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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the relationship between the degree of hypertension and experimentally-induced cerebral ischemia, brain metabolites, including lactate, pyruvate and adenosine triphosphate (ATP) were determined one hour after bilateral carotid occlusion in 119 spontaneously hypertensive rats (SHR) with a variety of mean arterial pressures (MAP). Of these, 36 SHR were given antihypertensive agents for 10 weeks to reduce blood pressure prior to the experiment. There was a significant linear correlation between MAP before and either supratentorial lactate (r = 0.482, p less than 0.001) or the lactate/pyruvate ratio (r = 0.388, p less than 0.001) in the brain after carotid occlusion. An inverse correlation was observed between supratentorial lactate and either ATP (r = -0.627, p less than 0.001) or arterial PCO2 (r = -0.477, p less than 0.001) after carotid occlusion. The changes suggest that the animals with a higher MAP had a greater increase in ischemic metabolites with a decrease in ATP and a more pronounced hypocapnia after carotid occlusion. This hypocapnia is believed to be due to hyperventilation induced by cerebral ischemia. It is concluded that hypertensive rats are more susceptible to cerebral ischemia and the susceptibility is related to the degree of hypertension. By long-term lowering of the blood pressure prior to carotid occlusion, the ischemic changes are lessened in this experimental model.
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PMID:Experimental cerebral ischemia in spontaneously hypertensive rats (SHR): Importance of degree of hypertension. 678 15

1 Because they affect isolated cerebral arteries, some calcium antagonists have been studied on the intact cerebral circulation of the rat.2 Global cerebral blood flow ((133)Xe clearance technique) was measured in anaesthetized rats. Neither perhexiline (0.1 mug/kg to 1.0 mg/kg, i.v.) nor diltiazem (0.06-0.6 mg/kg, i.v.) had any significant effect on resting cerebral blood flow when measured 5 min after each dose. A high dose of nifedipine (1.0 mg/kg, i.v.) was administered during induced hypocapnia. Nifedipine failed to modify the hypocapnic vasoconstriction of the cerebral vasculature when compared to vehicle-treated rats.3 The possibility of discrete changes in regional cerebral blood flow was investigated. Local cerebral blood flow was measured in a number of brain regions by the [(14)C]-ethanol technique 15 min after the administration of nifedipine (20 or 100 mug/kg, i.v.). Nifedipine had no apparent effect on regional blood flow in the rat brain.4 Acute arterial hypertension increases protein leakage into the brain, a phenomenon susceptible to drugs that act on endothelial pinocytosis which is known to be calcium-dependent. The increase in protein extravasation, induced by the intravenous administration of either angiotensin II or adrenaline, was unchanged in rats previously treated with either nimodipine (20 mug/kg, i.v.) or nifedipine (50 mug/kg, i.v.) when dissolved in ethanol alone. However, nifedipine (20 mug/kg, i.v.) when dissolved in a solution of polyethylene glycol and ethanol further enhanced the hypertension-induced increase in brain albumin permeability.5 In conclusion, we have been unable to demonstrate any apparent effects of various calcium antagonists on the intact cerebral circulation of the rat, despite the number of different experimental models used.
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PMID:Calcium antagonists: effects on cerebral blood flow and blood-brain barrier permeability in the rat. 687 38

Acute severe hypertension induced by intravenous norepinephrine or angiotensin in anesthetized cats equipped with a cranial window caused prolonged arteriolar vasodilation associated with reduced responsiveness to arterial hypercapnia or hypocapnia and passive response to changes in arterial blood pressure. Scanning and transmission electron microscopy of such pial arterioles showed discrete destructive endothelial lesions the density of which correlated with the degree of vasodilation. Abnormalities of the vascular smooth muscle were seen in all dilated arterioles but affected only a small number of smooth muscle cells. The oxygen consumption of pial arterioles from cats subjected to hypertension was significantly reduced in comparison to that of vessels from normal animals. The arteriolar abnormalities induced by hypertension were inhibited by pretreatment with inhibitors of cyclooxygenase (indomethacin or AHR-5850) or by topical application on the brain surface of scavengers of free oxygen radicals (mannitol or superoxide dismutase). The results suggest that the mechanism of the arteriolar abnormalities from acute hypertension involves a sudden increase in prostaglandin synthesis that leads to generation of free oxygen radicals.
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PMID:Mechanism of cerebral arteriolar abnormalities after acute hypertension. 722 3

Varying degrees of respiratory distress developed in 3 dogs in which hyperadrenocorticism was diagnosed. The respiratory distress was attributed to pulmonary artery thrombosis. Radiography revealed pleural effusion, increased diameter and blunting of the pulmonary arteries, lack of perfusion of the obstructed pulmonary vasculature, and overperfusion of the unobstructed pulmonary vasculature. Thrombosis was confirmed by nonselective angiocardiography in each case. In 1 case, selective angiocardiography showed marked reduction of the transit time of contrast medium from the right atrium to the aorta. Hypertension proximal to the site of thrombosis was confirmed in 2 cases by showing increases in the right ventricular systolic pressures (80 mm of Hg in one case and 54 mm of Hg in the other case). In 3 cases, there was moderate hypoxemia with hypocapnia, suggesting a ventilation-perfusion mismatch. Clinical findings other than respiratory distress included hepatomegaly, ventral edema, orthopnea, and a jugular pulse. Pulmonary artery thrombosis, as it occurred in these 3 cases, was compared with the disease in man. It was concluded that pulmonary artery thrombosis should be suspected in cases of intractable dyspnea, right-sided heart failure of unexplained origin, and acute unexplainable death.
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PMID:Pulmonary artery thrombosis in three dogs with hyperadrenocorticism. 723 99

We have developed a method for virtually continuous measurement of changes in cerebral blood flow (CBF) in cats and dogs. CBF was computed by multiplying cross-sectional area (CSA) and mean blood velocity in a pial artery. CSA was determined by measuring pial artery diameter with an electronic micrometer every 2-4 s through a cranial window. Velocity was measured continuously with a pulsed Doppler crystal positioned under a pial artery. CBF was determined in 12 anesthetized cats during 1) control, 2) hypocapnia, 3) hypercapnia, and 4) hypercapnia plus hypertension. Microspheres were injected under steady-state conditions to compare the two methods. During control, the diameter of the cerebral arteries observed was 388 +/- 28 (SE) micrometers, and CBF measured with microspheres was 40 +/- 4 ml.min-1.100 g-1. CBF decreased 18 +/- 2% during hypocapnia and increased 152 +/- 36% during hypercapnia. During steady-state conditions, the correlation coefficient between changes in CBF (CSA X velocity and microspheres) was 0.94, and the slope of the regression line was 1.02. In similar studies on seven anesthetized dogs, the correlation coefficient between CSA X velocity and microspheres was 0.98, and the slope of the regression line was 0.94. We conclude that the product of CSA and blood velocity of a pial artery provides accurate on-line measurement of changes in CBF.
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PMID:Continuous measurement of cerebral blood flow in anesthetized cats and dogs. 727 Jul 11

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74

The management of brain swelling that frequently occurs following severe traumatic brain injury (TBI) presents a difficult challenge for physicians treating these patients. A traditional cornerstone for the treatment of post-traumatic brain swelling has been prophylactic hyperventilation to reach PaCO2 levels of 25 to 28 torr. While there are anecdotal reports of improvement in intracranial pressure (ICP) and neurologic functioning following institution of this therapy, the only prospective, randomized trial of its use has found worse outcomes in those treated with prophylactic hyperventilation therapy for 5 days. That hyperventilation therapy might exacerbate secondary brain injury seems likely based on abnormalities in cerebral blood flow (CBF) and metabolism which result from TBI, and the potential for hyperventilation to worsen those abnormalities. Both global and regional CBF are critically reduced, and metabolism increased, during the first several hours and days after injury. As a result, focal ischemia is common following severe TBI. Hyperventilation causes a further decrease in CBF, often without a concomitant reduction in ICP. In some cases, TBI also causes an increase in cerebral vascular responsivity to hypocapnia, increasing the drop in regional CBF that occurs with hyperventilation. Thus, there is a well defined physiologic basis for expecting hyperventilation to cause worsened clinical outcomes following TBI. While this therapy clearly is indicated for the management of acute neurologic deterioration or intracranial hypertension refractory to all other forms of medical therapy, hyperventilation is no longer recommended as a first-line therapy for intracranial hypertension or as prophylactic therapy following severe TBI.
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PMID:Hyperventilation therapy for severe traumatic brain injury. 749 52

Deliberate hypocapnia during the anaesthetic management of the patient undergoing craniotomy has become an accepted standard of care. However there has been a resurgence of interest, in how hypocapnia should be applied in intra- and extra-operative settings. There are three possible therapeutic effects of hypocapnia, namely, (a) reduction of brain bulk through a reduction in cerebral blood volume, with a decrease cerebral blood flow; (b) developing an "inverse steal" by redistribution of blood from normal to ischaemic regions and (c) acting to offset cerebral acidosis by increasing pH in the extracellular space. In anaesthetic intraoperative practice, hypocapnia is used as a specific treatment of, or prophylaxis against, intracranial hypertension during induction of anaesthesia and the period before dural exposure. More commonly, hypocapnia is used for intraoperative brain relaxation (intracranial pressure = 0). Severe hypocapnia (< 20 mmHg) may result in cerebral production of lactate; however no studies have shown that a Paco2 in the range of 23-28 mmHg has deleterious effects. Recent studies in head-injured patients suggest that routine long-term hyperventilation, without an objective index of cerebral flow/metabolism coupling, may place the brain at risk for adverse outcome. The few data available for intraoperative management suggest that Paco2 figures of 30-35 mmHg result in acceptable operating conditions. Unless otherwise specifically indicated by surgical conditions or cerebral flow/metabolism coupling (e.g. jugular O2 saturation), routine application of profound (Paco2 < 28-30 mmHg) hyperventilation should probably be avoided and its use needs reevaluation.
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PMID:[Is there still a place for routine deep hypocapnia in intracranial surgery?]. 767 90

Cerebral vasodilation in response to hypotension is necessary to maintain adequate cerebral blood flow. This study in newborn pigs examines the hypothesis that endothelial injury in vivo inhibits cerebral vasodilation in response to hypotension in newborn pigs, thus suggesting that this response is endothelium dependent. Chloralose-anesthetized piglets with closed cranial windows were studied before and after injury caused by light/dye or before and after dye only sham control. Light/dye injury was produced by injecting sodium fluorescein i.v. and passing filtered light from a mercury arc lamp through the cranial window. Measurements of pial arteries and arterioles were made during normotensive and hypotensive periods. Hemorrhagic hypotension (to 50% of the mean arterial control value) caused pial arterial and arteriolar diameters to increase 49 +/- 8% and 66 +/- 8%, respectively. After the light/dye injury, dilation in response to hypotension was absent, whereas dilations in response to isoproterenol and constriction in response to hypertension (3.33 to 4.0 kPa increase in arterial pressure) and hypocapnia were retained. These findings are consistent with the hypothesis that hypotension-induced cerebral arteriolar vasodilation is dependent on endothelial signals influencing adjacent smooth muscle.
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PMID:Light/dye microvascular injury eliminates pial arteriolar dilation in hypotensive piglets. 770 Jul 23

The two major neurological complications of subarachnoid haemorrhage (SAH) due to an intracranial aneurysm are rebleeding and delayed cerebral ischaemia related to cerebral vasospasm. The best way to prevent rebleeding is early surgery. Even when surgery is performed within the first 72 hours posthaemorrhage, the risk of cerebral ischaemia due to vasospasm is high. Conventional medical treatment of cerebral vasospasm includes haemodilution, hypervolaemia and increase of arterial blood pressure. Haemodilution is of limited value as the patients suffering from SAH have usually a low haematocrit. The effectiveness of hypervolaemia is controversial and it may worsen cerebral and pulmonary oedema. Systemic hypertension is an effective therapy of vasospasm, but which can only be used once the aneurysm is controlled. Nimodipine and nicardipine, two calcium antagonists, have a beneficial effect on neurologic outcome following SAH. Today, it is still debated whether the beneficial effect of nimodipine results from the vascular effect of the drug or from a direct cerebral cytoprotective mechanism. Early surgery implies that surgeons operate on brains in acute inflammatory state. Thus, it is mandatory to use peroperative techniques improving cerebral exposure. These techniques include infusion of mannitol, lumbar cerebrospinal fluid (CSF) drainage, administration of anaesthetic agents known to decrease cerebral blood flow (CBF) and hypocapnia. Usually, the effect of CSF drainage is very effective and sufficient by itself. The second objective in the peroperative period is to avoid ischaemia. In areas with decreased flow distal to vasospasm, autoregulation is impaired and CBF is directly dependent on cerebral perfusion pressure. Furthermore, the safe practice of transient clipping of vessels supplying the aneurysm has dramatically reduced the indications of controlled hypotension. During temporary clipping, some authors recommend a pharmacological brain protection using barbiturates, etomidate or propofol, but this practice has not been validated by randomized studies. However, it is generally agreed that the arterial pressure should be increased during temporary clipping to improve collateral blood flow and to maintain it after the aneurysm has been secured. To conclude, together with lumbar CSF drainage and transient clipping, the anaesthetic management of the patients should include: maintenance of the arterial blood pressure close to its preoperative level, maintenance of PaCO2 between 30 and 35 mmHg and of normovolaemia through replacement of fluid and blood losses. After completion of surgery, recovery from anaesthesia should be rapid to allow fast diagnosis of neurological complications. The monitoring of the status of consciousness is the key of the diagnosis of early postoperative complications.
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PMID:[Anesthesia in surgery for intracranial aneurysms]. 781 6


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