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

It is known that cimetidine inhibits the hypoxia-induced increase in cerebral blood flow (CFB) in dogs, but the mechanism of this inhibition is not fully understood. Since the accepted mechanisms explaining the increase in CBF during hypercapnia are very different from those active during hypoxia, acute hypercapnia was induced in 12 conscious dogs in order to study the cimetidine effect in this condition. Six dogs were given i.v. saline (control group) and the other six, i.v. cimetidine (4 mg kg-1). After 15 min, CBF and various muscular blood flow measurements were performed, using the microspheres technique under two conditions: (1) breathing air and (2) after 2 h inhalation of a gas mixture with FiCO2 0.10, FiO2 0.21 in nitrogen. The CBF increase was similar in both series with or without cimetidine. The changes in muscular blood flow were unaffected by the H2-blocker. We conclude that cimetidine has no effect on the CBF and on muscular blood flow during acute hypercapnia.
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PMID:Preserved CO2 response in cerebral and muscular blood vessels during cimetidine treatment. 191 39

The hemodynamic, cerebrovascular, and neurologic effects of hypercapnia with 4% and 6% CO2 were retrospectively reviewed in 217 patients referred for regional CBF (rCBF) procedures. Inhalation of CO2 significantly increased rCBF, blood pressure, and pulse from baseline. The findings suggest a higher incidence of side effects with 6% CO2 concentration and an equivalent vasoreactivity to 4%. We recommend the use of 4% CO2 for hypercapnic stimulation, and present safety guidelines for its use.
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PMID:Safety of hypercapnic challenge: cardiovascular and neurologic considerations. 193 82

Impairment of cerebral autoregulation and development of hyponatraemia are both implicated in the pathogenesis of delayed cerebral ischaemia and infarction following subarachnoid haemorrhage (SAH) but the pathophysiology and interactions involved are not fully understood. We have studied the effects of hyponatraemia and SAH on the cerebral vasomotor responses of the rabbit. Cerebrovascular reactivity to hypercapnia and cerebral autoregulation to trimetaphan-induced hypotension were determined in normal and hyponatraemic rabbits before and 6 days after experimental SAH produced by two intracisternal injections of autologous blood. Hyponatraemia (mean plasma sodium of 119 mM) was induced gradually over 48 h by administration of Desmopressin and intraperitoneal 5% dextrose. Sham animals received normal saline. The cerebrovascular reactivity (% change +/- SD in cortical CBF/mm Hg PaCO2, measured by hydrogen clearance) of hyponatraemic (4.8 +/- 3.0%) and SAH (1.3 +/- 2.0%) animals was significantly less (p less than 0.05) than control (11.6 +/- 4.0%) and sham (8 +/- 2.0%) animals, whereas the reactivity of hyponatraemic-SAH animals was preserved (9.8 +/- 6.0%). Hyponatraemia and SAH alone each significantly impaired CBF autoregulation but their combined effects were not additive. Systemic hyponatraemia impairs normal cerebral vasomotor responses but does not augment the effects of experimental SAH in the rabbit.
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PMID:The effects of hyponatraemia and subarachnoid haemorrhage on the cerebral vasomotor responses of the rabbit. 205 Jul 54

The chemosensitive area on the ventral surface of the brain stem responds to local acidosis by eliciting hyperventilation and to local alkalosis by hypoventilation. The stimulus is conventionally thought to be the hydrogen ion concentration in the area's extracellular fluid. It is pointed out, however, that the elegant studies by Loeschcke & Ahmad have demonstrated that [pH]e and [pH]i are normally tightly and rapidly coupled (Loeschcke & Ahmad, 1980). For this reason, the stimulus might just as well be the intracellular hydrogen ion concentration in the chemoreceptor area. The administration of acetazolamide allows the dissociation of [pH]e from [pH]i. With acetazolamide a sharp acid shift of CSF pH [( pH]c) is measured and in two consonance with this shift a marked increase in CBF is seen. Comparing these two reactions to that obtained with CO2 breathing, it is apparent that 7% CO2 causes about the same decrease in [pH]e and the same increase in CBF. In other words CBF acidosis can quantitatively account for the CBF increase induced by acetazolamide. But CO2 and acetazolamide influence [pH]i quite differently, as CO2 drops [pH]i to almost the same extent as [pH]c, while two recent studies by MR spectroscopy have shown that acetazolamide does not drop [pH]i measurably, if tissue hypercapnia is prevented in artificially ventilated rabbits or by the mild spontaneous hyperventilation caused by acetazolamide in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is central chemoreceptor sensitive to intracellular rather than extracellular pH? 211 40

Cerebral blood oxyhemoglobin (HbO2), deoxyhemoglobin (HbR) and total hemoglobin (Hb) were examined in N2 and CO2 induced hypoxemia by near-infrared spectroscopy and compared with CBF examined by the H2 clearance method. HbO2 and HbR changed more sensitively than total Hb, reflecting the blood volume. Low CO2-loading showed marked increase in CBF with little change of blood volume, and higher CO2-induced hypoxemia was less increased and followed by a crossed after-reaction, probably because of persistent arterial dilatation due to the marked hypercarbia and acidosis. Neck venous compression showed a specific pattern of increased total Hb and HbR with little change in CBF. Thus, for near-infrared spectroscopy the intracranial blood volume may be affected mainly by arterial dilatation with an increase in CBF and venous dilatation with congestion. And Hb fractions of HbO2 and HbR may be influenced by cerebral blood oxygenation as well as the arteriovenous blood volume.
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PMID:Response on near-infrared spectroscopy and of cerebral blood flow to hypoxemia induced by N2 and CO2 in young rabbits. 212 62

Cerebral blood flow in the cat was studied before and after acute bilateral common carotid occlusion under normocapnic and hypercapnic conditions and after induced hypotension. Regional blood flow to different brain structures was studied with the microsphere method. Local blood flow in the caudate nucleus, the cerebral cortex and medulla oblongata was studied with H2-polarography. Although the blood flow to the anterior brain regions is significantly decreased after bilateral common carotid occlusion, their blood supply is kept above ischaemic levels by re-distribution of the vertebrobasilar flow. Cerebrovascular reserve in anterior brain regions, however, is lost as indicated by the severe impairment of both the flow response to hypercapnia and to blood pressure decrease. After bilateral common carotid occlusion paradoxical CO2-reactions, indicating intracerebral steal, were seen in the caudate nucleus. In posterior brain regions resting blood flow, flow-reaction to hypercapnia and to hypotension are better preserved under these conditions. Measurement of the CBF responses to induced hypercapnia is a dependable test for appreciation of cerebrovascular reserve after cerebrovascular occlusion but may be potentially hazardous where local flow is close to ischaemic levels.
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PMID:Cerebrovascular reserve in the cat after acute bilateral carotid occlusion. 245 18

The present study investigates the question of whether increases in CBF induced by hypercapnia in awake rats are accompanied by increases in the number of perfused capillaries. For the detection of perfused capillaries, gamma-globulin-coupled fluorescein isothiocyanate was injected intravenously. In 10 brain structures the density of perfused capillaries per square millimeter was determined from coronal sections using a highly sensitive fluorescent microscopical method that, in contrast to others, avoided air drying of the frozen brain sections. The results showed an inhomogeneous local distribution of the density of perfused capillaries during normo- and hypercapnia. The density of perfused capillaries was unchanged during hypercapnia compared with normocapnia, although blood flow was markedly increased. It is concluded that a capillary recruitment does not exist in the brain during the high-flow situation of hypercapnia.
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PMID:Lack of capillary recruitment in the brains of awake rats during hypercapnia. 210 67

CO2 reactivity of the brain vessels was investigated in 33 patients (Grade I-III after Hunt and Hess) with cerebral vasospasm after an aneurysmal subarachnoid haemorrhage (SAH) and after early operation within 72 hours. In all cases, transcranial Doppler sonography was used to measure flow velocities in the middle cerebral artery (MCA) and internal carotid artery (ICA) and vasomotor reactivity to CO2 changes. Vasospastic conditions lead to higher flow velocities through the narrow segment, lower peripheral stream resistance due to the post-stenotic pressure drop and lower vasodilating capacities of arterioles under hypercapnia. In severe vasospastic conditions, the peripheral stream bed is already maximally dilated and the hypercapnic response is weak. On the other hand, the peripheral vascular bed reacts normally to hypocapnia in all vasospastic situations. Our results point out two dangerous conditions of vasospastic disease: 1) exhaustion of peripheral vasodilating capacities, and 2) hyperventilatory therapy. Both of these situations can result in a reduction of CBF to brain tissue, mainly for two reasons: 1) In the former, a further increase in vasospasm cannot be compensated for anymore when the peripheral arterioles are maximally dilated, and 2) in the latter, hypocapnia produces a strong peripheral vasoconstrictor response with further reduction of CBF.
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PMID:CO2 reactivity of cerebral vasospasm after aneurysmal subarachnoid haemorrhage. 250 Aug 37

Respiratory insufficiency of any cause has significant effects on the nervous system. Headache, mental status changes, papilledema, and numerous motor abnormalities including asterixis are commonly seen. Abnormalities in ventilation and gas exchange result in hypoxia, hypercapnia, and respiratory acidosis, and these, in turn, interfere with cerebral metabolism, increase CBF, and may raise intracranial pressure. Chronic respiratory insufficiency can persist for many months with minimal neurologic symptoms, as numerous compensatory mechanisms, particularly renal, may take effect. Treatment includes restoring adequate ventilation and improving gas exchange and may require tracheal intubation and assisted ventilation. Supplemental oxygen therapy should be carefully monitored, as high rates of flow may suppress the hypoxic drive for respiration and lead to significant carbon dioxide retention. The sleep apnea syndromes are a group of disorders in which abnormal respiratory patterns during sleep result in hypercapnia and hypoxemia. Intermittent obstruction of the upper airway and abnormalities of brainstem respiratory centers cause frequent nocturnal awakenings and apneas in these patients. Treatments vary and include weight loss in obese subjects, respiratory stimulants, tracheostomy, and diaphragmatic pacing. Rapid ascent to high altitudes may result in headache, changes in mental status, papilledema, and other neurologic symptoms in certain individuals: a syndrome known as high-altitude sickness. Hypoxia leading to cerebral edema, nocturnal periodic breathing, and hypobaria produces neurologic symptoms in these individuals. Acetazolamide and dexamethasone may be effective in minimizing symptoms of this disorder. Sustained hyperventilation produces acral and circumoral paresthesias and lightheadedness in anxious individuals and can be maintained by relatively normal ventilatory patterns once established. These symptoms are due to hypophosphatemia and respiratory alkalosis, the latter reducing CBF and causing localized tissue hypoxia. Rebreathing into a paper bag at the first awareness of symptoms is the most effective form of treatment.
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PMID:Neurologic manifestations of pulmonary disease. 267 37

CPP reflects perfusion problems related to increased ICP or inadequate MAP. CPP is a most helpful and practical management tool. The relationship of CBF and CPP depends on cerebral vascular resistance (flow equals pressure divided by resistance). At present, we do not have a practical method to measure vascular resistance or CBV. A close relationship between an increase in CBV and increase in ICP exists. However, the relationship between CBF and ICP is more complex. Whereas CBV is strongly dependent on vasodilation and venous return, CBF is influenced by CPP, vascular resistance, viscosity changes, and focally or diffusely increased ICP. For instance, in hypotensive shock one finds a low CBF with an elevated CBV (and ICP) from vasodilation related to hypercapnia, anoxia, or acidosis. Nevertheless, about two thirds of patients with increased ICP after head injury have increased CBF (hyperemia) and increased CBV. This frequent hyperemia is one rationale for the wide usage of hyperventilation to treat increased ICP. It must be recognized that a group of patients may have ischemia caused by excessive hyperventilation therapy for increased ICP. The PaCO2 must not be allowed to decrease to 20 mmHg or lower, but in some patients a PaCO2 level of 21 to 25 may be predisposing to ischemia. Strong consideration is thus given to monitoring CBF and cerebral oxygen metabolism (arteriovenous oxygen content difference [AVDO2], CMRO2) in states of coma and increased ICP. In such patients, continuous infusion of mannitol may result in improved CBF, and hyperventilation therapy can be less aggressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonsurgical management of increased intracranial pressure. 270 May 10


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