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

The authors discuss the gross and microscopic anatomy and the physiology of the cerebral venous system. Cerebral veins under pathological circumstances (hypercapnia, arterial hypertension, and increased intracranial pressure), pharmacological observations, the venous blood-brain barrier, and traumatic involvement are reviewed. Neoplastic involvement and radiological aspects are included. Surgical reconstruction of venous sinuses (including the Donaghy technique), tumor removal, sinus thrombectomy, and extraanatomical bypass of the transverse sinus are discussed.
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PMID:The cerebral venous system. 390 42

The purpose of this study was to examine regional autoregulation of blood flow in the brain during acute hypertension. In anesthetized cats severe hypertension increased blood flow more in cerebrum (159%) and cerebellum (106%) than brain stem (58%). In contrast to the heterogeneous autoregulatory response, hypocapnia produced uniform vasoconstriction in the brain. We also compared vasodilatation during severe hypertension with vasodilatation during hypercapnia. During hypercapnia, blood flow increased as much in brain stem, as in cerebrum and cerebellum. Thus regional differences in autoregulation appear to be specific for autoregulatory stimulus and are not secondary to nonspecific differences in vasoconstrictor or vasodilator capacity. To determine whether the blood-brain barrier is more susceptible to hypertensive disruption in regions with less effective autoregulation, permeability of the barrier was quantitated with 125I-albumin. Severe hypertension produced disruption of the barrier in cerebrum but not in brain stem. Thus there are parallel differences in effectiveness of autoregulation and susceptibility to disruption of the blood-brain barrier in different regions of the brain.
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PMID:Heterogeneity of brain blood flow and permeability during acute hypertension. 392 26

This study describes the case of a 58 year old man who presented with an episode of acute respiratory failure and right heart decompensation. After recovery from the acute illness, hypoxaemia, hypercapnia and pulmonary arterial hypertension remained, the causes of which were not known. There was no airway obstruction, only a moderate restrictive ventilatory defect, a little weight increase and a unilateral diaphragmatic paralysis. Obstructive sleep apnoea was finally suspected and confirmed by sleep recording. The obstructive sleep apnoea probably explained the respiratory insufficiency and the pulmonary hypertension. Loss of weight was associated with the disappearance of hypercapnia and pulmonary hypertension. As a result of this study, the value of sleep recording is emphasized. When respiratory failure or pulmonary hypertension seem unexplained, think of obstructive sleep apnoea.
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PMID:[Value of sleep polygraph examination in the etiological diagnosis of apparently inexplicable respiratory insufficiency]. 404 63

The development of important respiratory disorders and significant hypertension in association with increasing body weight is not widely recognized. Altered respiratory function results from a combination of mechanical impedance to breathing exerted by thoracic and abdominal fat and a ventilation-perfusion mismatch. Sleep-disordered breathing with periods of hypoventilation, with or without apnoeic episodes, may commonly occur in patients with extreme obesity. Nocturnal hypercapnia and hypoxia in such patients may lead to a decrease in ventilatory drive, abnormal central respiratory control and possibly, in time, the development of the obese-hypoventilation syndrome. Respiratory abnormalities should be suspected in obese patients with a history of restlessness at night, loud snoring and daytime somnolence. Treatment is substantial weight reduction, but short-term measures include the use of compressed air via nasal cannulae for obstructive apnoea, and drugs which alter sleep pattern or stimulate respiration. The alterations in endocrine function, which accompany weight gain, may contribute to an increase in blood pressure and there appears to be a relationship between plasma insulin and catecholamine concentrations, fat cell size and the development of hypertension. The confirmation of a raised blood pressure requires that readings be taken with an adequately sized arm-cuff. In many instances endocrine function becomes normal with weight loss, and there is a corresponding decrease in blood pressure. The ideal management for an obese hypertensive patient is the combination of a suitable calorie-restricted diet with a programme of physical exercise.
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PMID:Clinical complications of obesity. 639 58

Although it is known that hypercarbia increases and benzodiazepines decrease cerebral blood flow (CBF), the effects of benzodiazepines on CBF responsiveness to CO2 are not well documented. The influence on CBF and CBF-CO2 sensitivity of placebo or midazolam, which is a new water-soluble benzodiazepine, was measured in eight healthy volunteers using the noninvasive 133Xe inhalation method for CBF determination. Under normocarbia, midazolam decreased CBF from 40.6 +/- 3.2 to 27.0 +/- 5.0 ml 100 g-1 min-1 (means +/- SD). At a later session under hypercarbia, CBF was 58.8 +/- 4.4 ml 100 g-1 min-1 after administration of placebo, and 49.1 +/- 10.2 ml 100 g-1 min-1 after midazolam. The mean of the slopes correlating PaCO2 and CBF was significantly steeper with midazolam (2.5 +/- 1.2 ml 100 g-1 min-1 mm Hg-1) than with placebo (1.5 +/- 0.4 ml 100 g-1 min-1 mm Hg-1). Our results suggest that midazolam may be a safe agent to use in patients with intracranial hypertension, since it decreases CBF and thus cerebral blood volume; however, it should be administered with caution in nonventilated patients with increased intracranial pressure, since its beneficial effects on cerebrovascular tone can be readily counteracted by the increase in arterial CO2 tension induced by this drug.
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PMID:Effects of midazolam on cerebral hemodynamics and cerebral vasomotor responsiveness to carbon dioxide. 640 14

In order to determine the relative roles of O2 tension and content, CO2 tension, hydrogen ion concentration, arterial blood pressure, and cardiac output in the regulation of fetal cerebral blood flow (CBF), we used radioactively labeled microspheres to measure flow to 20 major brain regions in 24 chronically catheterized fetal lambs. We continually monitored fetal heart rate and blood pressure, and periodically measured arterial PO2, PCO2, pH, and hematocrit. In addition to CBF measurements during control periods, we measured CBF during: 1) hypoxia (O2 content less than 6 ml X dl-1; O2 tension less than 15 torr) induced by having the ewe breathe a gas mixture with low O2 concentration, 2) hypercapnia (PCO2 greater than 50 torr) induced by increasing the maternal inspired CO2, 3) acidosis and alkalosis (7.60 greater than pH greater than 6.60) induced by infusing lactic acid or bicarbonate into the fetus, and 4) hypotension (blood pressure less than 35 mm Hg) and hypertension (blood pressure greater than 55 mm Hg) induced by rapidly phlebotomizing or transfusing the fetus. We used multiple regression analysis and analysis of covariance to examine the dependence of total cerebral blood flow on arterial O2 tension and content, CO2 tension, pH, blood pressure, and cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral blood flow: studies in the fetal lamb during hypoxia, hypercapnia, acidosis, and hypotension. 644 Nov 42

The major immediate goal in the treatment of a patient with central nervous system injuries is to prevent secondary injuries resulting from hypotension, hypoxemia, hypercapnia, intracranial hypertension, infection, and unnecessary motion of an unstable spinal column. This combined with application of the fundamentals of trauma resuscitation should achieve optimal results.
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PMID:Acute resuscitation of the patient with head and spinal cord injuries. 644 3

Little is known about the function of cholinesterase activity present in the walls of cerebral microvessels. It has been shown that systemically administered physostigmine, a cholinesterase inhibitor that penetrates the blood-brain barrier, causes barrier opening. This has led to suggestions that perivascular cholinesterase is involved in the maintenance of morphological blood-brain barrier function. The present study demonstrates that the physostigmine-induced barrier opening is fully attributable to the acute hypertension and hypercapnia the agent gives rise to. Thus, it is discussed whether the enzyme activity may function as an enzymatic barrier to cholinergic agents.
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PMID:Perivascular cholinesterase and morphological blood-brain barrier function. 651 93

The effect of unilateral, electrical stimulation of the cervical sympathetic chain in rabbits anesthetized with pentobarbital sodium and vasodilated by hypercapnia, acetazolamide, papaverine or PGI2 was investigated to determine to what extent the sympathetic nerves to the brain and the eye cause vasoconstriction and prevent overperfusion in previously vasodilated animals. Evans blue was given as a tracer for protein leakage. Blood flow determinations were made with the labelled microsphere method during normotension and acute arterial hypertension. Hypertension was induced by ligation of the thoracic aorta and in some animals metaraminol or angiotensin was also used. Acetazolamide caused a two to threefold increase in cerebral blood flow (CBF) and hypercapnia resulted in a fivefold increase. CBF was not markedly affected by papaverine or PGI2. In the choroid plexus, the ciliary body and choroid, papaverine and hypercapnia caused significant blood flow increases on the control side. Sympathetic stimulation induced a 12% blood flow reduction in the brain in normotensive, hypercapnic animals. Marked effects of sympathetic stimulation at normotension were obtained under all conditions in the eye. In the hypertensive state the CBF reduction during sympathetic stimulation was moderate, but highly significant in hypercapnic or papaverine-treated animals as well as in controls. Leakage of Evans blue was more frequently seen on the nonstimulated side of the brain. In the eye there was leakage only on the control side except in PGI2-treated animals where 2 rabbits had bilateral leakage. The effect of sympathetic stimulation on the blood flow in the cerebrum and cerebellum in vasodilated animals seems to be small or absent if the blood pressure is normal. In the eye pronounced vasoconstriction occurs under these conditions. In acute arterial hypertension sympathetic stimulation protects both the cerebral and ocular barriers even under conditions of marked vasodilation.
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PMID:Effects of sympathetic stimulation on cerebral and ocular blood flow. Modification by hypertension, hypercapnia, acetazolamide, PGI2 and papaverine. 675 90

The existence of treatable postischemic (PI) changes which influence neurological outcome has been documented by this group before. A global brain ischemia model without cardiac arrest was developed in monkeys. It includes high-pressure neck tourniquet inflation plus hypotension for a reproducible ischemic insult; survival with reproducible neurological deficit (ND) under continuous PI life-support for 7 days with control of extracranial variables; and new ND and histopathological damage scoring systems. Hypoxemia, hypercarbia, hypotension, uremia, sepsis, and other extracranial complications PI in 50 unsatisfactory experiments led to immediate worsening in ND and brain death (ND = 100%) in most of these monkeys. In contrast, all monkeys with the same initial insult, with life-support according to protocol, survived with a 7 day ND of 60% or less. In 46 experiments of seven treatment groups, after 16 or 18 min ischemia, life support was according to protocol for 7 days. The control 1 protocol (spontaneous breathing when feasible) resulted in a mean 7-day ND score of 53% (including quadriplegia). Immobilization with pancuronium and controlled ventilation ameliorate deficit to an ND score of 19% (P less than 0.05) (including quadriparesis); this became control 2 protocol. Immobilization resulted in less neuronal damage in the neocortex. Severe repetitive hypertension worsened ND to 46%, versus 19% in controls (P less than 0.05). In separate series, neither heparinization over 72 hours PI, nor hemodilution to hematocrit 25% with dextran 40, changed final ND significantly from that of their control groups. Histopathological damage scores correlated with ND scores.
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PMID:Effect of postcirculatory-arrest life-support on neurological recovery in monkeys. 676 78


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