Reduction in baroreflex cardiovascular responses due to venous infusion in the rabbit. (1/508)

We studied reflex bradycardia and depression of mean arterial blood pressure (MAP) during left aortic nerve (LAN) stimulation before and after volume infusion in the anesthetized rabbit. Step increases in mean right atrial pressure (MRAP) to 10 mm Hg did not result in a significant change in heart rate or MAP. After volume loading, responses to LAN stimulation were not as great and the degree of attenuation was propoetional to the level of increased MRAP. A change in responsiveness was observed after elevation of MRAP by only 1 mm Hg, corresponding to less than a 10% increase in average calculated blood volume. after an increase in MRAP of 10 mm Hg, peak responses were attenuated by 44% (heart rate) and 52% (MAP), and the initial slopes (rate of change) were reduced by 46% (heart rate) and 66% (MAP). Comparison of the responses after infusion with blood and dextran solutions indicated that hemodilution was an unlikely explanation for the attenuation of the reflex responses. Total arterial baroreceptor denervation (ABD) abolished the volume-related attenuation was still present following bilateral aortic nerve section or vagotomy. It thus appears that the carotid sinus responds to changes inblood volume and influences the reflex cardiovascular responses to afferent stimulation of the LAN. On the other hand, cardiopulmonary receptors subserved by vagal afferents do not appear to be involved.  (+info)

Quantification of baroreceptor influence on arterial pressure changes seen in primary angiotension-induced hypertension in dogs. (2/508)

We studied the role of the sino-aortic baroreceptors in the gradual development of hypertension induced by prolonged administration of small amounts of angiotensin II (A II) in intact dogs and dogs with denervated sino-aortic baroreceptors. Short-term 1-hour infusions of A II(1.0-100 ng/kg per min) showed that conscious denervated dogs had twice the pressor sensitivity of intact dogs. Long-term infusions of A II at 5.0 ng/kg per min (2-3 weeks) with continuous 24-hour recordings of arterial pressure showed that intact dogs required 28 hours to reach the same level of pressure attained by denervated dogs during the 1st hour of infusion. At the 28th hour the pressure in both groups was 70% of the maximum value attained by the 7th day of infusion. Both intact and denervated dogs reached nearly the same plateau level of pressure, the magnitude being directly related both the the A II infusion rate and the daily sodium intake. Cardiac output in intact dogs initially decreased after the onset of A II infusion, but by the 5th day of infusion it was 38% above control, whereas blood volume was unchanged. Heart rate returned to normal after a reduction during the 1st day of infusion in intact dogs. Plasma renin activity could not be detected after 24 hours of A II infusion in either intact or denervated dogs. The data indicate that about 35% of the hypertensive effect of A II results from its acute pressor action, and an additional 35% of the gradual increase in arterial pressure is in large measure a result of baroreceptor resetting. We conclude that the final 30% increase in pressure seems to result from increased cardiac output, the cause of which may be decreased vascular compliance. since the blood volume remains unaltered.  (+info)

Hypoxia inhibits baroreflex vagal bradycardia via a central action in anaesthetized rats. (3/508)

It is known that arterial baroreflexes are suppressed in stressful conditions. The present study was designed to determine whether and how hypoxia affects arterial baroreflexes, especially the heart rate component, baroreflex vagal bradycardia. In chloralose-urethane-anaesthetized rats, baroreflex vagal bradycardia was evoked by electrical stimulation of the aortic depressor nerve, and the effect of 15 s inhalation of hypoxic gas (4% O2) was studied. Inhalation of hypoxic gas was found to inhibit baroreflex vagal bradycardia. The inhibition persisted after bilateral transection of the carotid sinus nerve. Cervical vagus nerves were cut bilaterally and their peripheral cut ends were stimulated to provoke vagal bradycardia of peripheral origin so as to determine whether hypoxia could inhibit vagal bradycardia by acting on a peripheral site. In contrast to baroreflex vagal bradycardia, the vagus-induced bradycardia was not affected by hypoxic gas inhalation. It is concluded that baroreflex vagal bradycardia is inhibited by hypoxia and the inhibition is largely mediated by its direct central action.  (+info)

Responses of abdominal vascular capacitance in the anaesthetized dog to changes in carotid sinus pressure. (4/508)

1. The abdominal circulation of anaesthetized dogs was vascularly isolated without opening the abdomen, by cutting or tying all structures immediately above the diaphragm and tying the proximal ends of the hind limbs. The region was perfused at constant flow through the aorta and drained at constant pressure from the inferior vena cava. 2. Vascular resistance responses were expressed as the changes in perfusion pressure and capacitance responses were determined by integrating changes in vena caval outflow. 3. Decreasing the pressure in the isolated carotid sinuses over the whole baroreceptor sensitivity range increased mean perfusion pressure from 91 to 149 mmHg (a 67% increase in resistance) and decreased mean capacitance by 111 ml. (5 ml. kg-1). 4. The range of carotid sinus pressures over which capacitance responses occurred was at a significantly higher level than the corresponding range for resistance responses. 5. Comparison of the reflex responses with the responses to direct stimulation of efferent sympathetic nerves shows that quantitatively similar responses of resistance and capacitance to those induced by a large step decrease in carotid pressure could be produced by stimulating maximally the efferent sympathetic nerves at 5 Hz. These results also suggest that at all levels of carotid sinus pressure there is no difference in the impulse traffic to resistance and capacitance vessels.  (+info)

Carotid sinus hypersensitivity--a modifiable risk factor for fractured neck of femur. (5/508)

BACKGROUND: the potential impact on morbidity, mortality and health care economics makes it important to identify patients at risk of fracture, in particular fractured neck of femur (FNOF). Older patients with carotid sinus hypersensitivity (CSH) are more likely to have unexplained falls and to experience fractures, particularly FNOF. Our objective was to determine the prevalence of CSH in patients with FNOF. DESIGN: case-controlled prospective series. METHODS: consecutive cases were admissions over 65 years with FNOF. Controls were consecutive patients admitted for elective hip surgery, frail elderly people admitted to hospital medical wards and day-hospital patients. All patients had a clinical assessment of cognitive function, physical abilities and history of previous syncope, falls and dizziness, in addition to repeated carotid sinus massage with continuous heart rate and phasic blood pressure measurement. RESULTS: heart rate slowing and fall in systolic blood pressure was greater for patients with FNOF than those admitted for elective hip surgery (P < 0.05 and P < 0.001). CSH was present in 36% of the FNOF group, none of the elective surgery group, 13% of the acutely ill controls and 17% of the outpatients. It was more likely to be present in FNOF patients with a previous history of unexplained falls or an unexplained fall causing the index fracture. The heart rate and systolic blood pressure responses to carotid sinus stimulation were reproducible. CONCLUSION: older patients with an acute neck of femur fracture who do not give a clear history of an accidental fall or who have had previously unexplained falls are likely to have CSH. CSH may be a modifiable risk factor for older patients at risk of hip fracture.  (+info)

New analytic framework for understanding sympathetic baroreflex control of arterial pressure. (6/508)

The sympathetic baroreflex is an important feedback system in stabilization of arterial pressure. This system can be decomposed into the controlling element (mechanoneural arc) and the controlled element (neuromechanical arc). We hypothesized that the intersection of the two operational curves representing their respective functions on an equilibrium diagram should define the operating point of the arterial baroreflex. Both carotid sinuses were isolated in 16 halothane-anesthetized rats. The vagi and aortic depressor nerves were cut bilaterally. Carotid sinus pressure (CSP) was sequentially altered in 10-mmHg increments from 80 to 160 mmHg while sympathetic efferent nerve activity (SNA) and systemic arterial pressure (SAP) were recorded simultaneously under various hemorrhagic conditions. The mechanoneural arc was characterized by the response of SNA to CSP and the neuromechanical arc by the response of SAP to SNA. We parametrically analyzed the relationship between input and output for each arc using a four-parameter logistic equation model. In baseline states, the two arcs intersected each other at the point at which the instantaneous gain of each arc attained its maximum. Severe hemorrhage lowered the gain and offset of the neuromechanical arc and moved the operating point, whereas the mechanoneural arc remained unchanged. The operating points measured under the closed-loop conditions were indistinguishable from those estimated from the intersections of the two arc curves on the equilibrium diagram. The average root mean square errors of estimate for arterial pressure and SNA were 2 and 3%, respectively. Such an analytic approach could explain a mechanism for the determination of the operating point of the sympathetic baroreflex system and thus helps us integratively understand its function.  (+info)

Carotid baroreflex function during prolonged exercise. (7/508)

The present investigation was designed to uncouple the hemodynamic physiological effects of thermoregulation from the effects of a progressively increasing central command activation during prolonged exercise. Subjects performed two 1-h bouts of leg cycling exercise with 1) no intervention and 2) continuous infusion of a dextran solution to maintain central venous pressure constant at the 10-min pressure. Volume infusion resulted in a significant reduction in the decrement in mean arterial pressure seen in the control exercise bout (6.7 +/- 1.8 vs. 11.6+/- 1.3 mmHg, respectively). However, indexes of central command such as heart rate and ratings of perceived exertion rose to a similar extent during both exercise conditions. In addition, the carotid-cardiac baroreflex stimulus-response relationship, as measured by using the neck pressure-neck suction technique, was reset from rest to 10 min of exercise and was further reset from 10 to 50 min of exercise in both exercise conditions, with the operating point being shifted toward the reflex threshold. We conclude that the progressive resetting of the carotid baroreflex and the shift of the reflex operating point render the carotid-cardiac reflex ineffectual in counteracting the continued decrement in mean arterial pressure that occurs during the prolonged exercise.  (+info)

Chronic hypoxia enhances the phrenic nerve response to arterial chemoreceptor stimulation in anesthetized rats. (8/508)

Chronic exposure to hypoxia results in a time-dependent increase in ventilation called ventilatory acclimatization to hypoxia. Increased O(2) sensitivity of arterial chemoreceptors contributes to ventilatory acclimatization to hypoxia, but other mechanisms have also been hypothesized. We designed this experiment to determine whether central nervous system processing of peripheral chemoreceptor input is affected by chronic hypoxic exposure. The carotid sinus nerve was stimulated supramaximally at different frequencies (0.5-20 Hz, 0.2-ms duration) during recording of phrenic nerve activity in two groups of anesthetized, ventilated, vagotomized rats. In the chronically hypoxic group (7 days at 80 Torr inspired PO(2)), phrenic burst frequency (f(R), bursts/min) was significantly higher than in the normoxic control group with carotid sinus nerve stimulation frequencies >5 Hz. In the chronically hypoxic group, peak amplitude of integrated phrenic nerve activity ( integral Phr, percent baseline) or change in integral Phr was significantly greater at stimulation frequencies between 5 and 17 Hz, and minute phrenic activity ( integral Phr x f(R)) was significantly greater at stimulation frequencies >5 Hz. These experiments show that chronic hypoxia facilitates the translation of arterial chemoreceptor afferent input to ventilatory efferent output through a mechanism in the central nervous system.  (+info)

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