scholarly journals 3-Nitropropionic Acid-Induced Ischemia Tolerance in the Rat Brain is Mediated by Reduced Metabolic Activity and Cerebral Blood Flow

2014 ◽  
Vol 34 (9) ◽  
pp. 1522-1530 ◽  
Author(s):  
Oliver Bracko ◽  
Valentina Di Pietro ◽  
Giacomo Lazzarino ◽  
Angela M Amorini ◽  
Barbara Tavazzi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Structural Integrity ◽  
Energy Charge ◽  
Artery Occlusion ◽  
Metabolic Demand ◽  
Irreversible Damage ◽  
Nitropropionic Acid ◽  
Ischemia Tolerance ◽  
3 Nitropropionic Acid

Tissue tolerance to ischemia can be achieved by noxious stimuli that are below a threshold to cause irreversible damage (‘preconditioning’). Understanding the mechanisms underlying preconditioning may lead to the identification of novel therapeutic targets for diseases such as stroke. We here used the oxidative chain inhibitor 3-nitropropionic acid (NPA) to induce ischemia tolerance in a rat middle cerebral artery occlusion (MCAO) stroke model. Cerebral blood flow (CBF) and structural integrity were characterized by longitudinal magnetic resonance imaging (MRI) in combination with behavioral, histologic, and biochemical assessment of NPA-preconditioned animals and controls. Using this approach we show that the ischemia-tolerant state is characterized by a lower energy charge potential and lower CBF, indicating a reduced baseline metabolic demand, and therefore a cellular mechanism of neural protection. Blood vessel density and structural integrity were not altered by NPA treatment. When subjected to MCAO, preconditioned animals had a characteristic MRI signature consisting of enhanced CBF maintenance within the ischemic territory and intraischemic reversal of the initial cytotoxic edema, resulting in reduced infarct volumes. Thus, our data show that tissue protection through preconditioning occurs early during ischemia and indicate that a reduced cellular metabolism is associated with tissue tolerance to ischemia.

Assessing the Effects of Antihypertensive Medication on Cerebral Blood Flow: Demonstration in Internal Carotid Artery Occlusion

DICP ◽  
1991 ◽  
Vol 25 (12) ◽  
pp. 1299-1301 ◽  
Author(s):  
Susan C. Fagan ◽  
James R. Ewing ◽  
Steven R. Levine ◽  
Gretchen E. Tietjen ◽  
Nabih M. Ramadan ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Antihypertensive Medication ◽  
Internal Carotid ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Internal Carotid Artery Occlusion ◽  
Bilateral Carotid

Dynamic cerebral blood flow (CBF) studies using acetazolamide or hypercapnia as a vasodilatory challenge have attempted to evaluate intracranial hemodynamics. We report two patients with asymptomatic internal carotid artery occlusion in whom the vasodilatory stimulus was a single oral dose of antihypertensive medication (prazosin hydrochloride or enalapril maléate). In both patients, changes in regional CBF occurred that were larger than those seen in nine normal controls. One patient experienced an improvement in regional CBF with a reduction in probe pair asymmetry. In the other patient, who had bilateral carotid artery disease, a decrease in regional CBF in all 16 probes (mean decrease 12 percent) and an accentuation of the predose asymmetry were observed. Both patients remained asymptomatic throughout the study. Assessing these effects on cerebral circulation may help identify patients at risk for iatrogenic focal cerebral ischemia and provide information regarding the functional status of the cerebral vasculature.

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

Cerebral blood flow during exercise: mechanisms of regulation

2009 ◽  
Vol 107 (5) ◽  
pp. 1370-1380 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Philip N. Ainslie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Oxygenation ◽  
Central Fatigue ◽  
Future Research ◽  
Metabolic Demand ◽  
Heavy Exercise ◽  
Peripheral Vasculature ◽  
Cerebral Vasoconstriction ◽  
Methodological Considerations

The response of cerebral vasculature to exercise is different from other peripheral vasculature; it has a small vascular bed and is strongly regulated by cerebral autoregulation and the partial pressure of arterial carbon dioxide (PaCO2). In contrast to other organs, the traditional thinking is that total cerebral blood flow (CBF) remains relatively constant and is largely unaffected by a variety of conditions, including those imposed during exercise. Recent research, however, indicates that cerebral neuronal activity and metabolism drive an increase in CBF during exercise. Increases in exercise intensity up to ∼60% of maximal oxygen uptake produce elevations in CBF, after which CBF decreases toward baseline values because of lower PaCO2 via hyperventilation-induced cerebral vasoconstriction. This finding indicates that, during heavy exercise, CBF decreases despite the cerebral metabolic demand. In contrast, this reduced CBF during heavy exercise lowers cerebral oxygenation and therefore may act as an independent influence on central fatigue. In this review, we highlight methodological considerations relevant for the assessment of CBF and then summarize the integrative mechanisms underlying the regulation of CBF at rest and during exercise. In addition, we examine how CBF regulation during exercise is altered by exercise training, hypoxia, and aging and suggest avenues for future research.

scholarly journals Late Reversal of Cerebral Perfusion and Water Diffusion after Transient Focal Ischemia in Rats

2002 ◽  
Vol 22 (3) ◽  
pp. 253-261 ◽  
Author(s):  
Lei Wang ◽  
Victor E. Yushmanov ◽  
Serguei M. Liachenko ◽  
Pei Tang ◽  
Ronald L. Hamilton ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Focal Ischemia ◽  
Artery Occlusion ◽  
Tissue Water ◽  
Apparent Diffusion ◽  
Reperfusion Period ◽  
Adc Values ◽  
Transient Focal Ischemia ◽  
Late Reperfusion

Region-specific cerebral blood flow (CBF) and the apparent diffusion coefficient (ADC) of tissue water in the rat brain were quantified by high-field magnetic resonance imaging at 9.4 T in the rat suture occlusion model. Cerebral blood flow and ADC were compared during the short- (4.5 hours) and long-term (up to 6 days) reperfusion after 80 minutes of transient middle cerebral artery occlusion, and correlated with the histology analysis. On occlusion, average CBF fell from ∼100 to less than 50 mL 100 g−1 min−1 in the cortex, and to less than 20 mL 100 g−1 min−1 in the caudate putamen (CP). Corresponding ADC values decreased from (6.98 ± 0.82) × 10−4 to (5.49 ± 0.54) × 10−4 mm2/s in the cortex, and from (7.16 ± 0.58) × 10−4 to (4.86 ± 0.62) × 10−4 mm2/s in the CP. On average, CBF recovered to ∼50% of baseline in the first 24 hours of reperfusion. After 2 to 4 days, a strong hyperperfusion in the ipsilateral cortex and CP, up to ∼300 mL 100 g−1 min−1, was observed. The ADC ratio in the ipsilateral and contralateral CP was also inverted in the late reperfusion period. Histology revealed more severe tissue damage at the late stage of reperfusion than at 4.5 hours. Significant reversal of CBF and ADC during the late reperfusion period may reflect the impairment of autoregulation in the ischemic regions. Vascular factors may play an important role in the infarct development after 80-minute focal ischemia.

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