Lung fluid and protein exchange during intracranial hypertension and role of sympathetic mechanisms

Zee, H. van der; Malik, Asrar B.; Lee, B. C.; Hakim, T. S.

doi:10.1152/jappl.1980.48.2.273

Cited by 60 publications

(23 citation statements)

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“…of elevated intracranial pressure (ICP) in animals have almost uniformly found elevation in both systemic and pulmonary pressures [ 5 , 12, 16,20,22 [34), studying intracranial hypertension in sheep, have interpreted their data as being compatible with a change in pulmonary capillary permeability independent of any hemodynamic alterations. This point, however, is controversial.…”

Section: Specific Investigations Into the Cardiovascular Resultsmentioning

confidence: 99%

Pulmonary lymphatic flow alterations during intracranial hypertension in sheep

Simon

Bayne

1984

Annals of Neurology

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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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Section: Specific Investigations Into the Cardiovascular Resultsmentioning

confidence: 99%

Pulmonary lymphatic flow alterations during intracranial hypertension in sheep

Simon

Bayne

1984

Annals of Neurology

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“…In addition, a well-known complication of central nervous catastrophes is neurogenic pulmonary edema [16]. Second, the enhanced sympathic activity directly increases the permeability of the pulmonary capillary system and allows proteins and liquids to leave the intravasal space [17]. After this crucial hyperdynamic episode, a hypodynamic interval follows wherein the perfusion of peripheral organs decreases.…”

Section: Discussionmentioning

confidence: 99%

Organ-specific regulation of pro-inflammatory molecules in heart, lung, and kidney following brain death

Skrabal

Thompson

Potapov

et al. 2005

Journal of Surgical Research

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“…These increases in left atrial and pulmonary artery pressures result in a massive increase in pulmonary capillary pressure, and the accompanying pulmonary edema is a combined result of elevated hydrostatic pressure and structural damage to the capillary endothelium. 25 Stimulation of a-adrenergic receptors can increase the permeability of pulmonary capillaries independent of its hemodynamic effects, 26,27 but the pulmonary edema induced by this mechanism is less severe.…”

Section: Pulmonary Changesmentioning

confidence: 99%

Brain death and its implications for management of the potential organ donor

Bugge

2009

Acta Anaesthesiol Scand

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The systemic physiologic changes that occur during and after brain death affect all organs suitable for transplantation. Major changes occur in the cardiovascular, pulmonary, endocrine, and immunological systems, and, if untreated may soon result in cardiovascular collapse and somatic death. Understanding these complex physiologic changes is mandatory for developing effective strategies for donor resuscitation and management in such a way that the functional integrity of potentially transplantable organs is maintained. This review elucidates these physiological changes and their consequences, and based on these consequences the rationale behind current medical management of brain-dead organ donors is discussed.

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Lung fluid and protein exchange during intracranial hypertension and role of sympathetic mechanisms

Cited by 60 publications

References 0 publications

Pulmonary lymphatic flow alterations during intracranial hypertension in sheep

Pulmonary lymphatic flow alterations during intracranial hypertension in sheep

Organ-specific regulation of pro-inflammatory molecules in heart, lung, and kidney following brain death

Brain death and its implications for management of the potential organ donor

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