Regional differences in nitric oxide‐mediated vasorelaxation in porcine pulmonary arteries

Rimeika, D; Wiklund, Peter; Lindahl, Sten G. E.; Wiklund, Claes U.

doi:10.1111/j.1399-6576.2006.01060.x

Cited by 10 publications

(11 citation statements)

References 38 publications

(58 reference statements)

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“…iNOS activity was generally lower than cNOS activity in both groups, which concurred with findings from previous studies in healthy and endotoxemic pigs [22,23]. Enzymes operate at an optimal intracellular pH, which can differ depending on cell type.…”

Section: Discussionsupporting

confidence: 80%

Hypercapnic acidosis transiently weakens hypoxic pulmonary vasoconstriction without affecting endogenous pulmonary nitric oxide production

et al. 2012

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Section: Discussionsupporting

confidence: 80%

Hypercapnic acidosis transiently weakens hypoxic pulmonary vasoconstriction without affecting endogenous pulmonary nitric oxide production

et al. 2012

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“…Furthermore, if NO was formed preferentially in dorsal lung as suggested by prior research (Pelletier et al, 1998 andRimeika et al, 2004), redistribution of Q to ventral lung should result with blockage of cNOS. However, we found a small but significant redistribution of Q from ventral to dorsal regions, Figure 10, contrary to what would be expected (Pelletier et al, 1998, Rimeika et al, 2004, Rimeika et al, 2006. There was no difference in total V/Q heterogeneity as a result of this small redistribution, which was also supported by a preserved PaO 2 and (A-a)O 2 difference.…”

Section: Minimal Change In V/q Distributions By L-namecontrasting

confidence: 54%

“…Beck and Rehder (Beck and Rehder, 1986) showed that vascular conductance was higher in dorsal lung in dogs in the supine, lateral and head-up positions, but the prone position was not examined. Evidence for uneven formation of NO in the lung was provided by in vitro studies showing greater eNOS activity in dorsal than in ventral lung regions in animals and humans, and similar regional differences in NO-mediated vasorelaxation in equine and porcine pulmonary arteries (Pelletier et al, 1998, Rimeika 2004et al, Rimeika et al, 2006. Rimeika et al (Rimeika et al, 2004) tried to confirm this by examining humans with SPECT in the prone and supine positions after inhibition of NO production.…”

Section: Endogenous No and V/q Matching Paper Iv: Inhibition Of Constmentioning

confidence: 96%

Gas Exchange in the Normal Lung : Experimental studies on the effects of positive end-expiratory pressure and body position

Johansson¹

2014

Linköping University Medical Dissertations

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BACKGROUND:The principal function of the lung is gas exchange requiring adequate ventilation and perfusion at the level of the alveoli. The efficiency of gas exchange is depending on the distributions of regional ventilation (V) and pulmonary blood flow (Q) and their correlation. AIMS:To validate a high-resolution method to quantify regional V and to investigate the Radioactive microspheres, 15 m in diameter, were used for determining regional Q. Nitric oxide synthase (NOS) was inhibited with Nω-nitro-L-arginine methyl ester (L-NAME) to evaluate the role of NO on regional V/Q matching. The right lung was dried at total lung capacity and diced in approx. 1000 regions tracking the spatial location of each region. CONCLUSION: There were marked differences in redistribution of regional ventilation and regional pulmonary blood flow between prone and supine position when PEEP was applied. RESULTS:NO was not an active mechanism for V/Q matching in normal sheep lungs. VII List of original papershis thesis is based on the following four papers, which will be referred to by their Roman numerals: I.Positive end-expiratory pressure affects regional redistribution of ventilation differently in prone and supine sheep.

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“…VB, 1 and 2). Alternatively, alteration of HPV by endogenous modulators such as NO could vary among regions (1633,1634).…”

Section: Edema Formationmentioning

confidence: 99%

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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Regional differences in nitric oxide‐mediated vasorelaxation in porcine pulmonary arteries

Cited by 10 publications

References 38 publications

Hypercapnic acidosis transiently weakens hypoxic pulmonary vasoconstriction without affecting endogenous pulmonary nitric oxide production

Hypercapnic acidosis transiently weakens hypoxic pulmonary vasoconstriction without affecting endogenous pulmonary nitric oxide production

Gas Exchange in the Normal Lung : Experimental studies on the effects of positive end-expiratory pressure and body position

Hypoxic Pulmonary Vasoconstriction

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