Mechanism of encephalogenic heart injury

Eichbaum, F. W.; Gazetta, Ben-Hur

doi:10.1007/bf02047049

Cited by 4 publications

(1 citation statement)

References 1 publication

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“…Cushing [1,2] [3][4][5][6][7][8][9][10][11][12], An acute episode of pulmonary hyperten sion and edema constitutes one of the most serious problems after head injury [10][11][12][13][14][15], In the past, our laboratory had carried out a series of animal experiments on the neural and hemodynamic mechanisms involved in the neurogenic pulmonary edema (NPE) [10,12,[16][17][18][19][20][21][22][23][24][25][26]. This brief review presents and dis cusses early and recent studies on the patho genesis of pulmonary edema induced by cere bral compression (CC) or ICH.…”

Section: Hemodynamic Mechanisms Of Neurogenic Pulmonary Edema Abstractmentioning

confidence: 99%

Hemodynamic Mechanisms of Neurogenic Pulmonary Edema

1995

Neurosignals

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Section: Hemodynamic Mechanisms Of Neurogenic Pulmonary Edema Abstractmentioning

confidence: 99%

Hemodynamic Mechanisms of Neurogenic Pulmonary Edema

1995

Neurosignals

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Morphological Aspects of Myocardial Lesions Associated with Stress

Ferrans¹,

Vleet²

1985

Developments in Cardiovascular Medicine

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Some effects of propranolol on the cardiovascular responses of the monkey to simulated subarachnoid haemorrhage

McIntyre

Petruk

Weir

et al. 1972

Canad. Anaesth. Soc. J.

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StmAaaCHNOm ~EMOnnHAC~ rL~S BF_~N ASSOC~TED with electrocardiographic changes in in the experimental animal) ,z These may vary greatly in eharaoter and them have been changes consisterlt with increased activity of the sympathetic nervous system. Structural changes in the myoeardium have been described that could be produc ~d by a period of sympathetic nervous system overactivity ~ and increased tissue catecholamine levels have been measured following subaraehnoid haemorrhage and other forms of stimulation of the brain in the laboratory animals. 4 The importance of the cateeholamines is also suggested by the abolition of eneephalogenic cardhe arrhythmias in dogs following treatment with reserpine, s The portion of sympathetic nervous activity mediated by B-receptor stimulation has received some a~ention, not only because of the intrinsic interest in the mechanism of these arrhythmias, but because of the effect of rapid arrythmias on cardiac out-put and the possible reduction of cerebral blood flow. Accordingly it seemed of interest to study the effects of the prior administration of propranolol on such changes in cardiac rhythm and cerebral blood Bow as might occur following simulated subarachnoid haemorrhage in the monkey. METHODRhesus monkeys were sedated with intraperitoneal sodium pentobarbital 50 mg/kg body weight and the trachea was intubated. Anaesthesia was maintained with a mixture containing thirty per cent of oxygen in nitrous oxide. The animals were paralyzed with d-tubocurarine, artificially ventilated with a Harvard variable phase ventilator and then surgical preparations were made for measurements of cerebral blood flow, intracranial pressure, and systemic arterial pressure. During this period fluid balance was maintained, blood gases were measured at regular intervals, and normal body temperature was maintained. Four to six hours later, at which time cerebral blood flow was stable and a multichannel Grass encephalograph indicated brain activity consistent with light nitrous oxide anaesthesia, arrangements were made to simuhte a subaraehnoid haemorrhage. This was done by inserting a needle through a hole in the midline of the skull at a point 0.5 cm cephalad to the nasion and manipulatSng its tip alone the floor of the anterior fossa to a point about 0.75 cm anterior to the tubereulum sellae so that it lay in the

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Mechanism of encephalogenic heart injury

Cited by 4 publications

References 1 publication

Hemodynamic Mechanisms of Neurogenic Pulmonary Edema

Hemodynamic Mechanisms of Neurogenic Pulmonary Edema

Morphological Aspects of Myocardial Lesions Associated with Stress

Some effects of propranolol on the cardiovascular responses of the monkey to simulated subarachnoid haemorrhage

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