Acute alveolar hypoxia increases endothelin-1 release but decreases release of calcitonin generelated peptide in isolated perfused rat lungs

Helset, E.; Kjæve, J.; Bjertnæs, Lars J.; Lundberg, Jan M.

doi:10.3109/00365519509104975

Cited by 23 publications

(13 citation statements)

References 26 publications

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“…In some studies (419, 1180, 1250, 1508), hypoxia did not increase pulmonary ET-1 production. In others (288, 767,1175,1883), both induction of ET-1 production by hypoxia and reversal of pulmonary vasoconstriction induced by ET-1 occurred very slowly, whereas the onset and offset of HPV occur rapidly (see sect. IIA2).…”

Section: I) Endothelin-1mentioning

confidence: 94%

“…Adenosine-activated potassium current in smooth muscle cells isolated from the pig coronary artery. J Physiol 471:[767][768][769][770][771][772][773][774][775][776][777][778][779][780][781][782][783][784][785][786]1993.364. Daut J, Maier-Rudolph W, von Beckerath N, Mehrke G, Gunther K, Goedel-Meinen L. Hypoxic dilation of coronary arteries is mediated by ATP-sensitive potassium channels.…”

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confidence: 99%

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Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

607

621

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It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution.

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Section: I) Endothelin-1mentioning

confidence: 94%

mentioning

confidence: 99%

Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

607

621

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“…CGRP has one endothelium-dependent mode of action (6) and also dilates some systemic arteries and the pulmonary circulation, inde-pendent of endothelial factors such as nitric oxide (27,35). Our laboratory previously shown that endogenous CGRP has an essential protective role in hypoxiainduced PH (HPH) (37,38) and that circulating levels of immunoreactive CGRP are reduced in rats with HPH, thus allowing constrictors such as endothelin (ET)-1 to act unopposed (14,39). Vasoconstriction is further enhanced by increased ET-1 synthesis in hypoxia (24).…”

mentioning

confidence: 99%

Three-week neonatal hypoxia reduces blood CGRP and causes persistent pulmonary hypertension in rats

Keith

Tjen‐A‐Looi

Kraiczi³

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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To increase understanding of persistent pulmonary hypertension, we examined chronic pulmonary effects of hypoxia at birth and their relationships with immunoreactive levels of the potent vasodilator, calcitonin gene-related peptide (CGRP). Rats were born in 10% hypobaric hypoxia, where they remained for 1-2 days, or in 15% hypoxia, where they remained for 21 days. All were then reared in normoxia for 3 mo followed by reexposure to 10% hypoxia for 7 days (H-->H) or continued normoxia (H-->N); age-matched normoxic rats were hypoxic for the last 7 days (N-->H) or normoxic throughout (N-->N). Results are as follows. Pulmonary arterial pressure (P(PA)) in 10% H-->N rats was normal at the end of the experiment (13 wk), but in rats reexposed to hypoxia (H-->H), pressure rose to 19% above N-->H controls. In 15% H-->N rats, P(PA) remained high, similar to that of N-->H rats, and increased further by 40% on reexposure (H-->H). Medial thickness of small pulmonary arteries in 10% H-->H rats also increased by 40% over N-->H controls and was equally high in 15% H-->N and H-->H rats. In N-->H rats from both experiments, right ventricular hypertrophy index (RVH) was increased after hypoxia at 15-16 wk. Also, in the 15% study, RVH remained elevated in H-->N rats and increased in H-->H rats by 19% above N-->H controls. Blood CGRP was reduced by neonate and adult hypoxia, and hypoxic reexposure (H-->H) further lowered blood CGRP in the 15% but not 10% study. Declining left ventricular blood CGRP correlated highly with logarithmically increasing P(PA) in the 15% study (r = -0.81, P = 0.000). In conclusion, 1) short perinatal exposure to 10% O(2) exacerbated pulmonary hypertension with hypoxia later in life, 2) 15% O(2) at birth and for 21 days caused persistent pulmonary hypertension and exacerbation with reexposure, and 3) P(PA) correlated highly with declining blood CGRP levels in the 15% study.

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“…Helset et al. () found increased ET‐1 protein levels in the perfusate of isolated rat lungs even earlier, that is after 5 min exposure to FiO 2 0.02. FiO 2 0.21 in our study was not sufficient to maintain adequate oxygen saturation over 120 min of ventilation (SpO 2 ~78% after 120 min).…”

Section: Discussionmentioning

confidence: 98%

Mechanical ventilation strategies alter cardiovascular biomarkers in an infant rat model

et al. 2018

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Mechanical ventilation (MV) is routinely used in pediatric general anesthesia and critical care, but may adversely affect the cardiocirculatory system. Biomarkers are increasingly measured to assess cardiovascular status and improve clinical treatment decision‐making. As the impact of mechanical ventilation strategies on cardiovascular biomarkers in ventilated infants is largely unknown, we conducted this retrospective study in a healthy in vivo infant rat ventilation model using 14‐days old Wistar rats. We hypothesized that 2 h of mechanical ventilation with high and low positive end‐expiratory pressure (PEEP), hyperoxemia, hypoxemia, hypercapnia, and hypocapnia would significantly impact B‐type natriuretic peptide (BNP), vascular endothelial growth factor (VEGF), and endothelin‐1 (ET‐1). We found BNP to be driven by both high (9 cmH2O) and low (1 cmH2O) PEEP compared to ventilated control animals (P < 0.05). VEGF concentrations were associated with high PEEP, hyperoxemia, hypoxemia, and hypocapnia (P < 0.05), whereas ET‐1 levels were changed only in response to hypoxemia (P < 0.05). In conclusion, the mode of mechanical ventilation alters plasma biomarker concentrations. Moreover, BNP and VEGF might serve as surrogate parameters for ventilation induced cardiovascular compromise and lung tissue damage. Furthermore, our data support the hypothesis, that sudden onset of hyperoxemia may trigger a quick VEGF release as a possible cellular survival reflex.

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Acute alveolar hypoxia increases endothelin-1 release but decreases release of calcitonin generelated peptide in isolated perfused rat lungs

Cited by 23 publications

References 26 publications

Hypoxic Pulmonary Vasoconstriction

Hypoxic Pulmonary Vasoconstriction

Three-week neonatal hypoxia reduces blood CGRP and causes persistent pulmonary hypertension in rats

Mechanical ventilation strategies alter cardiovascular biomarkers in an infant rat model

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