scholarly journals Vagal baroreflex latency in circulatory control

2017 ◽  
Vol 595 (6) ◽  
pp. 2197-2198 ◽  
Author(s):  
John M. Karemaker ◽  
Roel W. DeBoer
Keyword(s):  
Circulatory Control

High-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and cholecystokinin: implications for circulatory control

2011 ◽  
Vol 300 (3) ◽  
pp. H961-H967 ◽  
Author(s):  
Jackie M. Y. How ◽  
Barbara C. Fam ◽  
Anthony J. M. Verberne ◽  
Daniela M. Sartor
Keyword(s):  
Arterial Pressure ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
High Fat ◽  
Lower Plasma ◽  
Lower Tertile ◽  
Circulatory Control ◽  
Plasma Leptin

Gastric leptin and cholecystokinin (CCK) act on vagal afferents to induce cardiovascular effects and reflex inhibition of splanchnic sympathetic nerve discharge (SSND) and may act cooperatively in these responses. We sought to determine whether these effects are altered in animals that developed obesity in response to a medium high-fat diet (MHFD). Male Sprague-Dawley rats were placed on a low-fat diet (LFD; n = 8) or a MHFD ( n = 24) for 13 wk, after which the animals were anesthetized and artificially ventilated. Arterial pressure was monitored and blood was collected for the determination of plasma leptin and CCK. SSND responses to leptin (15 μg/kg) and CCK (2 μg/kg) administered close to the coeliac artery were evaluated. Collectively, MHFD animals had significantly higher plasma leptin but lower plasma CCK levels than LFD rats ( P < 0.05), and this corresponded to attenuated or reversed SSND responses to CCK (LFD, −21 ± 2%; and MHFD, −12 ± 2%; P < 0.05) and leptin (LFD, −6 ± 2%; and MHFD, 4 ± 1%; P < 0.001). Alternatively, animals on the MHFD were stratified into obesity-prone (OP; n = 8) or obesity-resistant (OR; n = 8) groups according to their weight gain falling within the upper or lower tertile, respectively. OP rats had significantly higher resting arterial pressure, adiposity, and plasma leptin but lower plasma CCK compared with LFD rats ( P < 0.05). The SSND responses to CCK or leptin were not significantly different between OP and OR animals. These results demonstrate that a high-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and CCK and may impact on sympathetic vasomotor mechanisms involved in circulatory control.

The 2009 Carl Ludwig Lecture: pathophysiology of the human sympathetic nervous system in cardiovascular diseases: the transition from mechanisms to medical management

2010 ◽  
Vol 108 (2) ◽  
pp. 227-237 ◽  
Author(s):  
Murray Esler
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Heart Disease ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Clinical Translation ◽  
Organ Specific ◽  
Circulatory Control ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

Sympathetic nervous system responses typically are regionally differentiated, with activation in one outflow sometimes accompanying no change or sympathetic inhibition in another. Regional sympathetic activity is best studied in humans by recording from postganglionic sympathetic efferents (multiunit or single fiber recording) and by isotope dilution-derived measurement of organ-specific norepinephrine release to plasma (regional “norepinephrine spillover”). Evidence assembled in this review indicates that sympathetic nervous system abnormalities are crucial in the development of cardiovascular disorders, notably heart failure, essential hypertension, disorders of postural circulatory control causing syncope, and “psychogenic heart disease,” heart disease attributable to mental stress and psychiatric illness. These abnormalities involve persistent, adverse activation of sympathetic outflows to the heart and kidneys in heart failure and hypertension, episodic or ongoing cardiac sympathetic activation in psychogenic heart disease, and defective sympathetic circulatory reflexes in disorders of postural circulatory control. An important goal for clinical scientists is translation of knowledge of pathophysiology, such as this, into better treatment for patients. The achievement of this “mechanisms-to-management” transition is at differing stages of development with the different conditions. Clinical translation is mature in cardiac failure, knowledge of cardiac neural pathophysiology having led to introduction of β-adrenergic blockers, an effective therapy. With essential hypertension, perhaps we are on the cusp of effective translation, with recent successful testing of selective catheter-based renal sympathetic nerve ablation in patients with resistant hypertension, an intervention firmly based on demonstration of activation of the renal sympathetic outflow. With psychogenic heart disease and postural syncope syndromes, knowledge of the neural pathophysiology is emerging, but clinical translation remains for the future.

Hematocrit modifies the circulatory control of systemic and myocardial oxygen utilization in septic sheep

1994 ◽  
Vol 22 (3) ◽  
pp. 470-479 ◽  
Author(s):  
GEORGE A. FOX ◽  
ANDREW BERSTEN ◽  
CALVIN LAM ◽  
ANDREA NEAL ◽  
FRANK S. RUTLEDGE ◽  
...  
Keyword(s):  
Oxygen Utilization ◽  
Circulatory Control

Circulatory Control

2011 ◽  
pp. 253-282
Author(s):  
Abraham Noordergraaf
Keyword(s):  
Circulatory Control

Central and Peripheral Catecholamine Mechanisms in Circulatory Control

Cardiology ◽  
1976 ◽  
Vol 61 (1) ◽  
pp. 113-124 ◽  
Author(s):  
J.L. Reid ◽  
C.T. Dollery
Keyword(s):  
Circulatory Control

Intestinal capillary blood flow during metabolic hyperemia.

1979 ◽  
Vol 237 (6) ◽  
pp. E548 ◽  
Author(s):  
A P Shepherd
Keyword(s):  
Blood Flow ◽  
Metabolic Rate ◽  
Constant Pressure ◽  
Oxygen Demand ◽  
Capillary Density ◽  
Control Mechanisms ◽  
O2 Uptake ◽  
O2 Extraction ◽  
Circulatory Control ◽  
Parenchymal Cells

It has been postulated that local circulatory control mechanisms regulate the O2 flux to parenchymal cells by two vascular mechanisms: changes in blood flow that minimize capillary PO2 variations and changes in the density of the perfused capillary bed through which O2 extraction is regulated. To test this prediction, isolated loops of canine jejenum and ileum were perfused at either constant blood flow or constant pressure, and intraluminal glucose was used to increase metabolic rate. In the constant-flow series, glucose increased O2 extraction, O2 uptake, and rubidium extraction. Resistance fell when the metabolic rate was elevated. In the constant-pressure series, glucose increased blood flow, O2 extraction, O2 uptake, and capillary filtration coefficients. These results show that vascular resistance falls and that capillary density increases following an increase in oxygen demand. Thus, the glucose-stimulated gut loop seems to be a valid model of metabolic hyperemia, and its behavior would be difficult to reconcile with a purely myogenic theory of intestinal blood flow autoregulation.

Respiratory and cerebral circulatory control during exercise at .21 and 2.0 atmospheres inspired pO2

1959 ◽  
Vol 14 (6) ◽  
pp. 966-982 ◽  
Author(s):  
Christian J. Lambertsen ◽  
S. G. Owen ◽  
Herbert Wendel ◽  
Morris W. Stroud ◽  
Abraham A. Lurie ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Venous Blood ◽  
Work Load ◽  
Minute Volume ◽  
Bicarbonate Concentration ◽  
Oxygen Administration ◽  
Circulatory Control ◽  
Leg Exercise ◽  
Positive Correlations ◽  
Fixed Acid

Respiratory and cerebral hemodynamic responses to leg exercise during respiration of air at 1.0 atm. and O2 at 2.0 atm. were studied in relation to changes in arterial and internal jugular venous blood oxygen composition, pH, pCO2 and bicarbonate concentration. The hyperpnea of exercise at 1.0 atm. was accompanied by arterial and venous acidemia and hypocapnia. Oxygen administration during exercise at 2.0 atm. lowered ventilation, restored arterial pH and pCO2 toward resting levels and caused venous pCO2 to rise above the resting level; cerebral venous cH remained elevated in spite of reduction of blood fixed acid concentration. The ventilatory response to exercise showed positive correlations with work load, oxygen consumption, and with changes in arterial and internal jugular venous cH and fixed acid. The observed negative correlations of changes in respiratory minute volume with changes in arterial and internal jugular venous pCO2 and bicarbonate concentration suggest that these factors are functions, rather than primary determinants, of ventilation in exercise. Cerebral hemodynamics and oxygen consumption were not significantly altered by exercise at 1.0 atm. The data suggest either a slight elevation of cerebral blood flow or reduction in the rate of cerebral oxygen consumption during exercise breathing O2 at 2.0 atm., without gross elevation of cerebral venous pO2. Observed changes in cerebral vascular resistance during exercise at .21 and 2.0 atm. inspired pO2 appear related to concomitant alterations in arterial pCO2, with no detectable relationship either to brain oxygen requirement of cerebral venous acid-base composition. Submitted on November 25, 1958

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