Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoregulation of blood flow denotes the intrinsic ability of an organ or a vascular bed to maintain a constant perfusion in the face of blood pressure changes. Alternatively, autoregulation can be defined in terms of vascular resistance changes or simply arteriolar caliber changes as blood pressure or perfusion pressure varies. While known in almost any vascular bed, autoregulation and its disturbance by disease has attracted particular attention in the cerebrovascular field. The basic mechanism of autoregulation of cerebral blood flow (CBF) is controversial. Most likely, the autoregulatory vessel caliber changes are mediated by an interplay between myogenic and metabolic mechanisms. Influence of perivascular nerves and most recently the vascular endothelium has also been the subject of intense investigation. CBF autoregulation typically operates between mean blood pressures of the order of 60 and 150 mm Hg. These limits are not entirely fixed but can be modulated by sympathetic nervous activity, the vascular renin-angiotensin system, and any factor (notably changes in arterial carbon dioxide tension) that decreases or increases CBF. Disease states of the brain may impair or abolish CBF autoregulation. Thus, autoregulation is lost in severe head injury or acute ischemic stroke, leaving surviving brain tissue unprotected against the potentially harmful effect of blood pressure changes. Likewise, autoregulation may be lost in the surroundings of a space-occupying brain lesion, be it a tumor or a hematoma. In many such disease states, autoregulation may be regained by hyperventilatory hypocapnia. Autoregulation may also be impaired in neonatal brain asphyxia and infections of the central nervous system, but appears to be intact in spreading depression and migraine, despite impairment of chemical and metabolic control of CBF. In chronic hypertension, the limits of autoregulation are shifted toward high blood pressure. Acute hypertensive encephalopathy, on the other hand, is thought to be due to autoregulatory failure at very high pressure. In long-term diabetes mellitus there may be chronic impairment of CBF autoregulation, probably due to diabetic microangiopathy.
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PMID:Cerebral autoregulation. 220 48

The data, concerning anatomy of brain vessels and the main parameters of cerebral blood flow, including vascular dilation (nitric oxide, prostacyclin, endothelial hyperpolarising factor, estrogen, calcitonin) and vascular contracting (thomboxan A2, endotolin) agents, as well the interaction between them have been scrutinized. Emphasized the leeding role of vascular endothelium and nitric oxide in the regulation of cerebral circulation. Analysis have been done of mechanisms of neuron/vascular conjugent, autoregulation of the brain blood flow, effects of functional loading (hyperoxia, hypoxia, hypercapnia, hypocapnia, acidosis) on the cerebral circulation, the different reactions between them in central and peripheral circulations, oxidant stress, inflammantion. Pointed the significance of these data for the pathogenic mechanisms and therapy of cerebral insult, others physiological and pathophysiologic process in the brain.
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PMID:[Brain blood flow and cerebral insult. Part 2. Regulation of cerebral circulation]. 2380 22