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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The contractile effects of 19 factors on isolated human arterial segments at term pregnancy were quantified, and 14 contractile agents were similarly applied to preterm (23 to 35 weeks) umbilical arteries. Responses to potassium chloride were used to normalize the data. At comparison with the term vessel, the preterm artery contracted more to angiotensin II and arachidonic acid and was more sensitive to oxytocin. Contractions were greater in term arteries to vasopressin, norepinephrine, prostaglandin D2, and prostaglandin E2 but similar in both group of arteries to bradykinin, histamine, acetylcholine, and prostaglandin F2 alpha. Neuropeptide Y, linoleic acid, uridine triphosphate, and thrombin were ineffective. Hyperoxia inconsistently induced weak, short-lived contractions. Contractions to cooling manifested marked desensitization and tachyphylaxis. Serotonin was the only agonist that displayed the pharmacodynamic features most likely to be important for closure: potency, efficacy, and long duration of action (greater than 2.5 hours). It was postulated that cellular elements surrounding umbilical vessels are primary sources of vasoactive agents that are important to closure of the fetoplacental circulation at birth.
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PMID:Pharmacodynamic study of maturation and closure of human umbilical arteries. 291 87

For almost 10 years, numerous studies have shown that the pulmonary endothelium is endowed with a certain number of metabolic properties related to the uptake and hydrolysis of circulating vasoactive substances. Noradrenaline, serotonin, adenosine and possible certain prostaglandins are transported in the endothelial cells, according to processes which have now been clearly defined, and are there metabolised. Other compounds, including peptides (bradykinin, angiotensin I), or nucleotides (ATP, ADP, AMP) are hydrolysed in contact with the plasma membrane of the endothelium, without penetrating within the cell. For certain substrates (serotonin, angiotensin I), the properties of the pulmonary endothelial cell may be extended to systemic endothelial cells. For other substances, there would appear to be a specificity of endothelial function according to the site. It would appear that the lung, by virtue of its richness in endothelial cells, is capable of influencing concentrations of the circulating substances and, as a result, vascular tone. The existence of delicate processes of the uptake of substances has also been used to test the integrity of the cellular function of the pulmonary endothelium under experimental pathological condition, such as hyperoxia. However, before such a technique, based upon measurement os extraction of amines or other substances from various parts of the pulmonary circulation could be applied clinically, a critical consideration must be undertaken of the multiple factors involved in these processes. The major problem lies in the difficulty of distinguishing between dysfunction of the endothelial cells or a decrease in their number.
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PMID:[Measurement of pulmonary endothelial function; its potential clinical value]. 611 Dec 67

Angiotensin-converting enzyme (ACE) activity in the guinea pig fetal-placental unit was assessed at the different oxygen tensions found in utero, during labor, and at birth. To determine fetal-placental ACE activity, we separately perfused in situ term guinea pig fetuses and their placentas via the umbilical vessels under controlled conditions of flow, temperature, and pH. ACE activity was defined as the percent of angiotensin I (AO) or bradykinin (BK) in Krebs-Henseleit solution cleared by a single passage through the placenta or fetus. Peptide concentrations were measured by radioimmunoassay (RIA). Using BK as substrate, we found that placental and fetal ACE activities were reflected by 45% (SD = 10) and 24% (SD = 7) clearances, respectively, at a perfusate PO2 of 29 mm Hg. Maternal hypoxia (PaO2 = 28 mm Hg) decreased placental ACE activity to 16% (SD = 8) and maternal hyperoxia (PaO2 = 191 mm Hg) increased placental ACE activity to 56% (SD = 9). Using a perfusate PO2 of 95 mm Hg, fetal and placental ACE activity increased in less than 5 minutes to 75% (SD = 10) and 77% (SD = 9), respectively. Similar results were obtained using AI as substrate. We conclude that: fetal-placental ACE activity exhibits a chronically reduced level of activity appropriate to the low oxygen tension found in the fetal-placental unit; the placenta is the primary site of ACE activity in the fetus; maternal oxygenation modulates fetal-placental ACE activity; and fetal ACE activity acutely increases with increased fetal oxygenation and thus may play an important physiological role in the regulation of circulating levels of BK and AII and the circulatory adjustments at birth.
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PMID:Angiotensin-converting enzyme activity and its modulation by oxygen tension in the guinea pig fetal-placental unit. 389 3

Vascular tone has been shown to be importantly influenced by flow-induced release of endothelium-derived vasodilators. The purpose of the present study was to test the hypothesis that in porcine coronary resistance-size arterioles, flow-induced vasodilation is sensitive to oxygen tension. Arterioles (55-150 mu m) were studied in vitro under conditions of constant intraluminal pressure to dynamically measure arteriolar diameter in response to changes in flow or, alternatively, in response to bradykinin under three conditions: hyperoxia (pO(2) 400 mm Hg), normoxia (pO(2) 160 mm Hg), and hypoxia (p0(2) 40 mm Hg). Under conditions of constant pressure and no flow, hypoxia alone resulted in vasodilation that was blocked by the nitric oxide synthase inhibitor omega-nitro-L-arginine methyl ester (L-NAME). Hypoxia did not alter the vasodilator response to bradykinin when compared to the vasodilator response to bradykinin during normoxia. During hyperoxia, flow-induced vasodilation was significantly reduced by either indomethacin, or L-NAME. Indomethacin and L-NAME combined completely abolished flow-induced vasodilation under conditions of hyperoxia. Under conditions of normoxia and hypoxia, indomethacin or L-NAME alone only partially blocked flow-induced vasodilation. No further inhibition was observed when indomethacin and L-NAME were combined. Glybenclamide failed to alter flow-induced vasodilation either alone or in combination with indomethacin and L-NAME. The results suggest that the mechanisms responsible for flow-induced vasodilation in coronary arterioles are complex and are different depending upon the oxygen tension. During hyperoxia, vasodilation is due to the combined actions of prostanoids and nitric oxide, while under conditions of normoxia and hypoxia, flow-induced vasodilation is the result of not only prostanoids and nitric oxide, but of another as of yet unidentified oxygen-sensitive endogenous vasodilator.
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PMID:Effects of oxygen tension on flow-induced vasodilation in porcine coronary resistance arterioles. 899 34

Oxygenation with 95%O2 is routinely used in organ bath studies. However, hyperoxia may affect tissue responses, particularly in studies which involve reactive oxygen species (ROS). Here, the effects of the antioxidant, Tiron, were investigated under different gassing conditions in the porcine isolated coronary artery (PCA). Distal PCAs from male and female pigs were mounted in a wire myograph gassed with either 95%O2/5%CO2 or 95% air/5%CO2 and pre-contracted with U46619. Concentration-response curves to bradykinin were constructed in the presence of Tiron (1mM), a cell permeable superoxide scavenger and catalase (1000Uml(-1)) to breakdown H2O2. The H2O2 level in Krebs'-Henseleit solution was detected using Amplex Red. Bradykinin produced concentration-dependent vasorelaxations in male and female PCAs when gassed with either 95%O2 or air, with no differences in the Rmax or EC50. Tiron increased the potency of bradykinin only when gassed with 95%O2 in PCAs from both sexes. At 95%O2, catalase prevented the leftward shift caused by Tiron in both sexes indicating that catalase prevented the formation of H2O2 by Tiron. In female PCAs, addition of catalase to Tiron significantly reduced the Rmax. In the EDH-type response (using L-NAME and indomethacin), Tiron enhanced the potency of the bradykinin-induced vasorelaxation when gassed with 95%O2 in PCAs from both sexes. Biochemical analysis using Amplex Red demonstrated that H2O2 was generated in Krebs'-Henseleit solution when gassed with 95%O2, but not with air. Therefore, hyperoxic gassing conditions could alter the environment generating superoxide within the Krebs'-Henseleit buffer, which may, in turn, influence the in vitro pharmacological responses.
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PMID:Hyperoxic gassing with Tiron enhances bradykinin-induced endothelium-dependent and EDH-type relaxation through generation of hydrogen peroxide. 2545 Feb 47