Effect of acute nitrate and citrulline supplementation on muscle microvascular response to ischemia–reperfusion in healthy humans

2017 ◽  
Vol 42 (9) ◽  
pp. 901-908 ◽  
Author(s):  
Thibault Le Roux-Mallouf ◽  
Florence Vibert ◽  
Stéphane Doutreleau ◽  
Samuel Verges
Keyword(s):  
Near Infrared ◽  
Ischemia Reperfusion ◽  
Area Under The Curve ◽  
Vascular Occlusion ◽  
No Production ◽  
Control Mechanisms ◽  
Healthy Humans ◽  
Microvascular Response ◽  
Reperfusion Period ◽  
Ischemic Period

Nitric oxide (NO) is implicated in vasomotor control mechanisms altering the diameter of the vessels under various physiological and pathological conditions. There are 2 main NO production pathways, 1 NO synthase (NOS) independent (nitrate–nitrite–NO) and the other is NOS dependent (citrulline–arginine–NO). The objective of the study was to evaluate the effect of acute nitrate and citrulline supplementation on post-ischemic vascular response in healthy subjects. Fourteen subjects performed 2-leg vascular occlusion tests, 3 days apart. They were randomly assigned to consume a drink containing 1200 mg (19.4 mmol) of nitrate and 6 g of citrulline (N+C) or a placebo (Pl). Changes in total hemoglobin (Hbtot) and oxyhemoglobin (HbO2) concentrations were recorded by near-infrared spectroscopy on the thigh and calf muscles. No differences between N+C and Pl were observed during the ischemic period. Hbtot increased to a larger extent during the reperfusion period for the thigh (e.g., area under the curve, 821 ± 324 vs. 627 ± 381 mmol·s−1, p = 0.003) and the calf (515 ± 285 vs. 400 ± 275 mmol·s−1, p = 0.029) in the N+C versus Pl conditions. Similar results were found regarding HbO2 for the thigh (e.g., area under the curve, 842 ± 502 vs. 770 ± 491 mmol·s−1, p = 0.077) and the calf (968 ± 536 vs. 865 ± 275 mmol·s−1, p = 0.075). The larger postocclusive Hbtot and HbO2 responses observed after N+C intake suggests a greater post-ischemic vasodilation, which may be due to increased NO availability, via the activation of the 2 main NO production pathways.

Abstract 1904: Myocardial Postconditioning Against Ischemia and Reperfusion Injury by Near Infrared Electromagnetic Radiation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Phillip F Pratt ◽  
Martin Bienengraeber ◽  
Dorothee Weihrauch ◽  
Judy R Kersten ◽  
David C Warltier
Keyword(s):  
Infarct Size ◽  
Electromagnetic Radiation ◽  
Reperfusion Injury ◽  
Near Infrared ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
No Production ◽  
Ischemia And Reperfusion ◽  
Early Reperfusion

Near-infrared electromagnetic radiation (NIR) has been reported to stimulate biochemical processes within cells and tissue, but whether NIR is capable of acutely protecting myocardium against ischemia+reperfusion injury in vivo is unknown. We tested the hypothesis that NIR (670 nm, 30 nm bandwith, 50 mW/cm 2 ) exposure immediately before and during early reperfusion protects rabbit myocardium against infarction that is dependent upon reactive oxygen species (ROS), nitric oxide synthase (NOS), mitochondrial K ATP (mito K ATP ) channels and inhibition of mitochondrial permeability transition pore (mPTP) opening. Rabbits subjected to a 30 min left anterior descending coronary artery occlusion and reperfusion received no irradiation (control) or continuous NIR (beginning 3 min before and ending 7 min after reperfusion) in the presence or absence of ROS scavengers [N-acetylcysteine (NAC; 150 mg/kg), or tempol (30 mg/kg)], nonselective NOS inhibitor L-nitro-arginine methyl ester (L-NAME; 10 mg/kg), selective mitoK ATP channel antagonist 5-hydroxydecanoate (5-HD; 10 mg/kg) or mPTP opener atractyloside (5 mg/kg). Dihydroethidium and diaminofluroscein immunofluorescence were used to detect ROS and NO production, respectively, in additional rabbits with or without NIR exposure. NIR reduced infarct size (24±4% of the area at risk; triphenyltetrazolium chloride staining) compared with control (46±3%). NAC, tempol, L-NAME, 5-HD, and atractyloside alone did not affect infarct size, but these drugs abolished the cardioprotective effect of NIR. NIR increased ROS production independent of ischemia and reperfusion, and this effect was blocked by NAC. NIR also enhanced NO generation during early reperfusion. In addition, NIR increased ATP synthesis in isolated rabbit mitochondria. Thus, NIR postconditions myocardium against infarction concomitant with ROS and NO production. MitoK ATP channels and mPTP mediate cardioprotection by NIR.

scholarly journals EARLY AND REMOTE RESPONSE OF HIF-1Α PROTEIN IN THE HIPPOCAMPUS FIELDS TO ISCHEMIA-REPERFUSION IN RATS WITH DIABETES MELLITUS

2021 ◽  
Vol 9 (1) ◽  
pp. 101-106
Author(s):  
O.M. Nika ◽  
O.V. Zaliavska ◽  
O.V. Kaushanska
Keyword(s):  
Diabetes Mellitus ◽  
Transcription Factor ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Experimental Conditions ◽  
Ischemic Reperfusion ◽  
Reperfusion Period ◽  
Ischemic Period ◽  
The Brain ◽  
Activity Indices

The role of the transcription factor Hif-1α in pathogenesis of hypoxic lesions and diabetes mellitus (DM) has been confirmed, though molecular mechanisms underlying dysfunctions of the factor in the association of DM with ischemic-reperfusion lesion of the brain remain unknown. Objective: the investigation of Hif-1α protein content in the neurons of the hippocampus fields of rats with experimental DM in the dynamics of ischemic-reperfusion lesion of the brain. The study was conducted on 60 6-month rats with DM simulated at the age of 2 months by means of a single administration of streptozotocin (60 mg/kg of the body weight) (Sigma, USA). Disorders of the cerebral circulation were simulated by means of occlusion of both carotid arteries for 20 minutes. The content of Hif1-α protein was determined by means of fluoroimmunoassay after 20-minute ischemia with one hour reperfusion, and on the 12th day of the post-ischemic period in the hippocampus fields: СА1, СА2, СА3, СА4. In rats without DM 20-minute ischemia with one hour reperfusion increases the content of Hif-1α protein in all the hippocampus fields. On the 12th day of ischemic-reperfusion period in СА2-СА4 hippocampus fields the values of certain examined activity indices of the transcription factor Hif-1α continue to increase, and in СА1 field they are normalized or come closer to the values of animals from the control group. In rats with DM at the early post-ischemic period changes of Hif-1α protein content are lacking in СА1 field, the signs of its reduced activity are found in СА2 field, in СА3 field they are limited by the response of one index, and in СА4 field they are similar to those of the control rats under the experimental conditions. On the 12th day of ischemic-reperfusion period all the activity indices of the transcription factor Hif-1α increase in СА1 filed. They are higher than the corresponding indices in animals from the control group by absolute values under similar experimental conditions; changes of the examined parameters are limited in СА2 and СА3 fields in comparison with those from the control group; the parameters, which increased in the control group of animals, decreased in СА4 field. DM restricts Hif-1α protein response to ischemia-reperfusion in the neurons of СА1-СА3 field at the early ischemic-reperfusion period and in the neurons of СА2-СА4 fields — on the 12th day of the observation.

Hypoxia compared with normoxia alters the effects of nitric oxide in ischemia-reperfusion lung injury

1997 ◽  
Vol 273 (3) ◽  
pp. L504-L512 ◽  
Author(s):  
Y. C. Huang ◽  
P. W. Fisher ◽  
E. Nozik-Grayck ◽  
C. A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Average Rate ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
No Production ◽  
Protective Effects ◽  
Lung Weight ◽  
Edema Formation ◽  
No Donors

Because both the biosynthesis of nitric oxide (NO.) and its metabolic fate are related to molecular O2, we hypothesized that hypoxia would alter the effects of NO. during ischemia-reperfusion (IR) in the lung. In this study, buffer-perfused lungs from rabbits underwent either normoxic IR (AI), in which lungs were ventilated with 21% O2 during ischemia and reperfusion, or hypoxic IR (NI), in which lungs were ventilated with 95% N2 during ischemia followed by reoxygenation with 21% O2. Lung weight gain (WG) and pulmonary artery pressure (Ppa) were monitored continuously, and microvascular pressure (Pmv) was measured after reperfusion to calculate pulmonary vascular resistance. We found that both AI and NI produced acute lung injury, as shown by increased WG and Ppa during reperfusion. In AI, where perfusate PO2 was > 100 mmHg, the administration of the NO. synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) before ischemia worsened WG and Ppa. Pmv also increased, suggesting a hydrostatic mechanism involved in edema formation. The effects of L-NAME could be attenuated by giving L-arginine and exogenous NO. donors before ischemia or before reperfusion. Partial protection was also provided by superoxide dismutase. In contrast, lung injury in NI at perfusate PO2 of 25-30 mmHg was attenuated by L-NAME; this effect could be reversed by L-arginine. Exogenous NO. donors given either before ischemia or before reperfusion, however, did not increase lung injury. NO. production was measured by quantifying the total nitrogen oxides (NOx) accumulating in the perfusate. The average rate of NOx accumulation was greater in AI than in NI. We conclude that hypoxia prevented the protective effects of NO on AI lung injury. The effects of hypoxia may be related to lower NO. production relative to oxidant stress during IR and/or altered metabolic fates of NO.-mediated production of peroxynitrite by hypoxic ischemia.

Syncope, cerebral perfusion, and oxygenation

2003 ◽  
Vol 94 (3) ◽  
pp. 833-848 ◽  
Author(s):  
Johannes J. Van Lieshout ◽  
Wouter Wieling ◽  
John M. Karemaker ◽  
Niels H. Secher
Keyword(s):  
Cardiac Output ◽  
Cerebral Perfusion ◽  
Near Infrared ◽  
Vasovagal Syncope ◽  
Low Frequencies ◽  
Healthy Humans ◽  
Standing Up ◽  
Arterial Inflow ◽  
Cerebral Blood Velocity ◽  
Critical Reduction

During standing, both the position of the cerebral circulation and the reductions in mean arterial pressure (MAP) and cardiac output challenge cerebral autoregulatory (CA) mechanisms. Syncope is most often associated with the upright position and can be provoked by any condition that jeopardizes cerebral blood flow (CBF) and regional cerebral tissue oxygenation (cO2Hb). Reflex (vasovagal) responses, cardiac arrhythmias, and autonomic failure are common causes. An important defense against a critical reduction in the central blood volume is that of muscle activity (“the muscle pump”), and if it is not applied even normal humans faint. Continuous tracking of CBF by transcranial Doppler-determined cerebral blood velocity ( Vmean) and near-infrared spectroscopy-determined cO2Hb contribute to understanding the cerebrovascular adjustments to postural stress; e.g., MAP does not necessarily reflect the cerebrovascular phenomena associated with (pre)syncope. CA may be interpreted as a frequency-dependent phenomenon with attenuated transfer of oscillations in MAP to Vmeanat low frequencies. The clinical implication is that CA does not respond to rapid changes in MAP; e.g., there is a transient fall in Vmeanon standing up and therefore a feeling of lightheadedness that even healthy humans sometimes experience. In subjects with recurrent vasovagal syncope, dynamic CA seems not different from that of healthy controls even during the last minutes before the syncope. Redistribution of cardiac output may affect cerebral perfusion by increased cerebral vascular resistance, supporting the view that cerebral perfusion depends on arterial inflow pressure provided that there is a sufficient cardiac output.

scholarly journals Evaluation of Different Near-Infrared Spectroscopy Devices for Assessing Tissue Oxygenation with a Vascular Occlusion Test in Healthy Volunteers

2020 ◽  
Vol 57 (6) ◽  
pp. 341-347
Author(s):  
Jaeyeon Chung ◽  
Sang-Hwan Ji ◽  
Young-Eun Jang ◽  
Eun-Hee Kim ◽  
Ji-Hyun Lee ◽  
...  
Keyword(s):  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Pairwise Comparison ◽  
Vascular Occlusion ◽  
Tissue Oxygen Saturation ◽  
Vascular Occlusion Test ◽  
Occlusion Test ◽  
Significant Difference ◽  
Post Hoc

Near-infrared spectroscopy devices can measure peripheral tissue oxygen saturation (StO<sub>2</sub>). This study aims to compare StO<sub>2</sub> using INVOS® and different O3™ settings (O3<sup>25:75</sup> and O3<sup>30:70</sup>). Twenty adults were recruited. INVOS® and O3™ probes were placed simultaneously on 1 side of forearm. After baseline measurement, the vascular occlusion test was initiated. The baseline value, rate of deoxygenation and reoxygenation, minimum and peak StO<sub>2</sub>, and time from cuff release to peak value were measured. The parameters were compared using ANOVA and Kruskal-Wallis tests. Bonferroni’s correction and Mann-Whitney pairwise comparison were used for post hoc analysis. The agreement between StO<sub>2</sub> of devices was evaluated using Bland-Altman plots. INVOS® baseline value was higher (79.7 ± 6.4%) than that of O3<sup>25:75</sup> and O3<sup>30:70</sup> (62.4 ± 6.0% and 63.7 ± 5.5%, respectively, <i>p</i> &#x3c; 0.001). The deoxygenation rate was higher with INVOS® (10.6 ± 2.1%/min) than with O3<sup>25:75</sup> and O3<sup>30:70</sup> (8.4 ± 2.2%/min, <i>p</i> = 0.006 and 7.5 ± 2.1%/min, <i>p</i> &#x3c; 0.001). The minimum and peak StO<sub>2</sub> were higher with INVOS®. No significant difference in the reoxygenation rate was found between the devices and settings. The time to reach peak after cuff deflation was faster with INVOS® (both <i>p</i> &#x3c; 0.001). Other parameters were similar. There were no differences between the different O3™ settings. There were differences in StO<sub>2</sub> measurements between the devices, and these devices should not be interchanged. Differences were not observed between O3™ device settings.

scholarly journals Hydrogen Sulfide Prevents Ischemia-Reperfusion Injury in Muscle even when Delivered in the Post-ischemic Period

2009 ◽  
Vol 50 (4) ◽  
pp. 972
Author(s):  
P.W. Henderson ◽  
S.P. Singh ◽  
A.L. Weinstein ◽  
V. Nagineni ◽  
J.A. Spector
Keyword(s):  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Period

Evaluation of Ischemia-Reperfusion Liver Injury by Near-Infrared Spectroscopy in an Experimental Swine Model: The Effect of Desferoxamine

2011 ◽  
Vol 24 (4) ◽  
pp. 164-170 ◽  
Author(s):  
Maria. A. Kyriazi ◽  
Kassiani Theodoraki ◽  
Theodosios Thedosopoulos ◽  
Paraskevi Tsiantoula ◽  
George Fragulidis ◽  
...  
Keyword(s):  
Infrared Spectroscopy ◽  
Liver Injury ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Ischemia Reperfusion ◽  
Swine Model

Noninvasive measurement of forearm blood flow and oxygen consumption by near-infrared spectroscopy

1994 ◽  
Vol 76 (3) ◽  
pp. 1388-1393 ◽  
Author(s):  
R. A. De Blasi ◽  
M. Ferrari ◽  
A. Natali ◽  
G. Conti ◽  
A. Mega ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Healthy Subjects ◽  
Near Infrared ◽  
Forearm Blood Flow ◽  
Vascular Occlusion ◽  
Venous Occlusion ◽  
The Subject

We applied near-infrared spectroscopy (NIRS) for the simultaneous measurement of forearm blood flow (FBF) and oxygen consumption (VO2) in the human by inducing a 50-mmHg venous occlusion. Eleven healthy subjects were studied both at rest and after hand exercise during vascular occlusion. FBF was also measured by strain-gauge plethysmography. FBF measured by NIRS was 1.9 +/- 0.8 ml.100 ml-1.min-1 at rest and 8.2 +/- 2.9 ml.100 ml-1.min-1 after hand exercise. These values showed a correlation (r = 0.94) with those obtained by the plethysmography. VO2 values were 4.6 +/- 1.3 microM O2 x 100 ml-1.min-1 at rest and 24.9 +/- 11.2 microM O2 x 100 ml-1.min-1 after hand exercise. The scatter of the FBF and VO2 values showed a good correlation between the two variables (r = 0.93). The results demonstrate that NIRS provides the particular advantage of obtaining the contemporary evaluation of blood flow and VO2, allowing correlation of these two variables by a single maneuver without discomfort for the subject.

scholarly journals Anesthetic Considerations in Hepatectomies under Hepatic Vascular Control

HPB Surgery ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Aliki Tympa ◽  
Kassiani Theodoraki ◽  
Athanassia Tsaroucha ◽  
Nikolaos Arkadopoulos ◽  
Ioannis Vassiliou ◽  
...  
Keyword(s):  
Liver Surgery ◽  
Ischemia Reperfusion ◽  
Anesthetic Management ◽  
Vascular Occlusion ◽  
Air Embolism ◽  
Preoperative Assessment ◽  
Mortality Rates ◽  
Vascular Control ◽  
Hemodynamic Management ◽  
Anesthetic Considerations

Background. Hazards of liver surgery have been attenuated by the evolution in methods of hepatic vascular control and the anesthetic management. In this paper, the anesthetic considerations during hepatic vascular occlusion techniques were reviewed. Methods. A Medline literature search using the terms “anesthetic,” “anesthesia,” “liver,” “hepatectomy,” “inflow,” “outflow occlusion,” “Pringle,” “hemodynamic,” “air embolism,” “blood loss,” “transfusion,” “ischemia-reperfusion,” “preconditioning,” was performed. Results. Task-orientated anesthetic management, according to the performed method of hepatic vascular occlusion, ameliorates the surgical outcome and improves the morbidity and mortality rates, following liver surgery. Conclusions. Hepatic vascular occlusion techniques share common anesthetic considerations in terms of preoperative assessment, monitoring, induction, and maintenance of anesthesia. On the other hand, the hemodynamic management, the prevention of vascular air embolism, blood transfusion, and liver injury are plausible when the anesthetic plan is scheduled according to the method of hepatic vascular occlusion performed.

scholarly journals Structural changes in skeletal muscles of the hind limbs of rats in acute ischemia-reperfusion and its correction by carbacetam, detected by polarization microscopy

2020 ◽  
pp. 30-35
Author(s):  
T. O. Veresiuk ◽  
P. R. Selskyy ◽  
A. T. Televiak
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Structural Changes ◽  
Ischemia Reperfusion ◽  
Acute Ischemia ◽  
Polarization Microscopy ◽  
Early Reperfusion ◽  
Hind Limbs ◽  
Reperfusion Period ◽  
Muscle Remodeling

Arterial tourniquets are used in clinical practice for angioplasty and arthroplasty, and in case of limb injuries, their use often occurs according to vital signs. After removing the tourniquet and blood supply restoration to the limb arises a multifactorial lesion of tissues both ischemic and distant from the site of ischemia. A number of publications have been devoted to the study of morphological disorders in muscle tissue in acute ischemia-reperfusion in the medical literature. However, the researches for effective means for drug correction of these disorders still continues. The aim of the study was to explore peculiarities of skeletal muscle remodeling of the hind limbs of rats, detected by polarization microscopy, in acute ischemia-reperfusion, caused by the application of an arterial tourniquet, and in the correction of reperfusion disorders by carbacetam. Microscopic examination of histological sections of skeletal muscles of the hind limbs of 60 rats below the site of application of the tourniquet under conditions of experimental acute ischemia-reperfusion was performed. Acute ischemia for all animals was caused by application of SWAT rubber bands on the hind limbs of animals, 5–6 mm in width, at the inguinal fold level within 2 hours under thiopental anesthesia. A reperfusion was modeled by removing the tourniquet. Half of the experimental animals in the reperfusion period for the purpose of correction intraperitoneally was administered the nootropic drug 1-oxo-3.3.6-trimethyl-1.2.3.4-tetrahydroindolo[2.3-c]quinoline (carbacetam) at a dose of 5 mg per kilogram of body weight once a day during the entire reperfusion period. The histological specimens of the skeletal muscles were stained with hematoxylin and eosin, and were examined with a light microscope with polarization nozzle. Studies with using the polarization microscopy have shown that in the early reperfusion period morphological criteria for skeletal muscle remodeling expressed by deformation and anisotropy of muscle fibers, disappearance of their transverse striation, cracks and ruptures of fibers, and in the most severe cases there were signs of necrosis of the fibers with their fragmentation into separate lumps. Subject to the correction of reperfusion disorders by carbacetam, there is a decrease in the degree of damage and consistent acceleration of restoration of the skeletal muscles structure, which was the most pronounced in groups of animals with reperfusion terms after 1 and 14 days. Complex of features indicates, that at the tissue level the administration of carbacetam as reduces the ischemic-reperfusion lesion of the muscular fibers, as also accelerates the mechanisms of reparative rhabdomyohistogenesis. Thus, structural changes in the skeletal muscles of the limb after two-hour ischemia and subsequent reperfusion increased in the early reperfusion period and reached its peak after 1 day of reperfusion, and in the late period of reperfusion their reverse development took place. With the correction of disorders by carbacetam, the degree of damage was reduced and the recovery of the skeletal muscle structure of the limb was accelerated.

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