Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion.

Tisi, Gennaro M.; Wolfe, Walter G.; Fallat, Robert J.; Ja, Nadel

doi:10.1152/jappl.1970.28.5.570

Cited by 15 publications

(16 citation statements)

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“…A normal percentage of ventilated but unperfused alveoli can be explained in 10 of them by the minimal circulatory defect on the scan (not exceeding 15% of the total perfusion), in 14 others by pulmonary infarction with abolition of ventilation in this region; in other cases a possible cause of erroneous diagnosis is alveolar hypoventilation by bronchoconstriction in avascular areas, which improves the ventilationperfusion ratio. This bronchoconstriction was demonstrated in animals (Cahill, Attinger, and Byrne, 1961;Nadel, Colebatch, and Olsen, 1964;Severinghaus et al, 1961 ;Stein et al, 1961;Thomas et al, 1964;Tisi, Wolfe, Fallat, and Nadel, 1970) and in man (Gurewich, Thomas, Stein, and Wessler, 1963;Swenson, Finley, and Guzman, 1961). Finally, another cause of underestimation of the alveolo-arterial gradient of Pco2 is the .…”

Section: Methodsmentioning

confidence: 89%

“…This relationship shows that the scan has greater sensibility for the smaller emboli; the normal alveolo-arterial gradient in such cases is probably explained by bronchoconstriction and hypoventilation occurring in pulmonary embolism (Cahill et al, 1961;Gurewich et al, 1963;Nadel et al, 1964;Severinghaus et al, 1961 ;Stein et al, 1961;Thomas et al, 1964;Tisi et al, 1970). On the other hand, the discrepancy between both estimations of vascular defect could be due to the fact that only the anterior views of the scan were retained for planimetry.…”

Section: Methodsmentioning

confidence: 98%

See 1 more Smart Citation

Value of measurement of alveolo-arterial gradient of PCO2 compared to pulmonary scan in diagnosis of thromboembolic pulmonary disease

Vereerstraeten

Schoutens

Tombroff

et al. 1973

Thorax

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Section: Methodsmentioning

confidence: 89%

Section: Methodsmentioning

confidence: 98%

Value of measurement of alveolo-arterial gradient of PCO2 compared to pulmonary scan in diagnosis of thromboembolic pulmonary disease

Vereerstraeten

Schoutens

Tombroff

et al. 1973

Thorax

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“…Immediately after the interruption of pulmonary blood flow, gas exchange ceases in the affected lung, alveolar CO 2 (PACO 2 ) falls, airway smooth muscle constricts [8,10] and the lung with the obstructed pulmonary artery becomes more difficult to ventilate. The length of time that hypocapnic bronchoconstriction persists after ligation is unknown, but it probably depends on the speed and extent of neovascularization of the lung by bronchial collaterals [3].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies of the acute (<1 day) effects of pulmonary artery occlusion [7][8][9][10] showed that, upon cessation of gas exchange, alveolar CO 2 fell, the airways constricted and lung impedance increased. As a result, inspired gas was diverted to the contralateral lung and arterial oxygen tension (PaO 2 ) and arterial carbon dioxide tension (PaCO 2 ) were maintained without the need for an increase in minute ventilation (VE).…”

mentioning

confidence: 97%

Respiratory mechanics and gas exchange in postobstructive pulmonary vasculopathy

Kelly

Bates²,

Michel³

1995

Eur Respir J

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R Re es sp pi ir ra at to or ry y m me ec ch ha an ni ic cs s a an nd d g ga as s e ex xc ch ha an ng ge e i in n p po os st to ob bs st tr ru uc ct ti iv ve e p pu ul lm mo on na ar ry y v va as sc cu ul lo op pa at th hy y ABSTRACT: Chronic unilateral pulmonary artery ligation induces formation of new bronchial collateral vessels in the affected lung. These vessels form precapillary anastomoses with the pulmonary circulation and the lung is perfused with arterial blood. Inspired gas is diverted to the contralateral lung to maintain the ventilation/ perfusion ratio (VA/Q) and gas exchange. This study was designed to determine the mechanism responsible for this shift of ventilation, which has not previously been investigated. We studied six dogs, before and 6 months after ligation of the left main pulmonary artery. We measured pulmonary resistance (RL) and elastance (EL), minute ventilation (VE), O 2 consumption (VO 2 ) and CO 2 production (VCO 2 ) of the right and left lungs. We also examined the effect of CO 2 , atropine and isoproterenol on RL and EL.In the lung with ligated pulmonary artery: 1) VE was significantly reduced; 2) RL and EL were increased and were unresponsive to CO 2 , atropine and isoproterenol; and 3) VO 2 decreased more than VCO 2 and, consequently, respiratory quotient (RQ) was greater than 1.We conclude that, with chronic pulmonary artery obstruction, ventilation shifts to the contralateral lung because of an increase in RL and EL not related to airway smooth muscle tone.

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“…rather than being secondary to the increase in smooth muscle tone produced by reduced CO2 in the airways (95).…”

Section: Transduction Properties Of Stretch Receptorsmentioning

confidence: 99%

Sensory Inputs to the Medulla

Pack¹

1981

Annu. Rev. Physiol.

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INTRODUCTION +1298Respiratory neurons in the medulla receive afferent information from many different sensory systems. Principal among these are the central and pe ripheral chemoreceptors, mechanoreceptors in the lung, and proprioceptors in the chest and abdominal wall. These sensory systems have been investi gated with respect to both the information they provide to the medulla and the nature of their transduction mechanisms. This short review focuses on the pulmonary vagal receptors, and on literature that has appeared since the two most recent extensive reviews of this topic (32, 68); both the transduc tion mechanisms and refl ex role of the receptors are considered. Other sensory systems-peripheral and central chemoreceptors-have been the subject of recent symposia (1, 51, 69). PULMONARY VAGAL RECEPTORSDuring the 1960s different names were employed by different investigators for essentially the same pulmonary vagal receptor. Further ANNUAL REVIEWS PACK PULMONARY STRETCH RECEPTORSFrom a functional point of view the main interest is in the stretch receptors (PSR). Evidence indicates that their afferent activity is involved in control of inspiratory and expiratory durations, and the instantaneous magnitude of neural output to a number of the main respiratory muscles. Distribution of Stretch ReceptorsAnatomical studies on the stretch receptors remain scarce although anatomical information on their distribution within the bronchial tree has been obtained by indirect physiological means (5,57,58). The receptors are thought to be situated in the bronchial smooth muscle. In the trachea, when the receptor is silenced by local dissection, the last piece of tissue to be removed is smooth muscle (5). The majority of the receptors (55.6%) are in the extrapulmonary airways (57). The total surface area of the extrapul monary airways is orders of magnitude less than that of the intrapulmonary airways (98); this implies large differences in the density of these receptors (per unit surface area of bronchial wall) between the extra and intrapulmo nary airways. This density of receptors in the extrapulmonary airways may however not refl ect their functional significance (49, 50).Within the intrapulmonary airways the receptors are also denser proxi mally (58). Such a distribution may have advantages, relating the distorting force on the bronchial wall more to the overall degree of lung infl ation and being less infl uenced by local mechanical derangements. A significant number of stretch receptors (of the order of 17% of the total) are located in the extrathoracic trachea (5). The mechanical forces on the extrathoracic trachea during ventilation are completely different from those on the intrathoracic airways. Transmural pressure, which distorts the wall, in the extrathoracic trachea is dependent on intratracheal pressure alone, whereas in the intrathoracic airways it refl ects transpulmonary pres sure. Since airfl ow is related to intratracheal pressure, the presence of receptors in this site may allow the control system to moni...

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Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion.

Cited by 15 publications

References 0 publications

Value of measurement of alveolo-arterial gradient of PCO2 compared to pulmonary scan in diagnosis of thromboembolic pulmonary disease

Value of measurement of alveolo-arterial gradient of PCO2 compared to pulmonary scan in diagnosis of thromboembolic pulmonary disease

Respiratory mechanics and gas exchange in postobstructive pulmonary vasculopathy

Sensory Inputs to the Medulla

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