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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concept that reflex control of cerebral vessels is unimportant has been challenged by recent studies which suggest that carotid baroreceptors have an important role in regulation of cerebral blood flow (CBF). In this study we have tested the hypothesis that arterial baroreceptors contribute to regulation of total or regional CBF. CBF was measured in anesthetized dogs with 15 mu microspheres. Stimulation of carotid baroreceptors, by raising carotid sinus pressure, did not alter or redistribute cerebral flow. Responses to baroreceptor stimulation were intact, as manifested by vasodilation in skeletal muscle. CBF decreased during systemic hypocapnia and increased during hypercapnia, which indicates that failure of cerebral flow to change during baroreceptor stimulation was not due to unresponsiveness of cerebral vessels. During hypercapnia, baroreceptor stimulation also failed to alter CBF. In other studies CBF was measured during increases in systemic arterial pressure, before and after denervation of arterial baroreceptors. Increases in arterial pressure did not increase CBF either before or after denervation of baroreceptors. We conclude that baroreceptor stimulation does not alter total or regional CBF and that baroreceptors do not regulate cerebral flow during systemic hypertension.
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PMID:Total and regional cerebral blood flow during stimulation of carotid baroreceptors. 94 13

Reflex control of hind-limb and renal resistance vessels by cardiac and pulmonary receptors was studied by interrupting afferent vagal nerve traffic when only the heart or only the lungs were in situ in anesthetized dogs with sinoaortic denervation. During normocapnia, interruption of cardiac and of pulmonary vagal traffic decreased hind-limb blood flow (constant-pressure perfusion) by 23% and 21%, respectively. Corresponding decreases in renal blood flow were 23% and 33%. Hypercapnia augmented the decreases in renal blood flow due to the vagal block. Thus, the inhibitions exerted by the heart and lung receptores on these two beds were similar during normocapnia but were greater on the renal vessels during hypercapnia. In closed-chest dogs with their aortic nerves sectioned and their carotid sinus pressure controlled, combined withdrawal of carotid and cardiopulmonary inhibition decreased hind-limb and renal blood flow by about 80% and 40%, respectively, during both normovolemia and hypervolemia. Interruption of cardiopulmonary inhibition was responsible for 17% and 31% of the decrease in hind-limb blood flow at normal and increased blood volumes, respectively; values for the decreases in renal blood flow were 50% and 65%. Thus, cardiopulmonary receptors oppose the vasoconstriction due to carotid hypotension more effectively in the kidney than they do in the hind limb.
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PMID:Role of cardiac, pulmonary, and carotid mechanoreceptors in the control of hind-limb and renal circulation in dogs. 114 94

Activity was recorded from physiologically identified baroreceptor or chemoreceptor fibers in carotid sinus nerves of urethane-anesthetized spontaneously breathing rabbits. A carotid sinus area was vascularly isolated so that carotid sinus pressure and perfusion medium (Locke's solution or rabbit blood) could be controlled. The cervical sympathetic, vagus, and aortic depressor nerves were bilaterally cut to eliminate vagal and cardiopulmonary reflexes. Baroreceptor fibers could be divided into two groups: fibers with a mean firing threshold of 47.6 +/- 1.9 mm Hg and no activity below this threshold (37 fibers) and fibers that were active at low intrasinus pressures (18.1 +/- 2.2 impulses/sec at an intrasinus pressure of 0 mm Hg). The baroreceptor fibers that were spontaneously active at low pressures were also chemically sensitive: discharge rate was increased by 5-hydroxytryptamine (10 fibers, p less than 0.01), nicotine (10 fibers, p less than 0.01), or hypercapnia (13 fibers, p less than 0.001). The activity of baroreceptor fibers with a clear pressure threshold was usually decreased by hypercapnia (26 of 27 fibers, from 18.8 +/- 3.1 to 13.2 +/- 3.9 impulses/sec). Chemoreceptor fibers failed to respond to intrasinus pressure changes from 0 to 100 mm Hg (n = 25 fibers, p greater than 0.5) but were sensitive to chemical changes, as expected. Thus, there is a subset of baroreceptor fibers that, under certain conditions, is spontaneously active at very low intrasinus pressures and responds to changes in the chemical milieu.
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PMID:Low-pressure-sensitive baroreceptor fibers recorded from rabbit carotid sinus nerves. 195 80

Using awake, chronically catheterized newborn pigs, we measured cerebral blood flow (CBF), net cerebral vascular 6-keto-prostaglandin F1 alpha production, and cerebral metabolic rate of oxygen (CMRO2) during hypercapnia and during hypercapnia at increased mean airway pressure (Paw), both before and after treatment with indomethacin. CBF nearly doubled during hypercapnia. The hypercapnia-induced cerebral hyperemia was maintained when Paw was increased from 3 +/- 2 to 16 +/- 4 cm H2O during hypercapnia. Sagittal sinus pressure increased in proportion to the increase in Paw, and cardiac output was unchanged. Net cerebral production of 6-keto-prostaglandin F1 alpha increased from 9 +/- 1 to 15 +/- 1 ng/min/100 g tissue during hypercapnia and increased dramatically to 57 +/- 1 ng/min/100 g when hypercapnia was coupled with an increase in Paw. CMRO2 was not changed by either hypercapnia or increased Paw. After indomethacin, CBF decreased and cerebral vasodilation to hypercapnia did not occur. After indomethacin, adding increased Paw during hypercapnia dropped CBF below baseline, adversely affecting CMRO2. These results suggest that cerebral hypercapnia hyperemia requires brain prostanoid production and that when Paw is increased during hypercapnia, the contribution of prostanoids to maintaining CBF is increased. Increasing ventilation pressure during hypercapnia in piglets pretreated with indomethacin compromises CBF sufficiently to reduce CMRO2.
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PMID:Pressure ventilation increases brain vascular prostacyclin production in newborn pigs. 228 59

Cerebral blood flow (CBF) responsiveness to alterations in arterial CO2 tensions (PaCO2) during 1.4% and 2.8% isoflurane anesthesia was assessed. Dogs were initially anesthetized with thiopental (12 mg/kg, iv bolus), their tracheae intubated, after which anesthesia was maintained with 1.4% isoflurane. In eight animals three levels of PaCO2 (25, 40, and 60 mmHg) were studied during 1.4% and 2.8% isoflurane. Mean arterial blood pressure, sagittal sinus pressure, and cerebrospinal fluid pressure were measured and CBF was determined using radiolabeled microspheres. Cerebral perfusion pressure (CPP) was maintained constant at approximately 80 mmHg by inflation of a balloon in the midthoracic aorta. CBF during normocapnia was 70 +/- 14 and 118 +/- 18 ml.min-1.100 g-1 with 1.4% and 2.8% isoflurane, respectively. As PaCO2 was decreased and increased, CBF decreased and increased to 42 +/- 7% and 185 +/- 16% of control, respectively, during 1.4% isoflurane. During 2.8% isoflurane, hypocapnia decreased CBF to 39 +/- 6% of control, but CBF did not increase with hypercapnia. In a second group of animals (n = 8), the effects of changes in CPP during hypercapnia with 1.4% and 2.8% isoflurane were assessed. Increasing CPP approximately 25 mmHg with both 1.4% and 2.8% isoflurane increased CBF but did not change CVR from control. With 1.4% isoflurane, the cerebral vasculature constricts with hypocapnia and dilates with hypercapnia, whereas with 2.8% isoflurane, vasoconstriction to hypocapnia is retained but vasodilation to hypercapnia is absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebrovascular responsiveness to carbon dioxide in dogs with 1.4% and 2.8% isoflurane. 249 63

1. Cerebral blood flow was measured in 17 baboons, anaesthetized with pentobarbitone, paralysed with gallamine and mechanically ventilated and in which the right sinus and both aortic nerves had been cut and the left carotid sinus vascularly isolated. Later in each experiment, the head was artificially perfused with femoral arterial blood via the innominate artery.2. Stimulation of the carotid body chemoreceptors with venous blood invariably caused a rise in regional cerebral blood flow whether the head was naturally or artificially perfused. This response was almost completely abolished if the VIIth cranial nerves were cut intracranially.3. Regional cerebral blood flow varied inversely with carotid sinus pressure.4. After the remaining (left) sinus nerve had been cut, the cerebral vascular response to hypoxia was negligible and the response to hypercapnia was markedly reduced. Blood flow then varied with perfusion pressure.5. These results provide further evidence that cerebral blood vessels are reflexly controlled and that the peripheral arterial receptors are involved. Their action is most conspicuous in the vascular response to hypoxia and together with intrinsic factors in the cerebral vascular bed, they determine the size of the vascular response to changes in CO(2) and pressure.
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PMID:The role of the carotid body chemoreceptors and carotid sinus baroreceptors in the control of cerebral blood vessels. 420 55

1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. One week after the blood injections were started there was about 10-20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of PaCO2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.
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PMID:Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates. 682 30

Systems analysis of the systemic arterial (SAPW), cerebrospinal fluid (CSFPW), and sagittal sinus (SSPW) pulse waves was carried out in 13 dogs during hypercapnia (5% CO2), intracranial normotension (inhalation of 100% O2), and intracranial hypertension (inhalation of 100% O2 plus an intraventricular infusion). Power amplitude and phase spectra were determined for each wave, and the power amplitude and phase transfer functions calculated between the cerebrospinal fluid (CSF) pressure and systemic arterial pressures, and between the sagittal sinus pressure and CSF pressure. The study indicates that the CSFPW and SSPW were virtually identical when impedance between the cerebral veins and sagittal sinus was minimal, which argues that the CSF pulse was derived from the cerebral venous bed. During inhalation of 100% O2, transmission of the SAPW across the precapillary resistance vessels into the cerebral venous pulse (as represented by the CSFPW) was nonlinear, while transmission across the lateral lacunae into the sagittal sinus was linear. During intracranial hypertension, wave transmission across the precapillary resistance vessels was linear, and across the lateral lacunae was nonlinear. During hypercapnia, wave transmission across the precapillary resistance vessels and the lateral lacunae was linear. When the wave transmission was nonlinear, there was also suppression in transmission of the lower harmonics, particularly the fundamental frequency, and a more positive phase transfer function, suggesting an inertial effect or decrease in acceleration of the pulse. Conversion from a nonlinear to linear transmission across the precapillary resistance vessels is evidence of loss of vasomotor tone, and is accompanied by rounding of the CSFPW. A vascular model which encompasses the above data and is based on flow in collapsible tubes and changes in vasomotor tone is posited to explain control of pulsatile flow and pulse waveform changes in the cerebrovascular bed. The model helps to clarify the strong interrelationship between intracranial pressure, cerebral blood flow, and cerebral autoregulation.
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PMID:Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation. 706 79

Superior sagittal sinus pressure, intracranial pressure and arterial pressure were recorded in an experimental series on 10 cats. During drug-induced, severe, acute arterial hypertension and parallel hypercapnia, venous pressure could exceed intracranial pressure in both the supra- and infratentorial compartment. From these data it is concluded that cerebral venous pressure during acute arterial hypertension may contribute to protein extravasation at the postcapillary-venular level.
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PMID:Cerebral venous pressure during actively induced hypertension and hypercapnia in cats. 736 47

Asphyxia, which occurs during obstructive sleep apnoeic events, alters the baroreceptor reflex and this may lead to hypertension. We have recently reported that breathing an asphyxic gas resets the baroreceptor-vascular resistance reflex towards higher pressures. The present study was designed to determine whether this effect was caused by the reduced oxygen tension, which affects mainly peripheral chemoreceptors, or by the increased carbon dioxide, which acts mainly on central chemoreceptors. We studied 11 healthy volunteer subjects aged between 20 and 55 years old (6 male). The stimulus to the carotid baroreceptors was changed using graded pressures of -40 to +60 mmHg applied to a neck chamber. Responses of vascular resistance were assessed in the forearm from changes in blood pressure (Finapres) divided by brachial blood flow velocity (Doppler) and cardiac responses from the changes in RR interval and heart rate. Stimulus-response curves were defined during (i) air breathing, (ii) hypoxia (12% O(2) in N(2)), and (iii) hypercapnia (5% CO(2) in 95% O(2)). Responses during air breathing were assessed both prior to and after either hypoxia or hypercapnia. We applied a sigmoid function or third order polynomial to the curves and determined the maximal differential (equivalent to peak sensitivity) and the corresponding carotid sinus pressure (equivalent to 'set point'). Hypoxia resulted in an increase in heart rate but no significant change in mean blood pressure or vascular resistance. However, there was an increase in vascular resistance in the post-stimulus period. Hypoxia had no significant effect on baroreflex sensitivity or 'set point' for the control of RR interval, heart rate or mean arterial pressure. Peak sensitivity of the vascular resistance response to baroreceptor stimulation was significantly reduced from -2.5 +/- 0.4 units to -1.4 +/- 0.1 units (P < 0.05) and this was restored in the post-stimulus period to -2.6 +/- 0.5 units. There was no effect on 'set point'. Hypercapnia, on the other hand, resulted in a decrease in heart rate, which remained reduced in the post-stimulus period and significantly increased mean blood pressure. Baseline vascular resistance was significantly increased and then further increased in the post-control period. Like hypoxia, hypercapnia had no effect on baroreflex control of RR interval, heart rate or mean arterial pressure. There was, also no significant change in the sensitivity of the vascular resistance responses, however, 'set point' was significantly increased from 74.7 +/- 4 to 87.0 +/- 2 mmHg (P < 0.02). This was not completely restored to pre-stimulus control levels in the post-stimulus control period (82.2 +/- 3 mmHg). These results suggest that the hypoxic component of asphyxia reduces baroreceptor-vascular resistance reflex sensitivity, whilst the hypercapnic component is responsible for increasing blood pressure and reflex 'set point'. Hypercapnia appears to have a lasting effect after the removal of the stimulus. Thus the effect of both peripheral and central chemoreceptors on baroreflex function may contribute to promoting hypertension in patients with obstructive sleep apnoea.
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PMID:Interaction of chemoreceptor and baroreceptor reflexes by hypoxia and hypercapnia - a mechanism for promoting hypertension in obstructive sleep apnoea. 1610 27


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