Influence of bronchial arterial PO2 on pulmonary vascular resistance

Marshall, Bryan E.; Marshall, Carol Lynn; Magno, Michael G.; Lilagan, P.; Pietra, G G

doi:10.1152/jappl.1991.70.1.405

Cited by 41 publications

(17 citation statements)

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“…Most investigators believe this omission is reasonable, since bronchial blood flow is so much smaller than pulmonary blood flow. Nevertheless, when the bronchial circulation of sheep was perfused at a pressure 40 mmHg higher than mean systemic arterial pressure (and thus at higher bronchial blood flow), decreases in bronchial arterial PO 2 caused modest HPV during ventilation with air, but not during ventilation with 100% O 2 (1194). Whether P a O 2 is a significant determinant of P s O 2 in intact animals remains unclear.…”

Section: Measurement Of Stimulus and Responsementioning

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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Section: Measurement Of Stimulus and Responsementioning

confidence: 99%

Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

607

621

View full text Add to dashboard Cite

show abstract

“…First, the absolute lung volume-FRC-is related to PVR through direct static effects on vascular compression. Studies in ex vivo lungs suggested that the relationship of lung volume with PVR followed a "U" shaped curve, with the PVR nadir at FRC (47,48). Second, data from in vivo isolated lung lobes suggest that the effects of nous O 2 tension, rather than lung volume per se (49).…”

Section: Atelectasis and Right Ventricular Dysfunctionmentioning

confidence: 99%

Atelectasis Causes Vascular Leak and Lethal Right Ventricular Failure in Uninjured Rat Lungs

Duggan

McCaul

McNamara

et al. 2003

Am J Respir Crit Care Med

155

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During mechanical ventilation, lung recruitment attenuates injury caused by high VT, improves oxygenation, and may optimize pulmonary vascular resistance (PVR). We hypothesized that ventilation without recruitment would induce injury in otherwise healthy lungs. Anesthetized rats were ventilated with conventional mechanical ventilation (VT 8 ml/kg; respiratory frequency 40 per minute) and 21% inspired oxygen, with or without a recruitment strategy consisting of recruitment maneuvers plus positive end-expiratory pressure, in the presence or absence of a laparotomy. Additional experiments examined the impact of atelectasis on right ventricular function using echocardiography, as well as functional residual capacity and PVR. Lack of recruitment resulted in reduced overall survival (59% nonrecruited vs. 100% recruited, p < 0.05), increased microvascular leak, greater impairment of oxygenation and lung compliance, increased PVR, and elevated plasma lactate. Echocardiography demonstrated that right ventricular dysfunction occurred in the absence of recruitment. Finally, samples from nonrecruited lungs demonstrated ultrastructural evidence of microvascular endothelial disruption. Although such effects clearly do not occur with comparable magnitude in the clinical context, the current data suggest novel mechanisms (microvascular leak, right ventricular dysfunction) whereby derecruitment may contribute to development of lung injury and adverse systemic outcome.

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“…Possibly, the arterial oxygenation of the bronchial circulation may add to the response too (Marshall et al . ). The degree of HPV reflects the severity of the hypoxic stimulus until very low oxygen tensions are reached and the HPV response may be blunted at inspiratory oxygen fractions <0.10 (De Canniere et al .…”

mentioning

confidence: 97%

The principal pathways involved in the in vivo modulation of hypoxic pulmonary vasoconstriction, pulmonary arterial remodelling and pulmonary hypertension

Kylhammar

Rådegran

2016

Acta Physiologica

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Hypoxic pulmonary vasoconstriction (HPV) serves to optimize ventilation-perfusion matching in focal hypoxia and thereby enhances pulmonary gas exchange. During global hypoxia, however, HPV induces general pulmonary vasoconstriction, which may lead to pulmonary hypertension (PH), impaired exercise capacity, right-heart failure and pulmonary oedema at high altitude. In chronic hypoxia, generalized HPV together with hypoxic pulmonary arterial remodelling, contribute to the development of PH. The present article reviews the principal pathways in the in vivo modulation of HPV, hypoxic pulmonary arterial remodelling and PH with primary focus on the endothelin-1, nitric oxide, cyclooxygenase and adenine nucleotide pathways. In summary, endothelin-1 and thromboxane A may enhance, whereas nitric oxide and prostacyclin may moderate, HPV as well as hypoxic pulmonary arterial remodelling and PH. The production of prostacyclin seems to be coupled primarily to cyclooxygenase-1 in acute hypoxia, but to cyclooxygenase-2 in chronic hypoxia. The potential role of adenine nucleotides in modulating HPV is unclear, but warrants further study. Additional modulators of the pulmonary vascular responses to hypoxia may include angiotensin II, histamine, serotonin/5-hydroxytryptamine, leukotrienes and epoxyeicosatrienoic acids. Drugs targeting these pathways may reduce acute and/or chronic hypoxic PH. Endothelin receptor antagonists and phosphodiesterase-5 inhibitors may additionally improve exercise capacity in hypoxia. Importantly, the modulation of the pulmonary vascular responses to hypoxia varies between species and individuals, with hypoxic duration and age. The review also define how drugs targeting the endothelin-1, nitric oxide, cyclooxygenase and adenine nucleotide pathways may improve pulmonary haemodynamics, but also impair pulmonary gas exchange by interference with HPV in chronic lung diseases.

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Influence of bronchial arterial PO2 on pulmonary vascular resistance

Cited by 41 publications

References 0 publications

Hypoxic Pulmonary Vasoconstriction

Hypoxic Pulmonary Vasoconstriction

Atelectasis Causes Vascular Leak and Lethal Right Ventricular Failure in Uninjured Rat Lungs

The principal pathways involved in the in vivo modulation of hypoxic pulmonary vasoconstriction, pulmonary arterial remodelling and pulmonary hypertension

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