Perivascular Potassium and pH as Determinants of Local Pial Arterial Diameter in Cats

Kuschinsky, Wolfgang; Wahl, Michael; Bosse, O.; Thurau, Klaus

doi:10.1161/01.res.31.2.240

Cited by 281 publications

(107 citation statements)

References 36 publications

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“…Conclusions In summary, elevated [K+]O is associated with vasodilatation and increased blood flow in heart and brain under physiological and pathophysiological conditions (Buenger et al 1976;Cameron & Caronna, 1976;Paulson & Newman, 1987). K+ efflux from tissue is indicative of its metabolic state or activity and has been proposed as a local regulator of blood flow in the brain (Kuschinsky et al 1972). We have provided evidence that elevated [K+].…”

Section: Methods Preparationmentioning

confidence: 68%

Section: Methods Preparationmentioning

confidence: 99%

“…In the cerebral circulation, an increase in the [K+]o in the range 1-16 mm causes small arteries to dilate (Kuschinsky, Wahl, Bosse & Thurau, 1972;McCarron & Halpern, 1990). K+ ions are released as a consequence of neuronal activity, and may be one of the factors which increase local cerebral blood flow during increased cerebral activity (Kuschinsky et al 1972). Extracellular [K+] increases during cerebral hypoxia, ischaemia or hypoglycaemia from around 3 mm to values in excess of 10 mM (Sieber, Wilson, Hanley & Traystman, 1993;Somjen, 1979).…”

Section: Methods Preparationmentioning

confidence: 99%

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Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Knot

Zimmermann

Nelson

1996

The Journal of Physiology

302

261

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1. The hypothesis that inward rectifier K+ channels are involved in the vasodilatation of small coronary and cerebral arteries (100-200 ,um diameter) in response to elevated [K+]. was tested. The diameters and membrane potentials of pressurized arteries from rat were measured using a video-imaging system and conventional microelectrodes, respectively. 2. Elevation of [K+]o from 6 to 16 mm caused the membrane potential of pressurized (60 mmHg) arteries to hyperpolarize by 12-14 mV. Extracellular Ba2P (Ba20+) blocked K+-induced membrane potential hyperpolarizations at concentrations (IC50, 6 uM) that block inward rectifier K+ currents in smooth muscle cells isolated from these arteries. 5. These findings suggest that K+ dilates small rat coronary and cerebral arteries through activation of inward rectifier K+ channels. Furthermore, these results support the hypothesis that inward rectifier K+ channels may be involved in metabolic regulation of coronary and cerebral blood flow in response to changes in [K+]0.

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Section: Methods Preparationmentioning

confidence: 68%

Section: Methods Preparationmentioning

confidence: 99%

Section: Methods Preparationmentioning

confidence: 99%

See 1 more Smart Citation

Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Knot

Zimmermann

Nelson

1996

The Journal of Physiology

302

261

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“…Adenosine levels double after only five seconds of ischemia and increase six-fold after the onset of hypoxia during which time cerebral blood flow begins to rise significantly 38 . Prostaglandins and other eicosanoids (products of arachidonic acid metabolism) can be rapidly synthesized and released by cerebral microvessels and have been postulated as putative mediators coupling metabolism and blood flow 38,39,40,41,42 . With the exception of the vasodilator prostacyclin, arachidonic acid derivatives are potent vasoconstrictors at low concentrations.…”

Section: Coupling Of Cerebral Blood Flow To Metabolismmentioning

confidence: 99%

Cerebral hemodynamic and metabolic changes in fulminant hepatic failure

Paschoal

Nogueira

Oliveira

et al. 2017

Arq. Neuro-Psiquiatr.

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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. This is an uncommon, but not rare, condition with approximately 2,000 cases annually in the United States and a mortality rate ranging from 50% to 90%, despite intensive care therapy 1,2 . Cerebral edema leading to intracranial hypertension complicates approximately 50% to 80% of patients with severe FHF (grade III or IV coma), in whom it is the leading cause of death 2,3,4 . Brain edema in FHF patients is a relatively recent concept. In a 1944 report of 125 autopsies of military patients who had died from a condition he called fatal hepatitis (previously referred to as idiopathic acute yellow atrophy of the liver), Lucké 5 noted little alteration in the brain except for edema, but did not describe cerebral herniation. The first reports of brain edema and cerebral herniation as complications of FHF only emerged in the 1980s 6,7 . It is also noteworthy that brain edema and intracranial hypertension are not recognized common features of chronic liver failure, despite some case reports and small series 8,9 . The recent recognition of brain edema in FHF patients could be due to the advances in FHF patient care. Previously, FHF patients were dying from early hepatocellular insufficiency complications, mainly hemorrhage or sepsis ABSTRACTIntracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.Keywords: hepatic insufficiency; intracranial hypertension; brain edema. RESUMOO edema cerebral e a hipertensão intracraniana (HIC) são as principais causas de morbidade e mortalidade de pacientes com insuficiência hepática fulminante (IHF). A patogênese dessas complicações tem sido investigada no homem, em modelos experimentais e em sistemas celulares isolados. Atualmente, o mecanismo subjacente ao edema cerebral e HIC na presença de IHF é multifatorial em etiologia e pouco compreendido na literatura. O objetivo deste trabalho é revisar a fisiopatologia das alterações hemodinâmicas e metabólicas cerebrais na IHF, visando melhorar a compreensão da complicação da hemodinâmica encefálica na IHF.Palavras-chave: insuficiência hepatica; hipertenção intracraniana; edema encefálico.

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“…In newborn piglets, we have previously shown that a pressurepassive relationship exists between mean arterial blood pressure and cerebral blood flow during seizures and the subsequent postictal state (12,13). Several factors may mediate this loss of autoregulation, including changes in perivascular potassium and hydrogen ion concentrations, intracranial pressure, systemic blood pressure, cerebral oxygenation, and carbon dioxide production (14)(15)(16)(17)(18). Because hydrogen ion and carbon dioxide production have previously been observed to increase after seizures, the concomitant rise in cerebral blood flow has been attributed to an increase in the perivascular concentrations of these two elements (19).…”

mentioning

confidence: 99%

Hyperventilation Restores Autoregulation of Cerebral Blood Flow in Postictal Piglets

Monin

Stonestreet

1991

Pediatr Res

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Perivascular Potassium and pH as Determinants of Local Pial Arterial Diameter in Cats

Cited by 281 publications

References 36 publications

Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Cerebral hemodynamic and metabolic changes in fulminant hepatic failure

Hyperventilation Restores Autoregulation of Cerebral Blood Flow in Postictal Piglets

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