Intermittent hypoxia modulates nitric oxide-dependent vasodilation and capillary perfusion during ischemia-reperfusion-induced damage

Bertuglia, Silvia

doi:10.1152/ajpheart.01371.2007

Cited by 24 publications

(25 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…] period, proposing a cardioprotective role for NOSderived NO against the oxidative episodes occurring during H/R. In agreement with our results, other authors working in another organ and species reported that L-NAME increased the concentrations of TBARS after intermittent hypoxia in hamster-cheek-pouch microcirculation (Bertuglia et al, 2008). Actually, several mechanisms may explain the protective effects of NO against oxidative stress.…”

Section: Discussionsupporting

confidence: 93%

See 1 more Smart Citation

Nitric oxide averts hypoxia‐induced damage during reoxygenation in rat heart

Rus

Molina

Peinado

et al. 2011

Microscopy Res & Technique

View full text Add to dashboard Cite

Nitric oxide (NO), synthesized by the hemoproteins NO synthases (NOS), is known to play important roles in physiological and pathological conditions in the heart, including hypoxia/reoxygenation (H/R). This work investigates the role that endogenous NO plays in the cardiac H/R-induced injury. A follow-up study was conducted in Wistar rats subjected to 30 min of hypoxia, with or without prior treatment using the nonselective NOS inhibitor L-NAME (1.5 mM). The rats were studied at 0 h, 12 h, and 5 days of reoxygenation, analysing parameters of cell, and tissue damage (lipid peroxidation, apoptosis, and protein nitration), as well as in situ NOS activity and NO production (NOx). The results showed that after L-NAME administration, in situ NOS activity was almost completely eliminated in all the experimental groups, and consequently, NOx levels fell. Contrarily, the lipid peroxidation level and the percentage of apoptotic cells rose throughout the reoxygenation period. These results reveal that NOS inhibition exacerbates the peroxidative and apoptotic damage observed before the treatment with L-NAME in the hypoxic heart, pointing to a cardioprotective role of NOS-derived NO against H/R-induced injury. These findings could open the possibility of future studies to design new therapies for H/R-dysfunctions based on NO-pharmacology.

show abstract

Section: Discussionsupporting

confidence: 93%

“…2). Because it is well known that L-NAME is a NOS inhibitor (Bertuglia et al, 2008;Viñ as et al, 2006), the decrease reported here in both NOx levels and in situ NOS activity should be attributed to NOS inhibition.…”

Section: Discussionmentioning

confidence: 58%

Nitric oxide averts hypoxia‐induced damage during reoxygenation in rat heart

Rus

Molina

Peinado

et al. 2011

Microscopy Res & Technique

View full text Add to dashboard Cite

show abstract

“…Animal studies (2, 6) have indicated that acute intermittent hypoxia improves myocardial tolerance to ischemia by activating nitric oxide synthase (NOS) and mitochondrial ATP-sensitive K ϩ (K ATP ) channels (2,6). Moreover, the severity of intervened hypoxia is apparently a required condition for cardioprotection (2,3).…”

Section: Cardiac Hemodynamicsmentioning

confidence: 99%

Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans

Wang

Mao

et al. 2010

Journal of Applied Physiology

View full text Add to dashboard Cite

. Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans. J Appl Physiol 109: 219-229, 2010. First published April 29, 2010 doi:10.1152/japplphysiol.00138.2010.-Hypoxic preconditioning prevents cerebrovascular/cardiovascular disorders by increasing resistance to acute ischemic stress, but severe hypoxic exposure disturbs vascular hemodynamics. This study compared how various exercise regimens with/without hypoxia affect hemodynamics and oxygenation in cardiac, muscle, and cerebral tissues during severe hypoxic exposure. Sixty sedentary males were randomly divided into five groups. Each group (n ϭ 12) received one of five interventions: 1) normoxic (21% O 2) resting control, 2) hypoxic (15% O2) resting control, 3) normoxic exercise (50% maximum work rate under 21% O 2; N-E group), 4) hypoxic-relative exercise (50% maximal heart rate reserve under 15% O2; H-RE group), or 5) hypoxicabsolute exercise (50% maximum work rate under 15% O 2; H-AE group) for 30 min/day, 5 days/wk, for 4 wk. A recently developed noninvasive bioreactance device was used to measure cardiac hemodynamics, and near-infrared spectroscopy was used to assess perfusion and oxygenation in the vastus lateralis (VL)/gastrocnemius (GN) muscles and frontal cerebral lobe (FC). Our results demonstrated that the H-AE group had a larger improvement in aerobic capacity compared with the N-E group. Both H-RE and H-AE ameliorated the suppression of cardiac stroke volume and the GN hyperemic response (⌬total Hb/min) and reoxygenation rate by acute 12% O2 exposure. Simultaneously, the two hypoxic interventions enhanced perfusion (⌬total Hb) and O 2 extraction [⌬deoxyHb] of the VL muscle during the 12% O2 exercise. Although acute 12% O2 exercise decreased oxygenation (⌬O2Hb) of the FC, none of the 4-wk interventions influenced the cerebral perfusion and oxygenation during normoxic/ hypoxic exercise tests. Therefore, we conclude that moderate hypoxic exercise training improves cardiopulmonary fitness and increases resistance to disturbance of cardiac hemodynamics by severe hypoxia, concurrence with enhancing O2 delivery/utilization in skeletal muscles but not cerebral tissues.oxygen; physical activity; circulation CHRONIC INTERMITTENT HYPOXIA is known to enhance aerobic capacity by increasing pulmonary ventilation, adaptation of the hematopoetic system, and tissue utilization of O 2 in sedentary males (43, 44), endurance athletes (10, 13), and elderly subjects with or without vascular diseases (8). Animal studies have also indicated that hypoxic preconditioning reduced the volume of cerebral infarction and edema (41) and attenuated the loss of myocardial contractility (3) immediately after sublethal ischemic insult. Therefore, we speculate that increased O 2 delivery/utilization and resistance to acute hypoxic/ischemic stresses conferred by hypoxic interventions improves exercise performance and is effective for preventing and treating cerebrovascular/cardiovascular diseases.Howeve...

show abstract

“…Nonetheless, the administration of this nonselective NOS inhibitor significantly lowered NOx levels in all the experimental groups. Because it is well known that L-NAME is a NOS inhibitor (Viñ as et al, 2006;Bertuglia, 2008), the decrease reported here in NOx levels and in situ NOS activity should be attributed to the inhibition of NOS isoforms.…”

Section: Discussionmentioning

confidence: 60%

“…In this sense, while some authors showed that inhibition of NO synthesis by L-NAME decreased greatly the production of lung TBARS after ischemia/reperfusion (Ischiropoulos et al, 1995), others found that the same NOS inhibitor increased the concentrations of TBARS after intermittent hypoxia in hamster cheek pouch microcirculation (Bertuglia, 2008). Regarding apoptosis, Maejima et al (2003) reported that L-NAME greatly increased the apoptosis rate in neonatal rat cardiomyocytes under ischemia/reperfusion, indicating that the NO released during these situations exerts an antiapoptotic effect.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Nitric Oxide Can Act as Beneficial or Deleterious in the Hypoxic Lung Depending on the Reoxygenation Time

Rus

Molina

Peinado

et al. 2010

The Anatomical Record

View full text Add to dashboard Cite

Nitric oxide (NO) has been implicated in many pathophysiological situations in the lung, including hypoxia/reoxygenation. This work seeks to clarify the current controversy concerning the double protective/toxic role of endogenous NO under hypoxia/reoxygenation situations in the lung by using a nitric oxide synthase (NOS) inhibitor, in a novel approach to address the problems raised from assaults under such circumstances. A follow-up study was conducted in Wistar rats submitted to hypoxia/ reoxygenation (hypoxia for 30 min; reoxygenation of 0 h, 48 h, and 5 days), with or without prior treatment using the nonselective NOS inhibitor L-NAME (1.5 mM, in drinking water). Lipid peroxidation, apoptosis level, protein nitration, in situ NOS activity and NO production (NOx) were analyzed. This is the first work to focus on the time-course effects of L-NAME in the adult rat lung submitted to hypoxia/reoxygenation. The results showed that after L-NAME administration, in situ NOS activity was almost completely eliminated and consequently, NOx levels fell. Lipid peroxidation and the percentage of apoptotic cells rose at the earliest reoxygenation time (0 h), but decreased in the later period (48 h and 5 days). Also nitrated protein expression decreased at 48 h and 5 days posthypoxia. These results suggest that NOS-derived NO exerts two different effects on lung hypoxia/reoxygenation injury depending on the reoxygenation time: NO has a beneficial role just after the hypoxic stimulus and a deleterious effect in the later reoxygenation times. Moreover, we propose that this dual role of NO depends directly on the producer NOS isoform.

show abstract

Intermittent hypoxia modulates nitric oxide-dependent vasodilation and capillary perfusion during ischemia-reperfusion-induced damage

Cited by 24 publications

References 45 publications

Nitric oxide averts hypoxia‐induced damage during reoxygenation in rat heart

Nitric oxide averts hypoxia‐induced damage during reoxygenation in rat heart

Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans

Endogenous Nitric Oxide Can Act as Beneficial or Deleterious in the Hypoxic Lung Depending on the Reoxygenation Time

Contact Info

Product

Resources

About