Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been recently suggested that atrial natriuretic factor (ANF) might be involved in the physiological regulation of pulmonary circulation. Therefore, we investigated the pulmonary hemodynamic response to 20-min infusions of 0.05, 0.1, and 0.2 micrograms kg-1 min-1 of alpha human ANF in five dogs alternatively ventilated with hyperoxic (FIO2 0.4) and hypoxic (FIO2 0.1) gas mixtures. Cardiac output was held constant by the inflation of a balloon in the inferior vena cava or by opening of an arteriovenous femoral fistula, in order to discriminate between active and passive changes in pulmonary arterial pressure (Ppa). Hypoxia increased Ppa from 14 +/- 3 to 24 +/- 3 mm Hg (mean +/- SE, p less than 001). Circulating ANF and guanosine 3',5'-cyclic monophosphate (cGMP) were increased to 1,326 +/- 299 pmol L-1 (normal is less than 10 pmol L-1) and 75.5 +/- 5.8 pmol ml-1 (normal is less than 15 pmol ml-1) respectively, at the highest infused dose. After ANF infusion, heart rate (HR), Ppa, pulmonary capillary wedge pressure (Ppw), and right atrial pressure (Pra) did not change either in hyperoxia or hypoxia. Systemic arterial pressure (Psa) decreased after ANF, but only in hypoxia. Thus, ANF at pharmacological doses associated with a 100-150-fold increase in plasma levels proved to be a poor vasodilator and, in particular, did not inhibit hypoxic pulmonary vasoconstriction (HPV). These results do not support the speculation that ANF might be an endogenous vasodilating modulator of pulmonary vascular tone in the dog.
J Cardiovasc Pharmacol 1989 Dec
PMID:Pharmacological doses of atrial natriuretic factor do not inhibit canine hypoxic pulmonary vasoconstriction. 248 70

We tested the following hypothesis: if carotid body blood flow, and hence the relationship of the frequency of discharge in chemoreceptor afferent fibres to arterial PO2, were affected by atherosclerotic change, then a modification of the control of the respiratory and cardiovascular systems might result. Carotid body reflexes were therefore studied in conscious atherosclerotic rabbits and a control group of normal animals breathing 100% O2, three hypoxic gas mixtures to which was added sufficient CO2 to maintain the arterial PCO2 constant, and 2% and 4% CO2 in 21% O2 and N2. When breathing room air, the atherosclerotic rabbits breathed at a higher respiratory frequency and lower tidal volume than the normal animals, although there was no difference in the respiratory minute volume. The respiratory and cardiovascular responses to hyperoxia, isocapnic hypoxia and hypercapnia were essentially the same in both groups of animals. Serial sections of the carotid bodies showed pathological changes including interstitial fibrosis in the caudal part with interstitial haemorrhages. The proximal part of the ascending pharyngeal artery, the vessel supplying the organ, and its origin from the external carotid, and the arterioles in the caudal part of the carotid body were nearly always occluded to a varying extent by atheromatous plaques. The capillaries appeared normal under light microscopy. The rostral-caudal lengths of the carotid bodies were similar in the two groups. We conclude that the peripheral arterial chemoreceptor responses in atherosclerotic rabbits are relatively normal even though the arteries to, and arterioles within, the carotid body are partly occluded.
Cardiovasc Res 1989 Jun
PMID:Carotid chemoreceptor function and structure in the atherosclerotic rabbit: respiratory and cardiovascular responses to hyperoxia, hypoxia and hypercapnia. 259 Sep 27

Following acute occlusion of the proximal left anterior descending (LAD) coronary artery, dogs were exposed continuously for 4 days in an environmental chamber to either 21% or 40% oxygen. Regional transmural myocardial blood flow was then determined by means of radioactive microspheres (8 to 10 microD) while each animal breathed room air (approximately equal to 21% oxygen). Blood flows in the anterolateral and apical regions of the left ventricle in normoxic animals (n = 5) averaged 0.95 +/- 0.03 and 0.69 +/- 0.13 ml/min X gm-1, respectively. In hyperoxic dogs (n = 5), blood flows in these regions were significantly lower, averaging 0.71 +/- 0.07 and 0.28 +/- 0.08 ml/min X gm-1, respectively in the anterolateral free wall, the greatest disparity in perfusion between experimental groups occurred in the subendocardial layers, and macroscopic evidence of necrosis was more widespread after hyperoxia.
J Thorac Cardiovasc Surg 1983 Nov
PMID:Persistent myocardial ischemia following chronic hyperoxia in conscious dogs. 663 43

In the fetal lamb, oxygen-induced pulmonary vasodilation is attenuated by the combined use of purinergic receptor P1 and P2y antagonists, which block the effect of adenosine and adenosine triphosphate (ATP), respectively, and by N(omega)-nitro-L-arginine [an inhibitor of endothelium-derived nitric oxide (EDNO) synthesis]. In the newborn lamb, oxygen-induced pulmonary vasodilation is not blocked by N(omega)-nitro-L-arginine. We investigated the role of ATP and adenosine in oxygen-induced pulmonary vasodilation in eight newborn lambs with pulmonary hypertension induced by the thromboxane mimic, U46619. The hemodynamic effects of hyperoxia, ATP, adenosine, sodium nitroprusside (SNP), and acetylcholine (ACh) were compared before and after purinergic receptor blockade with Cibacron blue (CB, a P2y-receptor antagonist) and 8-phenyltheophylline (8PT, a P1-receptor antagonist) individually, together, and on a separate day, after infusion of N(omega)-nitro-L-arginine. During pulmonary hypertension, combined pretreatment with 8PT and CB attenuated the decrease in pulmonary arterial pressure caused by hyperoxia (11.3 vs. 35.2%), ATP (10.6 vs. 32.2%), and adenosine (1.9 vs. 33.7%) without change in the effect of ACh or SNP (p < 0.05). N(omega)-Nitro-L-arginine attenuated the pulmonary vasodilation caused by ATP and ACh but not by hyperoxia, adenosine, or SNP. In the newborn lamb, the pulmonary vasodilating effect of both oxygen and ATP are attenuated by combined P1 and P2y purinergic-receptor antagonists. Postnatally, oxygen-induced pulmonary vasodilation appears to be mediated by ATP through purinergic receptors.
J Cardiovasc Pharmacol 1997 Jul
PMID:Oxygen-induced pulmonary vasodilation is mediated by adenosine triphosphate in newborn lambs. 926 28

This article describes the experimental infrastructure and subsequent successful clinical application of a comprehensive bypass and cardioplegic strategy that limits intraoperative injury and improves postoperative outcomes in pediatric patients. The infant heart is at high risk of damage from poor protection because of preoperative hypertrophy, cyanosis, and ischemia. The background factors of vulnerability to damage caused by cyanosis and ischemia are discussed, together with studies of the infrastructure of strategies to use normoxia versus hyperoxia as bypass starts, white blood cell filtration, warm induction and reperfusion with substrate enhancements, multidose blood cardioplegia, and an integrated approach to allow ischemia only when vision is needed in pediatric surgeries. Data on cardioplegic management, including reducing calcium, increasing magnesium, and reducing perfusion pressure are shown, as used during this technique. These principles were applied to a consecutive series of 567 patients at the Heart Institute for Children and University of Illinois hospital over a 2-year period. Included also were 72 patients with hypoplastic left heart over a 4-year period with this myocardial management strategy. Application of these concepts may improve the safety of protection in infant hearts.
Semin Thorac Cardiovasc Surg 2001 Jan
PMID:Pediatric myocardial protection: an overview. 1130 28

Supplementary oxygen is commonly administered in current medical practice. However, attention has recently been drawn to the potentially disadvantageous hemodynamic consequences in certain patients. Possible mechanisms underlying the cardiovascular responses to acute hyperoxia are unclear. The effects of acute oxygen administration on heart rate, blood pressure, cardiac output, systemic vascular resistance, and baroreflex sensitivity were studied in a series of randomised, placebo-controlled studies in healthy individuals, using validated, non-invasive techniques. The effects of oxygen administration on forearm blood flow responses to locally administered acetylcholine, an endothelium-dependent vasodilator, sodium nitroprusside, an endothelium-independent vasodilator, and l-NG-monomethylarginine, a nitric oxide synthase inhibitor, were studied using venous occlusion plethysmography. Oxygen administration for 1 hour caused a reduction in heart rate (P < 0.01) and cardiac index (P < 0.05), and an increase in mean arterial pressure (P < 0.01), systemic vascular resistance (P < 0.05), large artery stiffness (P < 0.05), and baroreflex sensitivity (P < 0.05). There were no effects on vascular responses in the isolated forearm bed. These findings indicate that oxygen administration causes acute effects on cardiovascular function, which might be important in the context of acute illness.
J Cardiovasc Pharmacol 2003 Aug
PMID:Cardiovascular effects of acute oxygen administration in healthy adults. 1288 29

Focal coronary artery blockage followed by further reperfusion injury is commonly involved in myocardial infarction. The injured heart has some inherent reparative responses. Although such natural healing mechanisms seem to be inefficient, a clear understanding of the underlying principles of myocardial healing holds the key to successful therapy. Under normoxic conditions, pO(2) ranges from 90 to <3 Torr in mammalian organs with the heart at approximately 35 Torr (5%) and arterial blood at approximately 100 Torr. Thus, "normoxia" for cells is an adjustable variable. In response to chronic moderate hypoxia, cells lower their normoxia set-point such that reoxygenation-dependent relative elevation of pO(2) (+DeltapO(2)) results in perceived hyperoxia. Perceived hyperoxia induces differentiation of cardiac fibroblasts to myofibroblasts in the peri-infarct region and represents a significant factor supporting myocardial healing. The oxygen-sensitive signaling pathways involved have been characterized and point towards a central role of p21, TGFbeta and p38MAPK. That low oxygen ambience serves as a cue to trigger angiogenesis is a well-accepted notion. Studies related to perceived hyperoxia establish that the sensing of oxygen environment is not limited to hypoxia. It demonstrates that in addition to being a trigger for injury as is widely recognized, reoxygenation insult has a built-in component of tissue remodeling in the peri-infarct region induced by perceived hyperoxia. Understanding of the underlying mechanisms of this and other myocardial healing responses should prove to be instrumental in developing productive therapeutic approaches to mend the infarcted heart.
Cardiovasc Res 2006 Jul 15
PMID:Perceived hyperoxia: oxygen-induced remodeling of the reoxygenated heart. 1648 58

Cyanotic hearts are associated with depleted endogenous antioxidants (glutathione peroxidase, superoxide dismutase, and catalase), and thereby is more susceptible to myocardial ischemia/reperfusion injury during open heart surgery compared with acyanotic ones. Clinically, when surgery is performed on cyanotic infants, cardiopulmonary bypass (CPB) is usually initiated at high PaO(2), without consideration of possible cytotoxic effects of hyperoxia. The concept of "surgical reoxygenation injury of cyanotic myocardium" was proposed, wherein unintended abrupt reoxygenation of cyanotic myocardium at the onset of routine CPB causes oxygen-mediated injury, which may render the reoxygenated myocardium more susceptible to subsequent surgical ischemia/reperfusion injury and accentuates post-CPB myocardial dysfunction. The experimental studies using acute and chronic hypoxia models confirmed the role of reoxygenation injury mediated by reactive oxygen species in the pathogenesis of post-CPB myocardial dysfunction and addressed the importance of controlling PaO(2) at the onset of CPB. The clinical relevance of this injury was shown by subsequent clinical studies, which demonstrated depleted antioxidant reserve capacity and troponin release during the initial reoxygenation on hyperoxic CPB prior to cardioplegic arrest. Furthermore recent randomized clinical trials verified that hyperoxic CPB provokes biochemical multi-organ damage including myocardium, lung, liver, and brain after open heart surgery in cyanotic patients, which can be successfully reduce by normoxic CPB management (i.e., reducing PaO(2) at onset of CPB, gradual reoxygenation and controlled reoxygenation protocol). Based on these experimental and clinical studies, avoidance of using hyperoxic PaO(2) on routine CPB is strongly recommended in the cyanotic patients.
Gen Thorac Cardiovasc Surg 2012 Sep
PMID:Surgical reoxygenation injury of the myocardium in cyanotic patients: clinical relevance and therapeutic strategies by normoxic management during cardiopulmonary bypass. 2278 41

Neurological complications are an important cause of morbidity in the postoperative period of cardiac surgery and its incidence reaches up to 75% of patients. An important cause of these events is the formation of microbubbles in the bloodstream during cardiopulmonary bypass. Integrative review was carried out on gaseous microemboli in cardiopulmonary bypass. This study analyzed studies with different methodological approaches, but that address the issue. The result suggests the denitrogenation of blood by hyperoxia dissolved microbubbles in the blood and venoarterial shunt can balance the respiratory parameters changed with hyperoxia.
Rev Bras Cir Cardiovasc
PMID:Gaseous microemboli in cardiac surgery with cardiopulmonary bypass: the use of veno-arterial shunt as a preventive method. 2328 86

Mechanical ventilation (MV) is a life-saving intervention for respiratory failure, including decompensated congestive heart failure. MV can reduce ventricular preload and afterload, decrease extra-vascular lung water, and decrease the work of breathing in heart failure. The advantages of positive pressure ventilation must be balanced with potential harm from MV: volutrauma, hyperoxia-induced injury, and difficulty assessing readiness for liberation. In this review, we will focus on cardiac, pulmonary, and broader effects of MV on patients with decompensated HF, focusing on practical considerations for management and supporting evidence.
J Cardiovasc Dev Dis 2016 Dec 02
PMID:Management of Mechanical Ventilation in Decompensated Heart Failure. 2936 76


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