lipid deposition. This study shows that CuD leads to systolic and diastolic dysfunction in association with histopathological changes, which are indices commonly used to diagnose congestive heart failure.

Reduction of Carotid Arterial Blood Flow in Ventricular Septal Defect Associated With Severe Congestive Heart Failure

2000 ◽  
Vol 10 (4) ◽  
pp. 241-243 ◽  
Author(s):  
Masanobu Kojo ◽  
Katsuhiko Yamada ◽  
Shinnosuke Akiyoshi ◽  
Miwako Maeda ◽  
Keisuke Sato ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Ventricular Septal Defect ◽  
Septal Defect ◽  
Severe Congestive Heart Failure ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Carotid Arterial

Inhalation of the Phosphodiesterase-3 Inhibitor Milrinone Attenuates Pulmonary Hypertension in a Rat Model of Congestive Heart Failure

2007 ◽  
Vol 106 (1) ◽  
pp. 124-131 ◽  
Author(s):  
Thomas Hentschel ◽  
Ning Yin ◽  
Alexander Riad ◽  
Helmut Habbazettl ◽  
Jörg Weimann ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Vascular Resistance ◽  
Rat Model ◽  
Intravenous Infusion ◽  
Left Ventricular ◽  
Venous Hypertension ◽  
Systemic Hemodynamics ◽  
Phosphodiesterase 3 ◽  
Arterial Blood

Background Most patients with congestive heart failure (CHF) develop pulmonary venous hypertension, but right ventricular afterload is frequently further elevated by increased pulmonary vascular resistance. To investigate whether inhalation of a vasodilatory phosphodiesterase-3 inhibitor may reverse this potentially detrimental process, the authors studied the effects of inhaled or intravenous milrinone on pulmonary and systemic hemodynamics in a rat model of CHF. Methods In male Sprague-Dawley rats, CHF was induced by supracoronary aortic banding, whereas sham-operated rats served as controls. Milrinone was administered as an intravenous infusion (0.2-1 microg.kg body weight.min) or by inhalation (0.2-5 mg/ml), and effects on pulmonary and systemic hemodynamics and lung water content were measured. Results In CHF rats, intravenous infusion of milrinone reduced both pulmonary and systemic arterial blood pressure. In contrast, inhalation of milrinone predominantly dilated pulmonary blood vessels, resulting in a reduced pulmonary-to-systemic vascular resistance ratio. Repeated milrinone inhalations in 20-min intervals caused a stable reduction of pulmonary artery pressure. No hemodynamic effects were detected when 0.9% NaCl was administered instead of milrinone or when milrinone was inhaled in sham-operated rats. No indications of potentially adverse effects of milrinone inhalation in CHF, such as left ventricular volume overload, were detected. Moreover, lung edema was significantly reduced by repeated milrinone inhalation. Conclusion If these results can be confirmed in humans, inhalation of nebulized milrinone may present a novel, effective, safe, and pulmonary selective strategy for the treatment of pulmonary venous hypertension in CHF.

scholarly journals Comparative effects of vasodilating stimuli on limb arterial blood flow in patients with congestive heart failure

1990 ◽  
Vol 15 (2) ◽  
pp. A257
Author(s):  
Stuart Katz ◽  
Luigi Biasucei ◽  
Michele Nanna ◽  
Carlo Sabba ◽  
Joel Strom ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Arterial Blood Flow ◽  
Arterial Blood

Pulmonary Edema I: Cardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Pulmonary Edema ◽  
Clinical Characteristics ◽  
Distress Syndrome ◽  
Capillary Permeability ◽  
Treatment Options ◽  
Experimental Models ◽  
Lung Mechanics ◽  
Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 24 references. Key words: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

Alterations in diaphragm strength and fatiguability in congestive heart failure

1994 ◽  
Vol 76 (6) ◽  
pp. 2707-2713 ◽  
Author(s):  
G. Supinski ◽  
A. DiMarco ◽  
M. Dibner-Dunlap
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Arterial Occlusion ◽  
Arterial Blood Flow ◽  
Exercise Intolerance ◽  
Diaphragmatic Function ◽  
Arterial Blood ◽  
Phrenic Artery ◽  
Acute Study ◽  
Rapid Ventricular Pacing

Recent reports suggested that exercise intolerance associated with congestive heart failure (CHF) may be due to changes in peripheral limb muscle function. Our purpose was to determine whether CHF also elicits alterations in diaphragmatic function. CHF was induced in dogs by rapid ventricular pacing for a period of 4–6 wk. After signs of CHF developed, dogs were anesthetized and an acute study was performed to assess diaphragm function. Diaphragm strips were dissected in situ in the left costal diaphragm, the phrenic artery supplying these strips was cannulated, and strips were perfused with arterial blood at arteriovenous pressure gradient of 90 mmHg. Diaphragm strength and fatiguability were then determined, and phrenic flow response to transient arterial occlusion was assessed. A group of nonpaced normal dogs was similarly studied and served as controls. We found that CHF dogs had a significant reduction in diaphragm strength. For example, tetanic force in response to 100 Hz of stimulation was 25.5 +/- 1.0 N/cm2 in control dogs but only 19.6 +/- 1.9 kg/cm2 in CHF dogs (P < 0.02). In addition, CHF dogs had increased diaphragm fatiguability. Diaphragm force fell to 27 +/- 3% of its baseline value during a 30-min fatigue trial in CHF dogs but only to 44 +/- 4% in control dogs (P < 0.01). CHF dogs also had a altered phrenic arterial hyperemic response to arterial occlusion and a reduction in phrenic arterial blood flow achieved during the fatigue trial. We conclude that development of CHF is associated with significant alterations in diaphragmatic function, causing a marked increase in fatiguability.

scholarly journals Aortocaval Fistula in Rat: A Unique Model of Volume-Overload Congestive Heart Failure and Cardiac Hypertrophy

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Zaid Abassi ◽  
Ilia Goltsman ◽  
Tony Karram ◽  
Joseph Winaver ◽  
Aaron Hoffman
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Hypertrophy ◽  
Volume Overload ◽  
Experimental Models ◽  
Aortocaval Fistula ◽  
New Therapeutic Approaches ◽  
High Output Heart Failure ◽  
Continuous Progress ◽  
Cardiac Manifestations

Despite continuous progress in our understanding of the pathogenesis of congestive heart failure (CHF) and its management, mortality remains high. Therefore, development of reliable experimental models of CHF and cardiac hypertrophy is essential to better understand disease progression and allow new therapy developement. The aortocaval fistula (ACF) model, first described in dogs almost a century ago, has been adopted in rodents by several groups including ours. Although considered to be a model of high-output heart failure, its long-term renal and cardiac manifestations are similar to those seen in patients with low-output CHF. These include Na+-retention, cardiac hypertrophy and increased activity of both vasoconstrictor/antinatriureticneurohormonal systems and compensatory vasodilating/natriuretic systems. Previous data from our group and others suggest that progression of cardiorenal pathophysiology in this model is largely determined by balance between opposing hormonal forces, as reflected in states of CHF decompensation that are characterized by overactivation of vasoconstrictive/Na+-retaining systems. Thus, ACF serves as a simple, cheap, and reproducible platform to investigate the pathogenesis of CHF and to examine efficacy of new therapeutic approaches. Hereby, we will focus on the neurohormonal, renal, and cardiac manifestations of the ACF model in rats, with special emphasis on our own experience.

scholarly journals The regulation role of carotid body peripheral chemoreceptors in physiological and pathophysiological conditions

2016 ◽  
Vol 69 (11-12) ◽  
pp. 385-390 ◽  
Author(s):  
Biljana Lazovic ◽  
Mirjana Zlatkovic-Svenda ◽  
Tijana Durmic ◽  
Zoran Stajic ◽  
Vesna Djuric ◽  
...  
Keyword(s):  
The Body ◽  
Internal Organs ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Oxygen Homeostasis ◽  
Pathological Conditions ◽  
Obstructive Sleep ◽  
Functional Sympatholysis ◽  
The Common

Introduction. The major oxygen sensors in the human body are peripheral chemoreceptors, also known as interoreceptors-as connected with internal organs, located in the aortic arch and in the body of the common carotid artery. Chemoreceptor function under physiological conditions. Stimulation of peripheral chemoreceptors during enviromental hypoxia causes a reflex-mediated increased ventilation, followed by the increase of the muscle sympatic activity, aiming to maintain tissue oxygen homeostatis, as well as glucosae homeostatis. Besides that, peripheral chemoreceptors interact with central chemoreceptors, responsible for carbon dioxide changes, and they are able to modulate each other. Chemoreceptor function in pathophysiological conditions. Investigations of respiratory function in many pathological processes, such as hypertension, obstructive sleep apnea, congestive heart failure and many other diseases that are presented with enhanced peripheral chemosensitivity and impaired functional sympatholysis ultimately determine the peripheral chemoreceptor role and significance of peripheral chemoreceptors in the process of those pathological conditions development. Considering this, the presumed influence of peripheral chemoreceptors is important in patients having the above mentioned pathology. Conclusion. The importance and the role of peripheral chemoreceptors in the course of the breathing control is still controversial, despite many scientific attempts to solve this problem. The main objective of this review is to give the latest data on the peripheral chemoreceptor role and to highlight the importance of peripheral chemoreceptors for maintaining of oxygen homeostasis in pateints with hypoxia caused by either physiological or pathological conditions.

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