Cerebral Circulation and Cerebral Blood Flow

2019 ◽  
pp. 79-85
Author(s):  
Arnoley S. Abcejo ◽  
Jeffrey J. Pasternak
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neurologic Outcomes ◽  
The Us ◽  
Hospital Cardiac Arrest ◽  
Premonitory Symptoms

Cardiac arrest occurs suddenly, often without premonitory symptoms. Consciousness is lost within seconds to minutes because of insufficient cerebral blood flow in the midst of complete hemodynamic collapse. Anoxic-ischemic brain injury is most commonly caused by cardiac arrest, which is frequently lethal; of the US patients with out-of-hospital cardiac arrest treated by emergency medical services, almost 90% die. Among the patients who survive to hospital admission, inpatient mortality may be decreasing, but a substantial number of those survivors have poor neurologic outcomes from anoxic-ischemic brain injury.

Temporal profiles of cerebral blood flow in neonatal mice with hypoxic–ischemic brain injury

2011 ◽  
Vol 71 ◽  
pp. e403
Author(s):  
Makiko Ohshima ◽  
Masahiro Tsuji ◽  
Yukiko Kasahara ◽  
Akihiko Taguchi ◽  
Tomoaki Ikeda
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neonatal Mice ◽  
Hypoxic Ischemic Brain Injury ◽  
Temporal Profiles

scholarly journals Increased Susceptibility to Ischemic Brain Injury in Cyclooxygenase-1–Deficient Mice

2001 ◽  
Vol 21 (12) ◽  
pp. 1436-1441 ◽  
Author(s):  
Costantino Iadecola ◽  
Koreaki Sugimoto ◽  
Kiyoshi Niwa ◽  
Ken Kazama ◽  
M. Elizabeth Ross
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Cyclooxygenase 1 ◽  
Cox 1 ◽  
Increased Susceptibility

Cyclooxygenase-1 (COX-1), a rate-limiting enzyme in the synthesis of prostanoids, is involved in selected vasodilatatory responses of the cerebral circulation. Cyclooxygenase-1–null mice were used to determine whether COX-1 influences cerebral ischemic damage. The middle cerebral artery was occluded in COX-1 −/− and +/+ mice (n = 9/group), and lesion volume was determined in thionin-stained sections 24 or 96 hours later. Middle cerebral artery occlusion produced larger infarcts in COX-1 −/− mice, both at 24 (35 ± 17%; P < 0.05) and 96 hours (41 ± 16%; P < 0.05) after ischemia. The enlargement was not due to increased susceptibility to glutamate excitotoxicity, because microinjection of N-methl- d -asparatate or kainate in the parietal cortex produced comparable lesions in COX-1 +/+ and −/− mice ( P > 0.05; n = 8/group). To examine the contribution of hemodynamic factors to the enlargement of the infarct, cerebral blood flow was monitored by laser-Doppler flowmetry in the ischemic territory (n = 6/group). Although the reduction in cerebral blood flow was comparable in the ischemic core ( P > 0.05), at the periphery of the ischemic territory the reduction was greater in COX-1 −/− mice (−58 ± 4%) than in COX-1 +/+ mice (−34 ± 5%; P < 0.05). It is concluded that mice lacking COX-1 are more susceptible to focal cerebral ischemia, an effect that can be attributed to a more severe cerebral blood flow reduction in vulnerable regions at the periphery of the ischemic territory. Thus, the vascular effects of COX-1 may contribute to maintain cerebral blood flow in the postischemic brain and, as such, play a protective role in ischemic brain injury.

Acute and chronic triptan exposure neither alters rodent cerebral blood flow nor worsens ischemic brain injury

Neuroscience ◽  
2017 ◽  
Vol 340 ◽  
pp. 1-7 ◽  
Author(s):  
Mirko Muzzi ◽  
Daniela Buonvicino ◽  
Francesco De Cesaris ◽  
Alberto Chiarugi
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain

scholarly journals Electroacupuncture increased cerebral blood flow and reduced ischemic brain injury: dependence on stimulation intensity and frequency

2011 ◽  
Vol 111 (6) ◽  
pp. 1877-1887 ◽  
Author(s):  
Fei Zhou ◽  
Jingchun Guo ◽  
Jieshi Cheng ◽  
Gencheng Wu ◽  
Ying Xia
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Ischemic Injury ◽  
Artery Occlusion ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Stimulation Parameters ◽  
Cerebral Artery Occlusion ◽  
The Brain

Stroke causes ischemic brain injury and is a leading cause of neurological disability and death. There is, however, no promising therapy to protect the brain from ischemic stress to date. Here we show an exciting finding that optimal electroacupuncture (EA) effectively protects the brain from ischemic injury. The experiments were performed on rats subjected to middle cerebral artery occlusion (MCAO) with continuous monitoring of cerebral blood flow. EA was delivered to acupoints of “Shuigou” (Du 26) and “Baihui” (Du 20) with different intensities and frequencies to optimize the stimulation parameters. The results showed that 1) EA at 1.0–1.2 mA and 5–20 Hz remarkably reduced ischemic infarction, neurological deficit, and death rate; 2) the EA treatment increased the blood flow by >100%, which appeared immediately after the initiation of EA and disappeared after the cessation of EA; 3) the EA treatment promoted the recovery of the blood flow after MCAO; 4) “nonoptimal” parameters of EA (e.g., <0.6 mA or >40 Hz) could not improve the blood flow or reduce ischemic injury; and 5) the same EA treatment with optimal parameters could not increase the blood flow in naive brains. These novel observations suggest that appropriate EA treatment protects the brain from cerebral ischemia by increasing blood flow to the ischemic brain region via a rapid regulation. Our findings have far-reaching impacts on the prevention and treatment of ischemic encephalopathy, and the optimized EA parameters may potentially be a useful clue for the clinical application of EA.

scholarly journals Intravenous Infusion of Adrenomedullin and Increase in Regional Cerebral Blood Flow and Prevention of Ischemic Brain Injury after Middle Cerebral Artery Occlusion in Rats

1997 ◽  
Vol 17 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Aclan Dogan ◽  
Yoshio Suzuki ◽  
Naoki Koketsu ◽  
Koji Osuka ◽  
Kiyoshi Saito ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intravenous Infusion ◽  
Regional Cerebral Blood Flow ◽  
Ischemic Brain Injury ◽  
Dependent Manner ◽  
Regional Cerebral Blood ◽  
Ischemic Brain ◽  
Dose Dependent

The intravenous infusion of rat adrenomedullin, at concentrations ranging from 0.1 to 1.0 μg/kg/min, for 60 min increased the regional cerebral blood flow (rCBF) in a dose-dependent manner in rats. rCBF was measured using a laser Doppler flowmetry device placed on the surface of the parietal cortex. The increase in rCBF induced by 1.0 μg/kg/min of adrenomedullin was up to 145 ± 10.8% of controls at 60 min (n = 5, p < 0.001). These concentrations of adrenomedullin did not affect systemic blood pressure or other physiologic parameters, including pH, PaCO2, PaO2, hemoglobin, and blood glucose. Repeated infusion of 1.0 μg/kg/min of adrenomedullin at 2-h intervals caused tachyphylaxis (n = 5, p < 0.01). Rat adrenomedullin (1.0 μg/kg/min) demonstrated a more potent effect than the same dose of human adrenomedullin. The C-terminal fragment of human adrenomedullin (0.5 and 5.0 μg/kg/min), adrenomedullin22–52, which did not affect rCBF alone, inhibited the effect of rat adrenomedullin (0.5 μg/kg/min) as a receptor antagonist in a dose-dependent manner. In a model of middle cerebral artery (MCA) occlusion in spontaneously hypertensive rats, pre- and postinfusion of 1.0 μg/kg/min of adrenomedullin suppressed the reduction in rCBF following MCA occlusion (control, 29 ± 15.1%; adrenomedullin group, 45 ± 14.4%; not significant) and decreased the volume of ischemic brain injury (control, 288 ± 35 mm3; adrenomedullin group, 232 ± 35 mm3; p < 0.05). These results suggest that adrenomedullin increases rCBF and prevents ischemic brain injury, partly by increasing the collateral circulation.

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