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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral ischemia of 15 min was produced in rats by increasing intracranial pressure above the systolic blood pressure level by infusing artificial cerebrospinal fluid into the cisterna magna. Pulmonary edema was prevented by blocking the vasomotor response with a ganglioplegic agent, and reducing the fluid load by peritoneal dialysis. The EEG flattened after 10.1 +/- 1.5 sec. followed by a dilatation of the pupils after 1--2 min. The EEG began to recover in 21 of 32 rats after 8 to 35 min of recirculation. Spectral analysis revealed an initial return of slow waves and spindles followed by continuous fast frequency activity. The EEG did not recover or was secondarily suppressed in 12 animals after a few hours. Electrophysiological recovery depended on the cardiocirculatory and respiratory state, the recovery being optimal in animals with mild hypertension and a normal acid-base status of the blood.
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PMID:Electrophysiological recovery after compression ischemia of the rat brain. 7 50

Clinical pulmonary oedema is often persistent and of sudden onset, suggesting a vicious circle, i.e. positive feedback. It is difficult to produce in animals by any haemodynamic manoeuvres, but the important neurogenic component can be illustrated by acutely increasing cerebrospinal fluid pressure of rabbits to 300 mmHg (40 kPa). Breathing stops virtually at once, and restarts when cerebrospinal fluid pressure is again reduced. With cerebral ischaemia lasting for up to 2 min, all is well; with longer times pulmonary oedema is almost invariable and often eventually fatal, although the animals may otherwise apparently recover. Comparable events sometimes follow subarachnoid haemorrhage in man. A few hypotheses on the pathogenesis of pulmonary oedema in man are offered.
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PMID:Clinical disorders of lung liquid. 104 41

The effects of hyperdynamic therapy on patients with cerebral vasospasm following subarachnoid hemorrhage (SAH), under normal blood pressure (BP) and normal blood volume conditions, are reported. Forty-four patients, who underwent surgery for aneurysms in acute stage, received hydroxyethyl starch (500 ml/day) postoperatively to prevent dehydration. Twenty-four of the 44 patients with prominent SAH on the computed tomographic (CT) scan, anticipating to develop cerebral ischemia due to vasospasm, were given dobutamine (DOB). The BP was maintained within the normal range, and the heart rate was kept below 130/min. In the 24 patients treated with DOB, cerebral blood flow (CBF) was measured repeatedly by the 133Xe intravenous injection method. In 8 of these 24 patients, the cardiovascular function was monitored with Swan-Ganz (S-G) catheters. Twelve of the 44 patients (27%) developed delayed neurological deficits associated with cerebral vasospasm. The neurological deficits were reversed by the administration of DOB, at a dose of 8-25 (average 12.4) micrograms/kg/min. In 43 patients, the ischemic lesions associated with vasospasm did not appear on CT scan and the patients were of normal condition at discharge. However, one patient showed multiple low-density lesions on CT scan. This was because of the failure of hyperdynamic therapy due to pulmonary complications. No case of pulmonary edema or heart failure due to volume overload was noted. In the 24 patients with prominent SAH, CBF increased significantly by up to 20% following DOB administration, although the BP stayed in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperdynamic therapy for cerebral vasospasm. 169 47

Ten minutes of cerebral ischemia was produced in 12 dogs by temporary ligation of the venae cavae and aorta. After reperfusion the dogs received the calcium entry blocker, flunarizine, 6 micrograms/kg infused over a ten minute period. Cerebral blood flow (CBF) and metabolism (CMRO2) were measured pre-ischemia and for 2 h post-ischemia in 6 dogs. At the end of the study brain biopsies were analyzed for cerebral metabolites. Neurologic recovery was evaluated for up to 48 h post-ischemia in an additional 6 dogs. The results of each study were compared to those previously obtained in untreated animals. The cerebral blood flows (when expressed as a percent of the pre-ischemic control value) of the flunarizine-treated and untreated groups were similar throughout the post-ischemic period. Following an initial hyperemia, the CBF fell to significantly less than the pre-ischemic control values, and remained approximately 26% of control during the final 90 min in both groups. The CMRO2 was also the same for both groups. Cerebral metabolites were similar although abnormal in both groups. Flunarizine produced pulmonary edema in 5 of 6 dogs studied for neurologic recovery. Four of these dogs died within 12 h and another dog demonstrated severe neurologic damage. None of the untreated dogs developed pulmonary edema, but 6 of 7 dogs evidenced severe neurologic damage or were dead at 48 h. Thus, flunarizine failed to improve either cerebral blood flow or neurologic outcome when given after complete cerebral ischemia in the dog. A cardiodepressive effect of flunarizine might have contributed to the poor neurologic outcome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Failure of flunarizine to improve cerebral blood flow or neurologic recovery in a canine model of complete cerebral ischemia. 646 59

The role of intracranial hypertension in the genesis of neurogenic pulmonary edema was studied in 25 sheep; cardiopulmonary hemodynamics (aortic, pulmonary arterial, and left atrial pressures and cardiac output) and fluid and protein movement across the pulmonary capillary bed (efferent pulmonary lymph flow and lymph/plasma protein ratio) were monitored. Only when intracranial pressure was raised to equal the baseline mean systemic pressure (75 to 120 Torr) did we observe the expected Cushing response of increased aortic pressure, or any alteration in pulmonary hemodynamics or fluid movement. When pulmonary changes did occur, they included an increase in pulmonary arterial pressure of between 5 and 15 Torr without any notable rise in left atrial pressure, and a sustained doubling of the pulmonary lymph flow with no dilution of the lymph/plasma protein ratio. In 3 additional animals cerebral ischemia alone produced an elevation in systemic pressure (74 Torr over baseline) without change in pulmonary arterial pressure, left atrial pressure, or pulmonary lymph flow. Thus, intracranial hypertension and ischemia both affect systemic pressure, but only the elevated intracranial pressure is followed by changes in the pulmonary circuit. We suggest that these changes in pulmonary vascular pressure, independent of changes in left atrial pressure, produce increased pulmonary transcapillary fluid flux that may result in neurogenic pulmonary edema.
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PMID:Pulmonary lymphatic flow alterations during intracranial hypertension in sheep. 670 58

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

The current report summarized animal models of heatstroke experimentation that advance our current knowledge of therapeutic effects on cerebrovascular dysfunction, hypercoagulable state and/or systemic inflammation with various agents in the setting of heatstroke. This was a narrative review of selected published primary basic literature from MEDLINE for 1973-2006. It was found that rodents shared with humans almost the same heatstroke reactions such as hyperpyrexia, hypotension, hyperventilation, pulmonary edema, hepatic and renal failure, hypercoagulable state, metabolic acidosis, systemic inflammation, and cerebral ischemia, injury and dysfunction. Therefore, the rodent model would allow testing of new therapeutic strategies for heatstroke. It was found that brain cooling produced by infusion of cold (4 degrees C) normal saline via the jugular vein or whole body cooling improved survival during heatstroke by reducing cerebrovascular dysfunction, multiple organ failure, systemic inflammation and hypercoagulable state. However, even under the absence of brain or whole body cooling, these heatstroke reactions still could be reversed by treating with the following agents: (1) free radical scavengers; (2) human recombinant protein C: (3) platonin; (4) hyperbaric oxygen; (5) hydroxyethyl starch, hypertonic solution, or human albumin; (6) glucocorticoids; (7) interleukin-1 receptor antagonists; (8) L-arginine; (9) estrogen; and (10) human umbilical cord blood cells or CD +34 cells. Before initiation of heat stress, prior manipulations with one of the following measures were found to be able to protect against heatstroke syndromes: (1) systemic delivery of inducible nitric oxide synthase inhibitors, mu-opioid receptor antagonists, endothelin-1A receptor antagonists, dopaminergic or serotoninergic nerve depletor or receptor antagonists, or glutamate receptor antagonists; or (2) heat shock protein 72 preconditioning.
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PMID:Prevention and repair of circulatory shock and cerebral ischemia/injury by various agents in experimental heatstroke. 1716 3

Even a trivial increase in intracranial pressure is likely to induce cerebral ischemia, hernia, and neurogenic pulmonary edema in patients with intracranial hypertension. In this article, I have described several issues that are essential for safe perioperative management in patients undergoing neurosurgical procedures for treatment of subarachonoid hemorrhage, and intracerebral and subdural hematoma, as well as relevant information on basic physiology and pathology of the brain.
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PMID:[Risk management for neurosurgical anesthesia]. 1946 90

Subarachnoid hemorrhage (SAH) is a devastating disease with a high incidence of morbidity and mortality. The main aims of therapy are the prevention of rebleeding and the prevention and treatment of delayed cerebral ischemia. SAH is manifested with a variable combination of symptoms and is accompanied by various systemic disturbances, such as cardiac arrhythmias and insufficiency, neurogenic pulmonary edema, and electrolyte disorders.Successful perioperative treatment - apart from the surgical and endovascular techniques - requires solid knowledge and understanding of the regulation of cerebral hemodynamics, and the effects of subarachnoid hemorrhage and other diseases and various drugs, including the anesthetic agents, on it.In the following, the basic principles of neuroanesthesia for patients with SAH are reviewed.
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PMID:Principles of neuroanesthesia in stroke surgery. 1995 81

A two-day-old, full-term male infant was admitted to the neonatal intensive care unit with heart failure. He was found to be non-dysmorphic, with no clinical evidence of sepsis. Physical examination was significant for hepatomegaly, active precordium, pansystolic murmur and hypotension requiring ionotropic support. A cranial bruit was detected on auscultation. Chest radiography revealed cardiomegaly and pulmonary oedema due to heart failure. Electrocardiogram and two-dimensional echocardiography were normal. Magnetic resonance imaging of the brain showed a large vein of Galen malformation, extensive cerebral ischaemia and multiple cerebral infarcts. This case illustrates the importance of auscultation of the cranium to rule out vein of Galen malformation, a potential cause of high-output cardiac failure in neonates in the absence of other common causes of heart failure.
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PMID:Clinics in diagnostic imaging (132). Vein of Galen malformation. 2114 Jan 18


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