Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier.

MacKenzie, Eric T.; Strandgaard, Svend; Graham, David I.; Jones, J V; Harper, A. M.; Farrar, J. K.

doi:10.1161/01.res.39.1.33

Cited by 301 publications

(135 citation statements)

References 35 publications

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“…In Fig. 4, model predictions are compared with several sets of experimental data (7,12,21,22). When all three mechanisms are included, the autoregulation predicted by the model is consistent with that seen experimentally.…”

Section: Resultssupporting

confidence: 57%

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Carlson¹,

Arciero²,

Secomb³

2008

American Journal of Physiology-Heart and Circulatory Physiology

143

160

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Carlson BE, Arciero JC, Secomb TW. Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses. Am J Physiol Heart Circ Physiol 295: H1572-H1579, 2008. First published August 22, 2008; doi:10.1152/ajpheart.00262.2008The autoregulation of blood flow, the maintenance of almost constant blood flow in the face of variations in arterial pressure, is characteristic of many tissue types. Here, contributions to the autoregulation of pressure-dependent, shear stress-dependent, and metabolic vasoactive responses are analyzed using a theoretical model. Seven segments, connected in series, represent classes of vessels: arteries, large arterioles, small arterioles, capillaries, small venules, large venules, and veins. The large and small arterioles respond actively to local changes in pressure and wall shear stress and to the downstream metabolic state communicated via conducted responses. All other segments are considered fixed resistances. The myogenic, shear-dependent, and metabolic responses of the arteriolar segments are represented by a theoretical model based on experimental data from isolated vessels. To assess autoregulation, the predicted flow at an arterial pressure of 130 mmHg is compared with that at 80 mmHg. If the degree of vascular smooth muscle activation is held constant at 0.5, there is a fivefold increase in blood flow. When myogenic variation of tone is included, flow increases by a factor of 1.66 over the same pressure range, indicating weak autoregulation. The inclusion of both myogenic and shear-dependent responses results in an increase in flow by a factor of 2.43. A further addition of the metabolic response produces strong autoregulation with flow increasing by a factor of 1.18 and gives results consistent with experimental observation. The model results indicate that the combined effects of myogenic and metabolic regulation overcome the vasodilatory effect of the shear response and lead to the autoregulation of blood flow. conducted response; microcirculation; blood flow regulation; vascular smooth muscle; vascular tone THE ABILITY OF VASCULAR BEDS to maintain a relatively constant blood flow over a large range of arterial pressures is known as vascular autoregulation. With increasing arterial pressure, the degree of vascular smooth muscle (VSM) activation, VSM tone, increases in arterioles, resulting in decreased vessel diameter and increased flow resistance. Several mechanisms contribute to changes in vascular tone, including responses to intraluminal pressure (myogenic response), shear stress on the endothelial lining of vessels (shear-dependent response), metabolite concentrations in vessels and/or tissue (metabolic response), and neural stimuli. The cerebral and renal vasculature show the most stable flow over a wide range of arterial pressures (2, 25), whereas in other beds, such as those in the mesentery, autoregulation is less effective.Several theoretical models for the autoregulation of blood flow have been developed using a multicompartmen...

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Section: Resultssupporting

confidence: 57%

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Carlson¹,

Arciero²,

Secomb³

2008

American Journal of Physiology-Heart and Circulatory Physiology

143

160

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“…These abnormalities include increased cerebral vascular permeability to dye and proteins, 1 ' 2 a loss or "breakthrough" of autoregulation, and forced dilation of the arterial vasculature, which imparts a "sausage-string" appearance. 3 - 4 Additionally, we and our colleagues have shown that following acute hypertension induced by pressor agents or experimental traumatic brain injury, abnormalities of the cerebral arterioles are caused by oxygen radicals formed during increased arachidonic acid metabolism. 5 - 7 The abnormalities include sustained dilation, decreased reactivity to hypocapnia, endothelial leFrom the Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Va.…”

mentioning

confidence: 99%

Superoxide dismutase decreases mortality, blood pressure, and cerebral blood flow responses induced by acute hypertension in rats.

Zhang

Ellis

1991

Stroke

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Oxygen radicals are known to be produced by the cerebral vasculature during acute, pressor-induced hypertension and are also known to inactivate endothelium-derived relaxing factor. The objective of our present study was to determine if the oxygen radical scavenger superoxide dismutase (24,000 units/kg plus 1,600 units/kg/min) alters the pressor, cerebral blood flow, and mortality responses to systemic norepinephrine in rats. Increasing doses (0.01-30 /tg/kg i.v.) of norepinephrine were given by bolus injection to eight rats, and changes in the cortical microcirculatory blood flow were measured by laser-Doppler flowmetry. Superoxide dismutase shifted the norepinephrine-blood pressure and -cerebral blood flow dose-response curves moderately, but significantly, to the right such that it took more norepinephrine to reach a given blood pressure. However, superoxide dismutase had no effect on the autoregulation of cerebral blood flow. Additionally, whereas five (63%) of the eight control rats died after the 10 /tg/kg norepinephrine dose, all eight rats treated with superoxide dismutase survived this dose. The mechanism by which superoxide dismutase reduced mortality is uncertain. The blood pressure and cerebral blood flow results suggest that superoxide dismutase prevents oxygen radicals from destroying endothelium-derived relaxing factors, which reduce the pressor effects of norepinephrine. (Stroke 1991^2:489-494) A cute, drag-induced hypertension is known to cause abnormalities in the cerebral circulation. These abnormalities include increased cerebral vascular permeability to dye and proteins, 1 ' 2 a loss or "breakthrough" of autoregulation, and forced dilation of the arterial vasculature, which imparts a "sausage-string" appearance. 3 -4 Additionally, we and our colleagues have shown that following acute hypertension induced by pressor agents or experimental traumatic brain injury, abnormalities of the cerebral arterioles are caused by oxygen radicals formed during increased arachidonic acid metabolism. 5- 7 The abnormalities include sustained dilation, decreased reactivity to hypocapnia, endothelial le-

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“…Brain vessels also dilate or contract as a physiological response to cellular metabolic activity, but should not strictly be called autoregulation. The influence of neuronal metabolism on CBF should be referred to as metabolic regulation of the flow-metabolism coupling [47,48] . The methods used to estimate changes in cerebral perfusion are TCD ultrasound and clearance of xenon133, while CT demonstrates stable CBF.…”

Section: Cerebral Blood Flow Monitoringmentioning

confidence: 99%

Multimodal brain monitoring in fulminant hepatic failure

Paschoal¹,

Nogueira²,

Ronconi³

et al. 2016

WJH

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Acute liver failure, also known as fulminant hepatic failure (FHF), embraces a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction, and hepatic encephalopathy. Cerebral edema and intracranial hypertension are common causes of mortality in patients with FHF. The management of patients who present acute liver failure starts with determining the cause and an initial evaluation of prognosis. Regardless of whether or not patients are listed for liver transplantation, they should still be monitored for recovery, death, or transplantation. In the past, neuromonitoring was restricted to serial clinical neurologic examination and, in some cases, intracranial pressure monitoring. Over the years, this monitoring has proven insufficient, as brain abnormalities were detected at late and irreversible stages. The need for real-time monitoring of brain functions to favor prompt treatment and avert irreversible brain injuries led to the concepts of multimodal monitoring and neurophysiological decision support. New monitoring techniques, such as brain tissue oxygen tension, continuous electroencephalogram, transcranial Doppler, and cerebral microdialysis, have been developed. These techniques enable early diagnosis of brain hemodynamic, electrical, and biochemical changes, allow brain anatomical and physiological monitoring-guided therapy, and have improved patient survival rates. The purpose of this review is to discuss the multimodality methods available for monitoring patients with FHF in the neurocritical care setting.

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Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier.

Cited by 301 publications

References 35 publications

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Superoxide dismutase decreases mortality, blood pressure, and cerebral blood flow responses induced by acute hypertension in rats.

Multimodal brain monitoring in fulminant hepatic failure

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