Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maintenance of cerebral perfusion pressure is a prerequisite for the prevention of cerebral ischemia. Physiological fluctuations in systemic perfusion pressure are compensated by cerebrovascular autoregulation. Cerebral hypoperfusion could result from (1) systemic hemodynamic failure (eg, distal to severe arterial stenosis), overcharging the vasoregulatory capacity; (2) dysfunction and exhaustion of cerebrovascular autoregulation; or (3) both. Ultrasound offers an excellent temporal resolution, is noninvasive, and is easily applicable for follow-up investigations. Despite its poor spatial resolution, transcranial Doppler sonography has been used for determination of cerebral perfusion reserve studies measuring cerebral blood flow velocity (CBFV) during hypercapnia or application of vasoactive agents (eg, acetazolamide). This approach evaluates vasomotor regulation in patients with hemodynamic compromise distal to severe stenosis or occlusion of the brain supplying arteries. Monitoring CBFV during tilt table examinations directly measures cerebral autoregulation. In patients with systemic orthostatic hypotension, maintainance or failure of cerebrovascular compensation and, even more importantly, cerebrovascular dysautoregulation, despite normal systemic blood pressure regulation, may be demonstrated. Vasoneuronal coupling is reflected by CBFV variations during appropriate neuronal stimulation. Neuronal dysfunction is associated with CBFV abnormalities as exemplified by preconditions of focal cerebral dysfunction in the posterior cerebral artery (PCA) in migraineurs with aura, where massive alteration of vasoneuronal coupling and ischemia is threatening during spreading depression. A highly significant asymmetric gain of vasoneuronal coupling in the interictal state may act as a trigger mechanism in these patients. Testing for vasoneuronal coupling within the middle cerebral artery (MCA) territory is more difficult due to the poor spatial resolution with various neuronal stimuli (eg, motorsensory or cognitive paradigms), only eliciting local neuronal areas underrepresented in the MCA CBFV global changes. However, motor stimulation evoked CBFV may be used to indicate dysintegration of vasoneuronal coupling in the course of acute cerebral ischemia with sensorimotor hemiparesis and, moreover, seems to be of prognostic value regarding the motor deficit.
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PMID:Cerebrovascular regulation and vasoneuronal coupling. 769

This review summarizes evidence in humans for an association between hyperventilation (HV)-induced hypocapnia and a reduction in cerebral perfusion leading to syncope defined as transient loss of consciousness (TLOC). The cerebral vasculature is sensitive to changes in both the arterial carbon dioxide (PaCO2) and oxygen (PaO2) partial pressures so that hypercapnia/hypoxia increases and hypocapnia/hyperoxia reduces global cerebral blood flow. Cerebral hypoperfusion and TLOC have been associated with hypocapnia related to HV. Notwithstanding pronounced cerebrovascular effects of PaCO2 the contribution of a low PaCO2 to the early postural reduction in middle cerebral artery blood velocity is transient. HV together with postural stress does not reduce cerebral perfusion to such an extent that TLOC develops. However when HV is combined with cardiovascular stressors like cold immersion or reduced cardiac output brain perfusion becomes jeopardized. Whether, in patients with cardiovascular disease and/or defect, cerebral blood flow cerebral control HV-induced hypocapnia elicits cerebral hypoperfusion, leading to TLOC, remains to be established.
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PMID:Hyperventilation, cerebral perfusion, and syncope. 2426 79