Unilateral Hypoventilation in Man During Temporary Occlusion of One Pulmonary Artery*

129

A B S T R A C T We have examined the mechanisiis of abnormal gas exchange in seven patients with chroniic obliteration of the pulmonary vascular bed secondary to recurrent pulmonary emboli or idiopathic pulmonary hypertension. All ofthe patients had a widened alveolararterial oxygen gradient and four were significantly hypoxemic with arterial partial pressures of oxygen <80 torr. Using the technique of multiple inert gas elimination, we found that ventilation-perfusion (VA/Q) relationships were only minimally abnormlal w\ith a imiean of 10% (range, 2-19%) of cardiac output perfusing abnormal units. These units consisted of shunt ancd units with VA/0 ratios <0.1. In addition, the dead space was found to be normal in each patient. There was no evidence for diffusion impairment, and the widenied alveolar-arterial oxygen gradient was completely explained by VA/Q inequality. Significanit hypoxemila occurred only when VA/Q inequality was combined with a low mixed venous oxygen content.

Section: Resultsmentioning

confidence: 72%

Mechanisms of gas exchange abnormality in patients with chronic obliterative pulmonary vascular disease.

Dantzker¹,

Bower²

1979

129

“…Although these morphological changes are generally reversible over a period of several months, during which time a marked increase in the bronchial circulation occurs (3), the precise mechanisms responsible for producing the injury remain to be clarified. It is well established that acute pulmonary artery occlusion produces a severe reduction in the alveolar carbon dioxide tension in the occluded lung, which directly initiates the contraction of airway smooth muscle and leads to a reduction in lung volume and a shift in ventilation away from the occluded lung (4)(5)(6)(7). These changes in airway Received for publication 30 January 1980 and in revised form 7 March 1980. 36 mechanics are initially reversible with the administration of supplemental CO2 to the inspired gas (5,7).…”

Section: Introductionmentioning

confidence: 99%

Lamellar body depletion in dogs undergoing pulmonary artery occlusion.

Shepard¹,

Hauer²,

Miyai³

et al. 1980

A B S T R A C T We have investigated the relationship between pulmonary artery occlusion (PAO) and the surfactant system of the lung by studying the ultrastructural responses of type II alveolar pneumocytes to PAO of 4-12 h duration in 16 mongrel dogs. In six of these animals, the occluded lung was allowed to reperfuse for 6 h before killing and in four animals subjected to PAO of 4 h duration, the occluded lung was ventilated with 5% CO2 balance air. PAO by itself resulted in a dramatic 80% reduction in the volumetric density of lamellar bodies (LB) in the type II cells. This resulted predominantly from a decrease in volume of the individual LB. Although reperfusion was associated with an increase in LB volume density toward normal, 6 h of reperfusion was insufficient to re-establish normal type II cellular morphology. Ventilation of the occluded lung with 5% CO2 prevented LB depletion indicating that alveolar CO2 tension may affect the release and/or synthesis of LB in type II pneumocytes.

“…Bronchodilation following an increase in blood flow in the isolated left lower lobe ofthe dog (45) and after inhalation ofCO2 in the cat ( 18) have been reported. The time course of these changes in ventilation and airway resistance are rapid with responses occurring within 15 to 30 s (16,18) and are consistent with CA-catalyzed changes in local H+ concentration. The actions ofCO2 on bronchial tone appear to be local and at the level of the small airways since vagotomy and atropine (46, 47) and adrenergic stimulation (47) have no influence on C02-sensitive bronchomotor tone.…”

Section: Discussionmentioning

confidence: 56%

“…Swenson and colleagues (16,17) showed that during unilateral pulmonary occlusion in humans and dogs, changes in ventilation and airway resistance could be blocked by inhalation of 6% CO2 and this was confirmed later at the lobar and segmental level (43,44). Bronchodilation following an increase in blood flow in the isolated left lower lobe ofthe dog (45) and after inhalation ofCO2 in the cat ( 18) have been reported.…”

Section: Discussionmentioning

confidence: 94%

“…First, hypoxic pulmonary vasoconstriction is potentiated by high CO2 and H+ ( 15). Second, even in the absence of hypoxia, airways and vasculature and alveolar surfactant are pH sensitive and respond very rapidly to changes in ambient [H+] and [CO2] (15)(16)(17)(18)(19). Third, recent data suggest that the lung, heart, and skeletal muscle display temporal fluctuations in regional perfusion (20)(21)(22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of carbonic anhydrase inhibition on ventilation-perfusion matching in the dog lung.

Swenson¹,

Robertson²,

Hlastala³

1993

Lung carbonic anhydrase (CA) permits rapid pH responses when changes in regional ventilation or perfusion alter airway and alveolar Pco2. These pH changes affect airway and vascular resistances and lung compliance to optimize the balance of regional ventilation (VA) and perfusion (Q) in the lung. To test the hypothesis that these or other CA-dependent mechanisms contribute to VA/Q matching, we administered acetazolamide (25 mg/kg intravenously) to six anesthetized and paralyzed dogs and measured VA/Q relationships before and after CA inhibition by the multiple inert gas elimination technique. Four other groups of dogs were studied to control for possible confounding effects of time under anesthesia and nonselective CA inhibition by acetazolamide: (a) saline placebo as a control for duration of anesthesia, (b) 4% CO2 inhalation to mimic systemic CO2 retention, (c) 1 mg/kg benzolamide (a selective renal CA inhibitor) or 0.5 meq /kg HCO to mimic systemic metabolic acidosis, and (d) 500 mg/kg 4,4'-dinitrostilbene-2,2'-disulfonate (an inhibitor of red cell band 3 protein) to mimic the respiratory acidosis arising from an intracapillary block to rapid mobilization ofplasma HCO3 in CO2 exchange. Acetazolamide increased VA/Q mismatch and reduced arterial Po2 measured at equilibrium but these did not occur in the control group. There was no deterioration in VA/Q matching when systemic respiratory acidosis produced either by CO2 inhalation or 4,4'-dinitrostilbene-2,2'-disulfonate or metabolic acidosis (benzolamide or HCl) were imposed to mimic the effects of acetazolamide apart from its inhibition of lung CA. These results support the concept that lung CA subserves VA /Q matching in the normal lung. (J. Clin. Invest. 1993.92:702-709.)