Abstract TP269: Reduction of Human Brain Adenosine Levels Following Remote Ischemic Preconditioning

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Joshua R Dusick ◽  
Arzu Bilgin-Freiert ◽  
Kym F Faull ◽  
Nestor Gonzalez
Keyword(s):  
Blood Pressure ◽  
Ischemic Preconditioning ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Adenine Nucleotides ◽  
High Energy ◽  
Protective Mechanisms ◽  
Extracellular Adenosine ◽  
Pressure Cuff ◽  
Cell Energy ◽  
Csf Levels

Introduction: Prior studies demonstrate that ischemic preconditioning (IP) alters adenosine metabolism. The significance of this effect is not fully understood, but evidence suggests that reduction in extracellular adenosine may represent use as an alternative fuel. Transformation into AMP/ADP may also replenish intracellular total adenine nucleotides (TAN), improving the potential high-energy phosphate bonds available in cells facing ischemia. In both cases, adenosine supports cell energy requirements and may be a key component of IP’s protective mechanisms. There are no previous studies of brain adenosine in human patients undergoing remote IP. Methods: In adults with aneurysmal subarachnoid hemorrhage (SAH), 3-4 remote IP sessions were conducted on non-consecutive days, 4-12 days after hemorrhage. Each session consisted of 4 5-min cycles of lower extremity blood pressure cuff inflation to 30mmHg above systolic blood pressure, followed by 5-min reperfusion. Patients had microdialysis (MD) probes to compare brain adenosine, inosine, xanthine and hypoxanthine before, immediately after, and 24h after RIPC. MD samples from 4 SAH ICU patients without IP were used as controls. Results: Five RIPC sessions in 3 patients resulted in complete MD data for comparison over time. In all, brain adenosine levels dropped from their baseline (pre-RIPC) level. Average pre-RIPC adenosine went from 19.2 (SD 14.4) fmol/mg to 7.9 (SD 8.6) immediately following the session (p=0.095) and to 3.2 (SD 4.5) by 24h (p=0.048). Adenosine metabolites inosine, xanthine, and hypoxanthine decreased or did not change over the same period, suggesting adenosine consumption rather than non-energy related catabolism. These changes in adenosine were not reflected in CSF levels, which did not change (p=0.5). Brain adenosine in control subjects did not decrease (baseline 0.26±0.17, 24h 6.6±9.3, p=0.27). Conclusion: Remote IP leads to decreased brain adenosine in SAH patients by 24 hours. Failure to demonstrate a concomitant rise in levels of metabolites suggests that adenosine is consumed by cells in the brain, as previously shown in animal models. This shift toward the energetic metabolism of adenosine may play a key role in the mechanisms of protection induced by IP.

387 Ischemic Preconditioning Reduces the Incidence of Postoperative Ischemic Lesions in Patients Undergoing Surgical Resection of Brain Tumors: A Single Center, Randomized, Double-blind, Controlled Trial

Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 292-293
Author(s):  
Arthur H A Sales ◽  
Melanie Barz ◽  
Stefanie Bette ◽  
Benedikt Wiestler ◽  
Yu-Mi Ryang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Brain Tumor ◽  
Brain Tumors ◽  
Ischemic Preconditioning ◽  
Control Group ◽  
Tumor Surgery ◽  
Brain Tumor Surgery ◽  
Blood Pressure Cuff ◽  
Pressure Cuff ◽  
Ischemic Tissue

Abstract INTRODUCTION Postoperative ischemia is a frequent phenomenon in patients with brain tumors and is associated with postoperative neurological deficits and impaired overall survival. Previous clinical and experimental studies have shown that the application of a brief ischemic stimulus not only in the target organ but also in a remote tissue can prevent ischemia. We hypothesized that remote ischemic preconditioning (rIPC) in patients with brain tumors undergoing elective surgical resection reduces the incidence of postoperative ischemic tissue damage and its consequences. METHODS Sixty patients were randomly assigned to two groups, with 1:1 allocation, stratified after tumor type (glioma or metastasis) and previous treatment with radiotherapy. Remote ischemic preconditioning was induced by inflating a blood pressure cuff placed on the upper arm three times for 5 minutes at 200 mmHg in the treatment group after induction of anesthesia. Between the cycles, the blood pressure cuff was released to allow reperfusion. In the control group no preconditioning was performed. Early postoperative MR images were evaluated blinded to randomization for the presence of ischemia and its volume. RESULTS >Fifty-eight of the 60 patients were assessed for occurrence of postoperative ischemia. Of these 58 patients, 44 (75.9%) had new postoperative ischemic lesions. The incidence of new postoperative ischemic lesions was significantly higher in the control group (87.1%) (27/31) than in the rIPC group (63.0%) (17/27) (P = 0.03). The median infarct volume was 0.36 cm3 (IR: 0.0- 2.35) in the rIPC group compared with 1.30 cm3 (IR: 0.29- 3.66) in the control group (P = 0.09). CONCLUSION Application of rIPC significantly reduced the incidence of postoperative ischemic tissue damage in patients undergoing elective brain tumor surgery. This is the first study indicating a benefit of rIPC in brain tumor surgery.

scholarly journals Growth inhibition of transformed mouse fibroblasts by adenine nucleotides occurs via generation of extracellular adenosine.

1988 ◽  
Vol 263 (25) ◽  
pp. 12367-12372
Author(s):  
G A Weisman ◽  
K D Lustig ◽  
E Lane ◽  
N N Huang ◽  
I Belzer ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Adenine Nucleotides ◽  
Extracellular Adenosine ◽  
Mouse Fibroblasts

Reno-protective mechanisms of epoxyeicosatrienoic acids in cardiovascular disease

2012 ◽  
Vol 302 (3) ◽  
pp. R321-R330 ◽  
Author(s):  
Ahmed A. Elmarakby
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Animal Models ◽  
Vascular Function ◽  
Organ Damage ◽  
Reduce Blood Pressure ◽  
Experimental Models ◽  
Epoxyeicosatrienoic Acids ◽  
Protective Effects ◽  
Protective Mechanisms

Cardiovascular disease (CVD) is the leading cause of mortality worldwide, and it is well known that end-stage renal disease (ESRD) is a profound consequence of the progression of CVD. Present treatments only slow CVD progression to ESRD, and it is imperative that new therapeutic strategies are developed to prevent the incidence of ESRD. Because epoxyeicosatrienoic acids (EETs) have been shown to elicit reno-protective effects in hypertensive animal models, the current review will focus on addressing the reno-protective mechanisms of EETs in CVD. The cytochrome P-450 epoxygenase catalyzes the oxidation of arachidonic acid to EETs. EETs have been identified as endothelium-derived hyperpolarizing factors (EDHFs) with vasodilatory, anti-inflammatory, antihypertensive, and antiplatelet aggregation properties. EETs also have profound effects on vascular migration and proliferation and promote angiogenesis. The progression of CVD has been linked to decreased EETs levels, leading to the concept that EETs should be therapeutically targeted to prevent end-organ damage associated with CVD. However, EETs are quickly degraded by the enzyme soluble epoxide hydrolase (sEH) to their less active diols, dihydroxyeicosatrienoic acids (DHETs). As such, one way to increase EETs level is to inhibit their degradation to DHETs by using sEH inhibitors. Inhibition of sEH has been shown to effectively reduce blood pressure and organ damage in experimental models of CVD. Another approach to target EETs is to develop EET analogs with improved solubility and resistance to auto-oxidation and metabolism by sEH. For example, stable ether EET analogs dilate afferent arterioles and lower blood pressure in hypertensive rodent animal models. EET agonists also improve insulin signaling and vascular function in animal models of metabolic syndrome.

POSITIONING THE BLOOD PRESSURE CUFF

Nursing ◽  
1976 ◽  
Vol 6 (10) ◽  
pp. 18-29
Author(s):  
Rebecca Sills ◽  
Carolyn M. Jarvis
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Cuff ◽  
Pressure Cuff

Blood pressure, fatigue, and the pathogenesis of aneurysmal subarachnoid hemorrhage

2006 ◽  
Vol 66 (6) ◽  
pp. 574-580 ◽  
Author(s):  
Patrick Mitchell ◽  
Danny Birchall ◽  
A. David Mendelow
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage

Ischemic Preconditioning Prior to Aortic Cross-Clamping Protects High-Energy Phosphate Levels, Glucose Uptake, and Myocyte Contractility

2002 ◽  
Vol 105 (2) ◽  
pp. 153-159 ◽  
Author(s):  
Douglas Baldwin ◽  
Y. Chandrashekhar ◽  
Edward McFalls ◽  
Inder Anand ◽  
Daosheng Liu ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Ischemic Preconditioning ◽  
High Energy ◽  
High Energy Phosphate ◽  
Myocyte Contractility

Sensor Fused Blood Pressure Measuring Device Capable of Recording Korotkoff Sounds in Inflationary Curves

2020 ◽  
Author(s):  
Enrique Alvarez Vazquez ◽  
Daniel Ewert ◽  
Dave Jorgenson ◽  
Michael Sand
Keyword(s):  
Blood Pressure ◽  
Cuff Pressure ◽  
High Sensitivity ◽  
Skin Surface ◽  
Pressure System ◽  
Measuring Device ◽  
Arterial Blood ◽  
Pressure Cuff ◽  
System 2 ◽  
Control Electronics

Abstract This study describes a non-invasive medical device capable of measuring arterial blood pressure (BP) with a combination of inflationary and deflationary procedures. The device uses the pressure cuff pressure signal, arterial skin-surface acoustics, and photoplethysmography (PPG) to make a sensor-fusion estimation of blood pressure readings. We developed an apparatus composed of 1) a modified off-the-shelf oscillometric blood pressure system, 2) a contact microphone with an amplifier, 3) and high-sensitivity pulse oximeter, and its control electronics.

Incidence of Fractures From Perioperative Blood Pressure Cuff Use, Tourniquet Use, and Patient Positioning in Osteogenesis Imperfecta

2019 ◽  
Vol 39 (1) ◽  
pp. e68-e70 ◽  
Author(s):  
Brian T. Sullivan ◽  
Adam Margalit ◽  
Vaibhav S. Garg ◽  
Dolores B. Njoku ◽  
Paul D. Sponseller
Keyword(s):  
Blood Pressure ◽  
Osteogenesis Imperfecta ◽  
Patient Positioning ◽  
Blood Pressure Cuff ◽  
Pressure Cuff

Abstract P129: Role of the Autonomic Nervous System in Remote Postconditioning in Humans

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rupert P Williams ◽  
Michael I Okorie ◽  
Harminder Gill ◽  
John E Deanfield ◽  
Raymond J MacAllister ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Whole Body ◽  
Limb Ischaemia ◽  
Protective Effects ◽  
Blood Pressure Cuff ◽  
Autonomic Nervous ◽  
Pressure Cuff ◽  
Remote Postconditioning

Brief periods of ischaemia activate systemic mechanisms that induce whole-body tolerance to subsequent prolonged and injurious ischaemia. This phenomenon, remote ischaemic preconditioning (RIPC), is sufficiently acute to reduce ischaemia-reperfusion (IR) injury even when applied simultaneously with injurious ischaemia. This aspect of RIPC is termed remote postconditioning (RPostC). We have previously demonstrated a role for the autonomic nervous system in RIPC. Using an in vivo model of endothelial IR injury, we determined if RPostC is dependent on adrenergic autonomic mechanisms. Vascular ultrasound was used to assess endothelial function in healthy volunteers by measuring dilatation of the brachial artery in response to increased blood flow during reactive hyperaemia (flow-mediated dilatation; FMD). Endothelial IR injury was induced by 20 min of upper limb ischaemia (inflation of a blood pressure cuff to 200 mm Hg) followed by reperfusion. RPostC was induced by applying 2 cycles of 5 minutes ischaemia and 5 minutes reperfusion on the leg during arm ischaemia (via a second blood pressure cuff). In order to determine the dependence of RPostC on autonomic activation, we administered the alpha adrenoceptor blocker phentolamine (0.2– 0.7mg/min, intravenously) during the application of the RPostC stimulus. FMD was determined before ischaemia and at 20 minutes of reperfusion. FMD (percentage change from baseline diameter) was compared statistically by ANOVA. IR alone caused a significant reduction in FMD (5.9±0.7% pre- versus 2.2±0.4% post-IR, n=9, P<0.001). This reduction was prevented by RPostC (5.8±0.4% pre- versus 5.4±0.3% post-IR, n=8, P>0.05). Systemic phentolamine blocked the protective effects of RPostC (FMD 6.1±0.5% pre- versus 2.0±0.3% post-IR, n=7, P<0.001). These data indicate, for the first time in humans, that protection from RPostC depends on preservation of adrenergic signalling. Alpha blockade neutralises one of the endogenous mechanisms of ischemic protection in humans; the clinical consequences of this remain to be determined.

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