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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

Profound hypothermia below 20 degrees C achieved by surface cooling using simple ice water bath equipment and deep ether anaesthesia is used with the aid of autonomic nerve blocking agents to obtain cardiac arrest for periods of over one hour for open-heart surgery. Blood levels of ether were between 40.6 mg/dl and 285.7 mg/dl during anaesthesia. No arrhythmia occurred and vital signs were quite stable. Hypocarbia throughout the procedure, severe base deficit after circulatory arrest, spontaneous recovery of metabolic acidosis, and a nearly normal cH+ (pH) were observed. Catecholamine increased moderately after circulatory arrest, but was far below shock levels. Plasma renin activity was markedly elevated but angiotensin II stayed at non-significant levels throughout the procedure. Excess lactate showed no significant change. Hyperglycaemia was noted. The mortality rate was 7.7 per cent and neurological disorders occurred in less than 5.8 per cent of the recent 52 cases.
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PMID:A study of profound hypothermia by surface cooling. 677 40

Changes in body fluid homeostasis during acute hypoxaemia suggest a crucial role of renal function in acclimatization processes. Hypoxaemia stimulates sympathetic nervous activity, and also the cardiovascular system is affected with increases in heart rate and cardiac output. In most subjects, a hypoxic ventilatory response produces hypocapnia and respiratory alkalosis. Acute hypoxaemia depresses aldosterone secretion secondary to a direct effect on adrenal cells. Also plasma renin is decreased in resting hypoxaemic conditions, but the mechanism remains unknown. These hormonal changes may have the advantage of opposing excessive sodium and water retention, which characterizes acute mountain sickness. Short-term isocapnic or hypocapnic hypoxaemia in spontaneously breathing humans causes moderate if any increases in renal blood flow and only minor changes in GFR. In contrast, renal blood flow and GFR decreases during hypercapnic hypoxaemia. Renal clearance studies in humans after 24-48 hours in altitude hypoxia (4,350 m) demonstrate that glomerular and tubular function is only slightly changed in spite of marked depression of the renin-aldosterone system and increased plasma levels of norepinephrine. However, renal vascular tone may increase most probably secondary to the increased adrenosympathetic activity. In the first hours, acute hypoxaemia may induce an increased excretion of sodium and water. Previous studies suggest that the natriuretic response is caused by decreased reabsorption of sodium and bicarbonate in the proximal tubules secondary to the associated hyperventilation and hypocapnia. After 6 hours, sodium and water excretion is normalized or even depressed, dependent on the severity of acute mountain sickness. In view of the prompt increase in sodium and water excretion found during short-term hypoxaemia, the absence of such a response to more prolonged hypoxaemia suggests an adaptive time-dependent course of renal functional changes in hypoxaemia. Taken together, previous studies suggest that effects of acute hypoxaemia on renal haemodynamics are minor compared with effects on cerebral and coronary circulation. This might be the result of an appropriate resetting of autoregulatory mechanisms that would maintain the role of the kidney as a major sense organ to hypoxaemia and, subsequently, as a mediator of plasma volume regulation and erythropoietin synthesis.
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PMID:Effect of hypoxaemia on water and sodium homeostatic hormones and renal function. 859 71