Hypoxic contraction of pre-stretched human pulmonary artery

Ohe, Masatoshi; Ogata, Masahiko; Katayose, Dai; Takishima, Tamotsu

doi:10.1016/0034-5687(92)90103-4

Cited by 27 publications

(26 citation statements)

References 16 publications

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“…HV was also abolished by an exogenous source of NO, in agreement with previous experimental data documented by OHE et al [9] and clinical studies in healthy subjects [19] and COPD patients [12]. The authors found that the presence of endotheliumindependent vasodilators, such as SNP or NO gas bubbled directly in the organ bath chamber, were potent and effective antagonists of hypoxic contraction.…”

Section: Discussionsupporting

confidence: 79%

See 1 more Smart Citation

Response to hypoxia of pulmonary arteries in chronic obstructive pulmonary disease: anin vitrostudy

Peinado

Santos²,

Ramírez³

et al. 2002

Eur Respir J

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Response to hypoxia of pulmonary arteries in chronic obstructive pulmonary disease: an in vitro study. V.I. Peinado, S. Santos, J. Ramírez, J. Roca, R. Rodriguez-Roisin, J.A. Barberà. #ERS Journals Ltd 2002. ABSTRACT: Patients with chronic obstructive pulmonary disease (COPD) show impaired hypoxic pulmonary vasoconstriction that might contribute to abnormal gas exchange and could be related to endothelial dysfunction in pulmonary arteries. The aim of the study was to investigate the response of PA to hypoxic stimulus in vitro in COPD, and the role of endothelium-derived nitric oxide (NO) in this response.The pulmonary arteries of 25 patients who underwent lung resection were studied. Patients were divided into controls, COPDznormoxaemia (COPDN) and COPDz hypoxaemia (COPDH). Hypoxic vasoconstriction (HV) was evaluated before and after stimulation or inhibition of the endothelial release of NO, and in the presence of exogenous NO.Compared with the other groups, HV was reduced in COPDH. The magnitude of HV correlated with the oxygen tension in arterial blood. The hypoxic stimulus induced greater contraction after stimulating endothelial release of NO, whereas its inhibition practically abolished HV. Exogenous NO completely inhibited HV. Maximal relaxation induced by endothelium-dependent vasodilators correlated with the magnitude of HV.In conclusion, pulmonary arteries of patients with chronic obstructive pulmonary disease and hypoxaemia have an impaired response to hypoxic stimulus, and the endothelial release of nitric oxide modulates hypoxic vasoconstriction. The depressed response of pulmonary arteries to hypoxia may contribute to abnormal gas exchange in chronic obstructive pulmonary disease.

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Section: Discussionsupporting

confidence: 79%

“…In vitro studies, where pulmonary artery rings are exposed to hypoxia, have only been conducted in series of patients with undefined respiratory disease [7][8][9]. To the current authors9 knowledge, there are no studies where the profile of the response to hypoxic stimulus in pulmonary arteries of COPD patients had been characterised in vitro.…”

mentioning

confidence: 99%

Response to hypoxia of pulmonary arteries in chronic obstructive pulmonary disease: anin vitrostudy

Peinado

Santos²,

Ramírez³

et al. 2002

Eur Respir J

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“…3. Figure 3b shows the change in tension (in milligrams) developed by a 3-mm-long segment of human pulmonary artery of external diameter 2 mm when exposed for 15 min to hypoxia (PO 2 5.7 kPa) [53]. Note that the tension is generated at right angles to the long axis of the vessel (Fig.…”

Section: Measures Of Vasoconstrictor Activity In Isolated Pulmonary Amentioning

confidence: 98%

Human pulmonary vascular responses to hypoxia and hypercapnia

Dorrington¹,

Talbot²

2004

Pflugers Arch - Eur J Physiol

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The ability of alveolar gas composition to influence pulmonary vascular tone has been appreciated for over 50 years. In particular, it has been proposed that both O2 and CO2 could play a role in the matching of perfusion to ventilation within the lung, improving the overall efficiency of gas exchange. A wide variety of experimental approaches has been used to investigate pulmonary vascular effects of the respiratory gases in a range of mammalian species. In this article, we review experiments performed in healthy humans, identify particular difficulties in the interpretation of such experiments, and discuss possible approaches to future study.

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“…Conversely in hypoxic conditions, the contraction to 5-hydroxytryptamine increased, and this appears to implicate the cyclooxygenase pathway. In the same way Ohe et al [10] have shown in human pulmonary arteries that the contraction was enhanced by cyclooxygenase inhibitors. In contrast, Xie and Triggle [22] recently showed in human umbilical arteries that relaxations due to acetylcholine and the calcium ionophore A 23187 are independent of the endothelium, that they are not mediated by nitric oxide or cyclooxygenase products and that they are not affected by changes in PO 2 .…”

Section: Discussionmentioning

confidence: 54%

“…Cyclooxygenase inhibitors reduce hypoxia constriction in human, pig and sheep pulmonary artery rings [8,9]. However, other reports have shown that hypoxic contraction of the pulmonary artery is unaffected in rats but enhanced in humans by cyclooxygenase inhibitors [10]. In coronary artery rings indomethacin reduced the contractions but had no effect on the relaxation induced by hypoxia.…”

Section: Introductionmentioning

confidence: 79%

5-Hydroxytryptamine Induces Vasoconstriction of the Human Umbilical Artery: Effects of Hypoxia and Nicorandil

Tiritilli

2000

Gynecol Obstet Invest

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Human umbilical arteries are known to be modulated by oxygen partial pressure. To further understand the underlying mechanisms, rings were suspended in organ chambers for the measurement of isometric force. The effects of 5-hydroxytryptamine (10^–9 to 10^–5 M) were first investigated before and after hypoxic conditions (5% O₂–5% CO₂ in N₂). Then after pretreatment, we tested indomethacin (10^–5 M), N-nitro-L-arginine (L-NNA, 10^–5 M) and nicorandil (10^–5 M) each separately, then each of the three substances together with hypoxia. In separate experiments the contractions to 5-hydroxytryptamine (10^–9 to 10^–5 M) were effectuated in a glucose-free medium, and mitochondrial respiration was inhibited by cyanide (2 mM). Hypoxic conditions significantly reduced the contractive response to 5-hydroxytryptamine. Contractions were enhanced after indomethacin, but remained unchanged after L-NNA. Pretreatment with nicorandil decreased the contraction. Furthermore, hypoxia and nicorandil dramatically decreased the contraction to 5-hydroxytryptamine. In glucose-free medium under normoxia or in hypoxic conditions, 5-hydroxytryptamine did not induce any contraction. Moreover, cyanide (2 mM) remained without effect on the contraction obtained by 5-hydroxytryptamine. These results suggest that hypoxia and nicorandil attenuate vasoconstrictor responses to 5-hydroxytryptamine in human umbilical arteries. Furthermore, these findings suggest that prostacyclin acts as a functional antagonist to vasoconstriction whereas nitric oxide does not. Finally, glycolysis seems to be involved rather than mitochondrial metabolism.

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Hypoxic contraction of pre-stretched human pulmonary artery

Cited by 27 publications

References 16 publications

Response to hypoxia of pulmonary arteries in chronic obstructive pulmonary disease: anin vitrostudy

Response to hypoxia of pulmonary arteries in chronic obstructive pulmonary disease: anin vitrostudy

Human pulmonary vascular responses to hypoxia and hypercapnia

5-Hydroxytryptamine Induces Vasoconstriction of the Human Umbilical Artery: Effects of Hypoxia and Nicorandil

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