Effect of increases in cardiac contractility on cerebral blood flow in humans

Ogoh, Shigehiko; Moralez, Gilbert; Washio, Takuro; Sarma, Satyam; Hieda, Michinari; Romero, Steven A.; Cramer, Matthew N.; Shibasaki, Manabu; Crandall, Craig G.

doi:10.1152/ajpheart.00287.2017

Cited by 20 publications

(33 citation statements)

References 33 publications

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“…Methodological concerns and regional cerebrovascular reactivity CBF regulation involves a large spectrum of regulatory mechanisms that, in concert, maintain nutrient and oxygen delivery to the brain . MAP, CO and P aCO 2 , for example, have been indicated as important CBF regulators Ogoh et al 2017). Throughout the experimental protocol, both MAP and CO remained unchanged, indicating that the observed tCBF responses were not affected by these variables.…”

Section: Discussionmentioning

confidence: 90%

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Human brain blood flow and metabolism during isocapnic hyperoxia: the role of reactive oxygen species

Mattos

Campos

Rocha

et al. 2018

The Journal of Physiology

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Key points It is unknown whether excessive reactive oxygen species (ROS) production drives the isocapnic hyperoxia (IH)‐induced decline in human cerebral blood flow (CBF) via reduced nitric oxide (NO) bioavailability and leads to disruption of the blood–brain barrier (BBB) or neural‐parenchymal damage. Cerebral metabolic rate for oxygen (CMRnormalO2) and transcerebral exchanges of NO end‐products, oxidants, antioxidants and neural‐parenchymal damage markers were simultaneously quantified under IH with intravenous saline and ascorbic acid infusion. CBF and CMR normalO2 were reduced during IH, responses that were followed by increased oxidative stress and reduced NO bioavailability when saline was infused. No indication of neural‐parenchymal damage or disruption of the BBB was observed during IH. Antioxidant defences were increased during ascorbic acid infusion, while CBF, CMR normalO2, oxidant and NO bioavailability markers remained unchanged. ROS play a role in the regulation of CBF and metabolism during IH without evidence of BBB disruption or neural‐parenchymal damage. Abstract To test the hypothesis that isocapnic hyperoxia (IH) affects cerebral blood flow (CBF) and metabolism through exaggerated reactive oxygen species (ROS) production, reduced nitric oxide (NO) bioavailability, disturbances in the blood–brain barrier (BBB) and neural‐parenchymal homeostasis, 10 men (24 ± 1 years) were exposed to a 10 min IH trial (100% O2) while receiving intravenous saline and ascorbic acid (AA, 3 g) infusion. Internal carotid artery blood flow (ICABF), vertebral artery blood flow (VABF) and total CBF (tCBF, Doppler ultrasound) were determined. Arterial and right internal jugular venous blood was sampled to quantify the cerebral metabolic rate of oxygen (CMRnormalO2), transcerebral exchanges (TCE) of NO end‐products (plasma nitrite), antioxidants (AA and AA plus dehydroascorbic acid (AA+DA)) and oxidant biomarkers (thiobarbituric acid‐reactive substances (TBARS) and 8‐isoprostane), and an index of BBB disruption and neuronal‐parenchymal damage (neuron‐specific enolase; NSE). IH reduced ICABF, tCBF and CMR normalO2, while VABF remained unchanged. Arterial 8‐isoprostane and nitrite TCE increased, indicating that CBF decline was related to ROS production and reduced NO bioavailability. AA, AA+DA and NSE TCE did not change during IH. AA infusion did not change the resting haemodynamic and metabolic parameters but raised antioxidant defences, as indicated by increased AA/AA+DA concentrations. Negative AA+DA TCE, unchanged nitrite, reductions in arterial and venous 8‐isoprostane, and TBARS TCE indicated that AA infusion effectively inhibited ROS production and preserved NO bioavailability. Similarly, AA infusion prevented IH‐induced decline in regional and total CBF and re‐established CMR normalO2. These findings indicate that ROS play a role in CBF regulation and metabolism during IH without evidence of BBB disruption or neural‐parenchymal damage.

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Section: Discussionmentioning

confidence: 90%

“…; Ogoh et al . ). Throughout the experimental protocol, both MAP and CO remained unchanged, indicating that the observed tCBF responses were not affected by these variables.…”

Section: Discussionmentioning

confidence: 97%

Human brain blood flow and metabolism during isocapnic hyperoxia: the role of reactive oxygen species

Mattos

Campos

Rocha

et al. 2018

The Journal of Physiology

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“…These two vascular beds appear to have different regulatory mechanisms in controlling blood flow [44][45][46]. Previous reports suggest that external cerebral vasculature plays a dynamic role in intracranial CBF regulation [44,47]. In fact, it was shown that changes in external carotid artery are more distinctive than internal carotid artery changes under acute hypotensive and hypertensive conditions in healthy individuals [44,47].…”

Section: Strengths and Weaknesses Of The Studymentioning

confidence: 99%

Protocol for the Isolation and Super-resolution dSTORM Imaging of RyR2 in Cardiac Myocytes

Hou¹,

Le²,

Soeller³

et al. 2018

BIO-PROTOCOL

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Heart failure is associated with low cardiac output (CO) and low brain perfusion that imposes a significant risk for accelerated brain ageing and Alzheimer's disease (AD) development. Although clinical heart failure can emerge several years following acute myocardial infarction (AMI), the impact of AMI on cerebral blood flow (CBF) at early stages and up to 30 days following MI is unknown. Sixteen months old male mice underwent left anterior descending (LAD) coronary artery ligation. Hemodynamics analyses were performed at baseline and at days 1, 7, and 30 post-MI. Left ventricular (LV) ejection fraction (EF), LV volumes, CO, and right common carotid artery (RCCA) diameter were recorded by echocardiography. RCCA flow (RCCA FL) was measured by Doppler echocardiography. LV volumes consistently increased (P<0.0012) and LV systolic function progressively deteriorated (P<0.0001) post-MI. CO and RCCA FL showed a moderate but significant decrease over the course of MI with similar fluctuation pattern such that both variables were decreased at day 1, increased at day 7, and decreased at 30 days post-MI. Correlation and regression analyses between CO and RCCA FL showed a strong correlation with significance at baseline and day 30 post-MI (R = 0.71, P=0.03, and R = 0.72, P=0.03, respectively). Days 1 and 7 analyses between CO and RCCA FL showed moderate correlation with non-significance post-MI (R = 0.51, P=0.2, and R = 0.56, P=0.12, respectively). In summary, CBF significantly decreased following AMI and remained significantly decreased for up to 30 days, suggesting a potential risk for brain damage that could contribute to cognitive dysfunction later in life.

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“…xia, dynamic or resistance exercise, orthostatic stress and heat stress (Hashimoto et al, 2018;Hirasawa et al, 2016;Ogoh et al, 2013Ogoh et al, , 2014aOgoh et al, , b, 2015bOgoh et al, , 2017bSato et al, 2012a, b;Sato, Ogoh, Hirasawa, Oue, & Sadamoto, 2011). These findings indicate that this heterogeneous CBF response between the anterior and posterior circulation might be attributable to different physiological roles between different brain areas (e.g.…”

Section: Introductionmentioning

confidence: 96%

Arterial and venous cerebral blood flow responses to long‐term head‐down bed rest in male volunteers

Ogoh

Sato

Abreu

et al. 2019

Experimental Physiology

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In this study, we investigated the whole cerebral haemodynamic response to long-term headdown bed rest (HDBR). We hypothesized that long-term exposure to weightlessness influences cerebral blood flow (CBF) or CBF distribution among cerebral arteries and veins because of the different physiological roles of each cerebral vessel. To test this hypothesis, 10 male volunteers were exposed to −6 deg HDBR for 60 days. Blood flows in the internal carotid artery, external carotid artery and vertebral artery or internal jugular vein and vertebral vein were measured using ultrasonography before and on days 30 and 57 of the HDBR. The internal carotid artery blood flow was reduced on day 30 (P = 0.019) and had returned to the baseline level by day 57. In contrast, the vertebral artery blood flow remained unaltered throughout the HDBR (P = 0.626). The internal jugular vein blood flow was reduced on day 30 (P = 0.009), whereas the vertebral vein blood flow remained unaltered (P = 0.397). These findings suggest that long-term HDBR causes a heterogeneous CBF response between the anterior and posterior cerebral circulation in the both arteries and veins. The posterior arterial and venous CBFs were well maintained throughout HDBR, and these CBF responses to HDBR were different from the anterior cerebral circulation.

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Effect of increases in cardiac contractility on cerebral blood flow in humans

Cited by 20 publications

References 33 publications

Human brain blood flow and metabolism during isocapnic hyperoxia: the role of reactive oxygen species

Human brain blood flow and metabolism during isocapnic hyperoxia: the role of reactive oxygen species

Protocol for the Isolation and Super-resolution dSTORM Imaging of RyR2 in Cardiac Myocytes

Arterial and venous cerebral blood flow responses to long‐term head‐down bed rest in male volunteers

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