Induction of Filtration Edema by Extreme Reduction of Cerebrovascular Resistance Associated with Hypertension

Meinig, G.; Reulen, H. J.; Hadjidimos, A.; Siemon, C.; Bartko, D; Schürmann, K.

doi:10.1159/000114558

Cited by 27 publications

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“…In the injured brain, these autoregulatory mechanisms are often impaired, and large increases in systemic blood pressure are directly referred to the cerebral capillaries, resulting in breakdown of the blood-brain barrier, worsened cerebral edema, and increased ICP 40 . With absence of autoregulatory vasoconstriction, increases in systemic blood pressure may cause increased regional cerebral blood flow and transudation of fluid across the disrupted blood-brain barrier, thus resulting in cerebral edema 41-44 . Furthermore, increased cerebral edema and elevated ICP may impair cerebral perfusion and result in cerebral ischemia 45 .…”

Section: Impact Of Hypertension Following Traumatic Brain Injurymentioning

confidence: 99%

Hypertension After Severe Traumatic Brain Injury: Friend or Foe?

Krishnamoorthy

Chaikittisilpa

Kiatchai

et al. 2017

Journal of Neurosurgical Anesthesiology

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Traumatic brain injury (TBI) is a major public health problem, with severe TBI contributing to a large number of deaths and disability worldwide. Early hypotension has been linked with poor outcomes following severe TBI, and guidelines suggest early and aggressive management of hypotension after TBI. Despite these recommendations, no guidelines exist for the management of hypertension after severe TBI, although observational data suggests that early hypertension is also associated with an increased risk of mortality after severe TBI. The purpose of this review is to discuss the underlying pathophysiology of hypertension after TBI, provide an overview of the current clinical data on early hypertension after TBI, and discuss future research that should test the benefits and harms of treating high blood pressure in TBI patients.

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Section: Impact Of Hypertension Following Traumatic Brain Injurymentioning

confidence: 99%

Hypertension After Severe Traumatic Brain Injury: Friend or Foe?

Krishnamoorthy

Chaikittisilpa

Kiatchai

et al. 2017

Journal of Neurosurgical Anesthesiology

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“…19 ' 24 The results of the present experiments seem to indicate that the reactivity of the cerebral blood vessels is altered in cats who had a hypertensive insult. CBF is about 15% lower than in control cats at normocapnia, and the increase in CBF during hypercapnia is less pronounced ( fig.…”

Section: Discussionmentioning

confidence: 49%

Cerebral Blood Flow in Cats After an Acute Hypertensive Insult With Damage to the Blood-Brain Barrier

Pannier¹,

Leusen²

1975

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Xenon clearance method in anesthetized cats under controlled ventilation. An acute pressure increase in the carotid system increases the cerebrovascular permeability to Evans blue, indicating damage to the blood-brain barrier. In these conditions the reactivity of cerebral blood vessels toward changes in the acid-base balance is altered: the CO 2 reactivity is less pronounced, while the effect of increasing the plasma [HCO 3 ] is more pronounced than in normal cats. Autoregulatory capacity toward moderate alterations in arterial blood pressure or in intracranial pressure is well maintained in these conditions. Additional Key Wordshypertension pH autoregulation intracranial pressure D Evidence, summarized by Lassen, 1 suggests that the cerebrovascular response to CO 2 alterations is the result of extravascular pH changes occurring in brain tissue. In view of this hypothesis, the different diffusion characteristics of CO 2 and HCO 3 through the blood-brain barrier 2 could explain the contrast between the marked effects of acute respiratory changes and the inconsistent effects of acute metabolic changes in blood pH on cerebral blood flow (CBF).3 ' 4 Accordingly, a lesion of the blood-brain barrier could be expected to alter the reactivity of the cerebral vessels toward changes in the acid-base balance. This possibility was investigated in anesthetized cats in which the blood-brain barrier was acutely damaged by an abrupt hypertensive insult. MethodsThe experiments were carried out on adult cats. Under light thiopental anesthesia, the trachea was cannulated; polyethylene catheters were introduced in a femoral vein, femoral artery, and thyroid artery; the surface of the skull was widely exposed, and a needle was placed in the cisterna magna or in a lateral cerebral ventricle. After completion of the surgical preparation the animals were paralyzed with gallamine (Flaxedil®, 5 mg per kilogram per hour) and mechanically ventilated with a gas mixture containing 67.5% N 2 O, 25% O 2 , and 7.5% N 2 . Procaine (2%) was applied locally on the surface of the skin wounds.

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“…However, he also described in the same model, a diffuse water increment unrelated .to tracer-identified vascular leakage. Meinig 7 found a similar diffuse increase in water content confined primarily to white matter following induction of hypertension in dogs. The increase in water content depended on the duration of sustained pressure elevation and did not correspond to areas of Evan's blue dye extravasation, which occurred cortically.…”

Section: Discussionmentioning

confidence: 80%

Brain water alterations after unilateral nephrectomy. A study of regional circulatory factors in squirrel monkeys.

Anderson¹,

Jordan

Jacobson

et al. 1977

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SUMMARY White and regional gray matter distributions of water, blood flow, and the protein tracer pertechnetate were measured in five normal squirrel monkeys. A second group of fire monkeys, which had undergone unilateral nephrectomy six months previously, were found at the time of study to have blood pressures similar to those of the control animals but increased brain water and altered distribution of blood flow which was increased in white matter. No alteration of capillary permeability to the protein tracer attended these changes, which appeared to be influenced by blood pressure.Nephrectomy without hypertension influences brain water content, perhaps because of an effect on cerebral resistance vessels. In hypertensive encephalopathy renal lesions, as well as intraluminal pressure changes, may be related to cerebral edema.THE PATHOGENESIS of hypertensive encephalopathy has been subject to research attention for some time and has recently stirred considerable controversy. Most investigators are in agreement that excess brain water is a critical characteristic of clinical and experimental hypertensive encephalopathy. Keen interest in the behavior of the socalled "blood-brain barrier" has characterized most studies, which have been designed to demonstrate the escape of a variety of protein tracers from vessels subjected to increased intraluminal pressure. The assumption has been made that a surplus of brain water is related to dysfunction of the plasma-brain interface as demonstrated by such tracer leakage. Attention has been directed to the course of events leading to injury of the barrier to tracer.The current study was undertaken with the objective of determining the relationships among water, tracer leakage, and blood flow in identical focal areas of brain in an animal model of chronic hypertension. Despite unilateral nephrectomy and wrapping of the remaining kidney, at the time of sacrifice, the experimental animals did not have blood pressures different on the average from those of control animals. The results, however, demonstrate the presence of increased brain water in the monkeys with nephrectomy and suggest that other factors besides increased intraluminal pressure may be important in experimental and clinical hypertensive encephalopathy. Furthermore, the data suggest that the basic assumption concerning water distribution and its relationship to tracer barriers may be incomplete since these data show increased brain water without evident barrier leakage of the protein tracer. MethodsFive adult male squirrel monkeys (Saimiri sciureus) weighing 780-900 gm underwent unilateral right nephrectomy under sodium pentobarbital anesthesia (25 mg/kg) approximately six months prior to investigation. The remain- ing kidney was compromised by cellophane wrapping at the same operation, with the objective of producing experimental renal hypertension. The monkeys developed no signs of illness to suggest development of either hypertension or uremia.At the time of study six months later, the five nephrectomized monkey...

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Induction of Filtration Edema by Extreme Reduction of Cerebrovascular Resistance Associated with Hypertension

Cited by 27 publications

References 0 publications

Hypertension After Severe Traumatic Brain Injury: Friend or Foe?

Hypertension After Severe Traumatic Brain Injury: Friend or Foe?

Cerebral Blood Flow in Cats After an Acute Hypertensive Insult With Damage to the Blood-Brain Barrier

Brain water alterations after unilateral nephrectomy. A study of regional circulatory factors in squirrel monkeys.

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