Direct injury to the bronchial vasculature in anesthetized sheep.

Injury to the bronchial vasculature may contribute to liquid and solute leakage into the lung during noncardiac pulmonary edema. The purpose of this study was to measure changes in hemodynamics, pulmonary mechanics, extravascular lung water, and lung morphometry after selectively injuring the bronchial vasculature in anesthetized sheep. In two groups of seven sheep, we injected oleic acid (0.1 ml/kg) or normal saline directly into the bronchoesophageal artery. We measured systemic and pulmonary arterial pressures, cardiac output, oxygen saturation, pulmonary resistance and compliance, and lung volumes before and 1 and 4 h after injection. The lungs were removed for measurement of extravascular water, histology, and morphometry. Four hours after injection of oleic acid, cardiac output decreased but pulmonary arterial pressure did not change. In addition, pulmonary resistance increased and dynamic compliance and vital capacity decreased. Extravascular lung water was slightly but significantly greater in the oleic acid group. Histological examination showed interstitial edema and leukocytes in airway walls and sloughing of bronchial epithelium but little or no alveolar edema. Morphometric analysis showed significant thickening of airway walls. We conclude that direct injury to the bronchial vasculature increases lung resistance, decreases dynamic compliance, and increases extravascular lung water by the accumulation of an inflammatory infiltrate in airway walls.     

Regulation of increase in anastomotic blood flow following pulmonary arterial occlusion

We have previously shown that there is an acute increase in anastomotic bronchial blood flow (Qbr) after pulmonary arterial obstruction in dogs. We examined the role of arachidonic acid metabolites in mediating this increase. The left lower lobe (LLL) was isolated and perfused (zone 2) with autologous blood in open-chested anesthetized dogs (n = 19). Qbr was measured from the amount of blood that overflowed from the closed vascular circuit of the suspended LLL and changes in its weight. In the control animals, there was a prompt and significant increase in Qbr following pulmonary arterial obstruction. Pretreatment with indomethacin (n = 6) or sodium salicylate (n = 4) almost completely blocked this rise in Qbr. Following pulmonary arterial occlusion, there was a rise in both thromboxane and a prostacyclin metabolite (6-keto-PGF1 alpha) in the blood of the pulmonary circulation of the LLL, although the 6-keto-PGF1 alpha rose relatively more. Pretreatment with indomethacin caused a fall in both thromboxane and prostacyclin levels (n = 3), which no longer rose after pulmonary arterial occlusion. These findings suggested that the balance of the vasodilator (prostacyclin) and vasoconstrictor (thromboxane) prostaglandins may play an important role in mediating the rise in Qbr that follows pulmonary arterial obstruction.     

Effect of a local disorder of bronchial patency on the circulation and gas exchange in the lungs

Acute and chronic experiments on dogs have demonstrated the onset of local alveolar hypoxia in disturbed bronchial patency. Alveolar hypoxia caused a rise in the pulmonary vascular resistance. Pulmonary hypertension is predetermined by an increased number of pulmonary zones of hypoxic vasoconstriction due to higher incidence and degree of bronchial obstruction. Despite pulmonary circulation redistribution confirmed by radioactive indicator 99mTc distribution, the perfusion of hypoventilated pulmonary regions is retained leading to venous shunt generation and the reduction of oxygen tension in the arterial animal blood.     

Acute increase in anastomotic bronchial blood flow after pulmonary arterial obstruction

We examined the acute changes in anastomotic bronchial blood flow (Qbr) serially for the 1st h after pulmonary arterial obstruction and subsequent reperfusion. We isolated and perfused the pulmonary circulation of the otherwise intact left lower lobe (LLL) with autologous blood in the widely opened chest of anesthetized dogs. Qbr was measured from the amount of blood overflowing from the closed pulmonary vascular circuit and the changes in the lobe weight. The right lung and the test lobe (LLL) were ventilated independently. The LLL, which was in zone 2 (mean pulmonary arterial pressure = 14.8 cm H2O, pulmonary venous pressure = 0, alveolar pressure = 5-15 cmH2O), was weighed continuously. The systemic blood pressure, gases, and acid-base status were kept constant. In control dogs without pulmonary arterial obstruction, the Qbr did not change for 2 h. Five minutes after pulmonary arterial obstruction, there was already a marked increase in Qbr, which then continued to increase for 1 h. After reperfusion, Qbr decreased. The increase in Qbr was greater after complete lobar than sublobar pulmonary arterial obstruction. It was unaltered when the downstream pulmonary venous pressure was increased to match the preobstruction pulmonary microvascular pressure. Thus, in zone 2, reduction in downstream pressure was not responsible for the increase in Qbr; neither was the decrease in alveolar PCO2, since ventilating the lobe with 10% CO2 instead of air did not change the Qbr. These findings suggest that there is an acute increase in Qbr after pulmonary arterial obstruction and that is not due to downstream pressure or local PCO2 changes.     

Pulmonary hypertension induced with an intra-arterial balloon: an alternate mechanism

The Laks catheter is a triple-lumen balloon catheter used to distend the canine main pulmonary artery while recording right ventricular pressure and the arterial pressure distal to the balloon. A rise in arterial pressure reported to occur during distension has been attributed to vasoconstriction rather than passive obstruction by the balloon. We tested this in six anesthetized dogs by inflating the Laks catheter-balloon while recording pressure distal to the balloon from the Laks catheter as well as from additional catheters in right and left pulmonary arteries placed retrogradely through lobar branches following thoracotomy. We found that balloon inflation increased pressures in the arterial port of the Laks catheter and in the left pulmonary artery catheter but reduced it in the right pulmonary artery. Tightening a snare around the right pulmonary artery had the same effects on pressures. Similar results were obtained while cardiac output was controlled by left ventricular bypass perfusion in four dogs. We conclude that the Laks catheter-balloon obstructs flow to the right lung and that the arterial pressure rise recorded in it during balloon inflation cannot be distinguished from that caused by occlusion of the right pulmonary artery.     

Angiogenesis in the Ischemic Rat Lung

The adult lung is perfused by both the systemic bronchial artery and the entire venous return flowing through the pulmonary arteries. In most lung pathologies, it is the smaller systemic vasculature that responds to a need for enhanced lung perfusion and shows robust neovascularization. Pulmonary vascular ischemia induced by pulmonary artery obstruction has been shown to result in rapid systemic arterial angiogenesis in man as well as in several animal models. Although the histologic assessment of the time course of bronchial artery proliferation in rats was carefully described by Weibel ¹, mechanisms responsible for this organized growth of new vessels are not clear. We provide surgical details of inducing left pulmonary artery ischemia in the rat that leads to bronchial neovascularization. Quantification of the extent of angiogenesis presents an additional challenge due to the presence of the two vascular beds within the lung. Methods to determine functional angiogenesis based on labeled microsphere injections are provided.     

Measurement of bronchial blood flow with radioactive microspheres in awake sheep

Distribution of bronchial blood flow was measured in unanesthetized sheep by the use of two modifications of the microsphere reference sample technique that correct for peripheral shunting of microspheres: 1) A double microsphere method in which simultaneous left and right atrial injections of 15-microns microspheres tagged with different isotopes allowed measurement of both pulmonary blood flow and shunt-corrected bronchial blood flow, and 2) a pulmonary arterial occlusion method in which left atrial injection and transient occlusion of the left pulmonary artery prevented delivery to the lung of microspheres shunted through the peripheral circulation and allowed systemic blood flow to the left lung to be measured. Both methods can be performed in unanesthetized sheep. The pulmonary arterial occlusion method is less costly and requires fewer calculations. The double microsphere method requires less surgical preparation and allows measurement without perturbation of pulmonary hemodynamics. There was no statistically significant difference between bronchial blood flow measured with the two methods. However, total bronchial blood flow measured during pulmonary arterial occlusion (1.52 +/- 0.98% of cardiac output, n = 9) was slightly higher than that measured with the double microsphere method (1.39 +/- 0.88% of cardiac output, n = 9). In another series of experiments in which sequential measurements of bronchial blood flow were made, there was a significant increase of 15% in left lung bronchial blood flow during the first minute of occlusion of the left pulmonary artery. Thus pulmonary arterial occlusion should be performed 5 s after microsphere injection as originally described by Baile et al. (1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary arterial distension does not cause pulmonary vasoconstriction

Distension of the main pulmonary artery or its major branches with an intraluminal balloon has been reported to cause pulmonary vasoconstriction by an unknown mechanism. This study was an attempt to confirm the pressor response and explore its cause. Several balloon distension methods were tried and discarded because they caused unintentional obstruction. Ultimately, I inflated a balloon placed retrogradely and confined to the left main pulmonary artery of six anesthetized open-chest dogs after ligating left lobar arterial branches. Blood flow and systemic gas composition were controlled by interposing an external pump oxygenator between the left ventricle and aorta. Pressures in the aorta, main pulmonary artery, and left atrium were recorded. Alveolar hypoxia was used as an independent test of pulmonary vasoreactivity. Although hypoxic pressor responses occurred, challenges with arterial distension did not change lung perfusion pressure. Silicone rubber casts were made of the arteries of six dogs used in pilot experiments. These revealed the limited lengths in which distenders can be placed without unintentional encroachment on flow. I could not support the conclusion that arterial distension causes vasoconstriction and am suspicious that the perfusion pressure increases reported by others may have been caused by undetected obstruction of a major arterial branch.     

Role of the rise of pressure in the pulmonary artery in the distribution of perfusion and gas exchange in bronchial obstruction

The experiments on the dogs revealed that the damage of lobar bronchus conduction resulted in the decrease of O2 tension in pulmonary venous blood of this lobe. The decrease in the ventilation and blood flow was found in the zone of obstruction by using tracers 133Xe and 99mTc. The pressure rise in the pulmonary artery caused by the spread of bronchial obstruction is one of the factors promoting the redistribution of perfusion into the reserve zones of lungs. The decrease of pressure by the ganglio-blocking preparation results in the increase of arterial hypoxemia.     

Effect of Salbutamol on Spirometry and Blood-gas Tensions in Bronchial Asthma

A new bronchodilator drug, salbutamol, reduced airway obstruction in 37 patients with bronchial asthma but did not lead to a significant fall in lowered arterial oxygen tension. This drug, unlike other bronchodilators, appears to have little or no effect on the cardiovascular system, and it is suggested that it does not therefore lead to an intensification of the ventilation/perfusion disturbance in the lung leading to a worsening of hypoxaemia.     

肺部感染对支气管封堵治疗影响的实验研究

目的:探讨肺部感染对支气管封堵治疗影响的动物实验性研究。方法:取健康杂种犬18条,分为3组(A、B、C组)(n=6),经支气管镜每只犬置入致密螺栓状支气管封堵器2枚,其中A、B组为肺部感染组,C组仅为单纯封堵(A、C组封堵后使用抗生素,而B组封堵后未使用抗生素)。观察实验动物的耐受性,定期复查血象、支气管镜、胸部CT扫描,8周后观察封堵器附近支气管组织及远端肺组织变化。结果:观察期内,除1例因给药管不慎封堵入靶支气管内而死亡外,其余犬耐受性良好;截至封堵第8周,36只封堵器中,脱落共有0只(0/36)。胸部CT扫描和组织病理学检查证实,部分封堵的肺叶有萎陷,封堵部位远端肺泡腔缩小,5例封堵部位及其周围有轻度阻塞性炎症改变,未出现肺脓肿及坏死。肺部感染因素对犬的恢复有延迟;而感染组术后肌注抗生素与否,并未能缩短实验动物的不适反应过程,亦未能预防或减少阻塞性炎症的发生。结论:试制的支气管封堵器置入方便,组织相容性好;无论单纯封堵还是肺部感染组的封堵,各组实验动物均有较好的耐受性,但是肺部感染因素对犬的恢复有延迟;肺部感染组术后肌注抗生素与否,对提高动物的耐受程度无明显作用。     

Systemic blood flow to the lung after bronchial artery occlusion in anesthetized sheep.

To compare the effectiveness of different embolizing agents in reducing or redistributing bronchial arterial blood flow, we measured systemic blood flow to the right lung and trachea in anesthetized sheep by use of the radioactive microsphere method before and 1 h after occlusion of the bronchoesophageal artery (BEA) as follows: injection of 4 ml ethanol (ETOH) into BEA (group 1, n = 5), injection of approximately 0.5 g polyvinyl alcohol particles (PVA) into BEA (group 2, n = 5), or ligation of BEA (group 3, n = 5). After occlusion, angiography showed complete obstruction of the bronchial vessels. There were no changes in tracheal blood flow in any of the groups. Injection of ETOH produced a 75 +/- 14% (SD) reduction in flow to the middle lobe (P less than 0.02) and a 75 +/- 13% reduction to the caudal lobe (P less than 0.01), whereas injection of PVA produced a smaller reduction in flow to these two lobes (41 +/- 66 and 51 +/- 54%, respectively). After BEA ligation there was a 52 +/- 29% reduction in flow to the middle lobe and a 53 +/- 38% reduction to the caudal lobe (P less than 0.05). This study has significant implications both clinically and experimentally; it illustrates the importance of airway collateral circulation, in that apparently complete radiological obstruction of the BEA does not necessarily mean complete obstruction of systemic blood flow. We also conclude that, in experimental studies in which the role of the bronchial circulation in airway pathophysiology is examined, ETOH is the agent of choice.     

Effects of embolus size on hemodynamics and gas exchange in canine embolic pulmonary hypertension

We examined the effects of different-sized glass-bead embolization on pulmonary hemodynamics and gas exchange in 12 intact anesthetized dogs. Pulmonary hemodynamics were evaluated by multipoint pulmonary arterial pressure (Ppa)/cardiac output (Q) plots before and 60 min after sufficient amounts of 100-microns (n = 6 dogs) or 1,000-microns (n = 6 dogs) glass beads to triple baseline Ppa were given and again 20 min after 5 mg/kg hydralazine in all the animals. Gas exchange was assessed using the multiple inert gas elimination technique in each of these experimental conditions. Embolization increased both the extrapolated pressure intercepts (by 6 mmHg) and the slopes (by 5 mmHg.l-1.min.m2) of the linear Ppa/Q plots, together with an 80% angiographic pulmonary vascular obstruction. These changes were not significantly different in the two subgroups of dogs. However, arterial PO2 was most decreased after the 100-microns beads, and arterial PCO2 was most increased after the 1,000-microns beads. Both bead sizes deteriorated the distribution of ventilation (VA)/perfusion (Q) ratios, with development of lung units with higher as well as with lower than normal VA/Q. Only 100-microns beads generated a shunt. Only 1,000-microns beads generated a high VA/Q mode and increased inert gas dead space. Hydralazine increased the shunt and decreased the slope of the Ppa/Q plots after 100-microns beads and had no effect after 1,000-microns beads. We conclude that in embolic pulmonary hypertension, Ppa/Q characteristics are unaffected by embolus size up to 1,000 microns.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left and Right Lung Asynchrony as a Physiological Indicator for Unilateral Bronchial Obstruction in Interventional Bronchoscopy

Background

In patients with bronchial obstruction, pulmonary function tests may not change significantly after intervention. The airflow asynchrony in both lungs due to unilateral bronchial obstruction may be applicable as a physiological indicator. The airflow asynchrony is reflected by the difference in the left and right lung sound development at tidal breathing.

Objectives

To investigate the usefulness of left and right lung asynchrony due to unilateral bronchial obstruction as a physiological indicator for interventional bronchoscopy.

Methods

Fifty cases with central airway obstruction were classified into three groups: tracheal, bronchial and extensive obstruction. The gap index was defined as the absolute value of the average of gaps between the left and right lung sound intensity peaks for a 12-second duration.

Results

Before interventional bronchoscopy, the gap index was significantly higher in the bronchial (p<0.05) and extensive obstruction groups (p<0.05) than in the tracheal group. The gap index in cases with unilateral bronchial obstruction of at least 80% (0.18±0.04 seconds) was significantly higher than in cases with less than 80% obstruction (0.02±0.01 seconds, p<0.05). After intervention for bronchial obstruction, the dyspnea scale (p<0.001) and gap index significantly improved (p<0.05), although no significant improvements were found in spirometric assessments. The responder rates for dyspnea were 79.3% for gap indexes over 0.06 seconds and 55.6% for gap indexes of 0.06 seconds or under.

Conclusions

Assessment of left and right lung asynchrony in central airway obstruction with bronchial involvement may provide useful physiological information for interventional bronchoscopy.     

Application of respiratory heat exchange for the measurement of lung water.

A noninvasive method for measuring pulmonary blood flow and lung mass (called airway thermal volume), based on the measurements of lung heat exchange with environment, is described. The lungs function as a steady-state heat exchange system, having an inner heat source (pulmonary blood flow) and an external heat sink (ventilation). Sudden changes in the steady-state condition, such as caused by hyperventilation of dry air, lead to a new steady state after a few minutes. The expired air temperature difference between the initial and final steady states is proportional to pulmonary blood flow, whereas the rate at which the new steady state is achieved is proportional to airway thermal volume. The method was tested in 20 isolated dogs lungs, 9 perfused goat lungs, and 27 anesthetized sheep. The expired air temperature fall during hyperventilation was inversely proportional to the perfusion rate of the isolated lungs, and half-time of the temperature fall was proportional to the lung tissue mass. Experiments in anesthetized sheep showed that the measured airway thermal volume is close to the total mass of the excised lungs, including its residual blood (r = 0.98). Pulmonary edema and fluid instillation into the bronchial tree increased in the measured lung mass.     

The ischemic lung: Role of the bronchial arteries in lung function

A patient with a dissecting aortic aneurysm, Type 1, developed acute pulmonary edema unexplained by the usual etiologic factors. Pathologic evidence that bronchial arterial circulation was interrupted led us to hypothesize that pulmonary edema could be due to ischemia of the bronchial circulation. To test this hypothesis, two chronic studies were done in dogs. The first study consisted of selective ligation of the right posterior bronchial artery at its origin at the fifth or sixth intercostal artery. After recovery from surgery, biopsies were taken from the ipsilateral and contralateral lung at time periods from 5 hours to 11 days. Ischemic damage was found in seven of eight dogs (87.5%), and was confined to the right lung. Histological examination revealed initial congestion within 8 hours, followed by pulmonary edema within 72 hours, and finally, disruption of alveolar septa with small emphysematous bullae on the eleventh postoperative day. The left lung remained normal in histological appearance. The second study consisted of transplanting the bronchial artery to the pulmonary artery to create a low pressure system and low O(2) content, and to simulate a regional shock situation. In five of six dogs (83.3%), the anastomosis was occluded within 72 hours, probably due to pressure competition from small collateral bronchial circulation. However, in these five dogs, pulmonary vascular resistance increased by 53%, intrapulmonary shunting increased by 83%, and the alveolar-to-arterial oxygen gradient increased by 150 mm Hg. Pulmonary edema was again confined to the right lung. Bronchial arteriograms demonstrated the extensive and variable distribution of the bronchial circulation in dogs. In the sixth dog, the anastomosis remained patent with a left-to-right shunt, due to a larger bronchial arterial collateral circulation. In this animal, the pulmonary arterial resistance, intrapulmonary shunting, and alveolar-arterial O(2) gradient were normal. Pulmonary edema was absent in lung biopsies. Bronchial circulation is discussed with respect to its clinical implications for lung transplants, shock, thoracic aneurysms, and mediastinal surgery. The results of this study suggest that the systemic bronchial circulation is important for normal lung function.     

Reflex tracheal smooth muscle contraction and bronchial vasodilation evoked by airway cooling in dogs

Pisarri, Thomas E., and Gordon G. Giesbrecht. Reflextracheal smooth muscle contraction and bronchial vasodilation evoked byairway cooling in dogs. J. Appl.Physiol. 82(5): 1566-1572, 1997.Coolingintrathoracic airways by filling the pulmonary circulation with coldblood alters pulmonary mechanoreceptor discharge. To determine whetherthis initiates reflex changes that could contribute to airwayobstruction, we measured changes in tracheal smooth muscle tension andbronchial arterial flow evoked by cooling. In ninechloralose-anesthetized open-chest dogs, the right pulmonary artery wascannulated and perfused; the left lung, ventilated separately, providedgas exchange. With the right lung phasically ventilated, filling theright pulmonary circulation with 5°C blood increased smooth muscletension in an innervated upper tracheal segment by 23 ± 6 (SE) gfrom a baseline of 75 g. Contraction began within 10 s of injection andwas maximal at ~30s. The response was abolished by cervical vagotomy.Bronchial arterial flow increased from 8 ± 1 to 13 ± 2 ml/min, withlittle effect on arterial blood pressure. The time course wassimilar to that of the tracheal response. This response was greatlyattenuated after cervical vagotomy. Blood at 20°C also increasedtracheal smooth muscle tension and bronchial flow, whereas 37°Cblood had little effect. The results suggest that alteration ofairway mechanoreceptor discharge by cooling can initiate reflexes thatcontribute to airway obstruction.

     

Bronchial vascular contribution to lung lymph flow

The lymphatic vessels of thelung provide an important route for clearance of interstitial edemafluid filtered from pulmonary blood vessels. However, the importance oflung lymphatics for the removal of airway liquid filtered from thesystemic circulation of the lung has not been demonstrated. We studiedthe contribution of the bronchial vasculature to lung lymph flow inanesthetized, ventilated sheep (n = 35). With the bronchial artery cannulated and perfused (control flow = 0.6 ml · min¹ · kg¹),lymph flow from the efferent duct of the caudal mediastinal lymph nodewas measured 1) during increasedbronchial vascular perfusion (300% of control flow);2) with a hydrated interstitium induced by a 1-h period of left atrial hypertension and subsequent recovery, both with and without bronchial perfusion; and3) during infusion (directly intothe bronchial artery) of bradykinin, an inflammatory mediator known tocause changes in bronchial vascular permeability. Increased bronchialperfusion for 90 min resulted in an average 35% increase in lung lymphflow. During left atrial hypertension, the increase in lung lymph flowwas significantly greater with bronchial perfusion (339% increase overbaseline) than without bronchial perfusion (138% increase).Furthermore, recovery after left atrial hypertension was more completeafter 90 min without bronchial perfusion (91%) than with bronchialperfusion (63%). Infusion of bradykinin into the bronchial arteryresulted in a prompt and prolonged 107% increase in lung lymph flow.This was not seen if the same dose was infused into the pulmonaryartery. Thus bronchial vascular transudate contributes significantly to lymph flow from the efferent duct of the caudal mediastinal lymph node.These results demonstrate that lymph vessels clear excess fluid fromthe airway wall and should be considered when evaluating the effect ofvascular leak in airway obstruction.

     

Bronchial collateral vessel micropuncture pressure in postobstructive pulmonary vasculopathy.

Postobstructive pulmonary vasculopathy, produced by chronic ligation of one pulmonary artery, markedly increases bronchial blood flow. Previously, using arterial and venous occlusion, we determined that bronchial collaterals enter the pulmonary circuit at the distal end of the arterial segment. In this study, we tested the hypothesis that pressure in bronchial collaterals (Pbr) closely approximates that at the downstream end of the arterial segment (Pao). We pump perfused [111 +/- 10 (SE) ml/min] left lower lobes of seven open-chest live dogs 3-15 mo after ligation of the left main pulmonary artery. Bronchial blood flow was 122 +/- 16 ml/min. We measured pulmonary arterial and venous pressures and, by arterial and venous occlusion, respectively, Pao and the pressure at the upstream end of the venous segment (Pvo). Pbr was obtained by micropuncture of 34 pleural surface bronchial vessels 201 +/- 16 microns in diameter. We found that Pbr (14.4 +/- 1.0 mmHg) was similar to Pao (15.0 +/- 0.8 mmHg) but differed significantly (P < 0.01) from Pvo (11.3 +/- 0.5 mmHg). In addition, Pbr was independent of systemic arterial pressure and bronchial vessel diameter. Light and electron microscopy revealed that, in the lobes with the ligated pulmonary artery, the new bronchial collaterals entered the thickened pleura from the parenchyma via either bronchovascular bundles or interlobular septa and had sparsely muscularized walls. We conclude that, in postobstructive pulmonary vasculopathy, bronchial collateral pressure measured by micropuncture is very close to the pressure in precapillary pulmonary arteries and that most of the pressure drop in the bronchial collaterals occurs in vessels > 350 microns in diameter.     

Advances in magnetic resonance imaging of lung physiology.

This review presents an overview of some recent magnetic resonance imaging (MRI) techniques for measuring aspects of local physiology in the lung. MRI is noninvasive, relatively high resolution, and does not expose subjects to ionizing radiation. Conventional MRI of the lung suffers from low signal intensity caused by the low proton density and the large degree of microscopic field inhomogeneity that degrades the magnetic resonance signal and interferes with image acquisition. However, in recent years, there have been rapid advances in both hardware and software design, allowing these difficulties to be minimized. This review focuses on some newer techniques that measure regional perfusion, ventilation, gas diffusion, ventilation-to-perfusion ratio, partial pressure of oxygen, and lung water. These techniques include contrast-enhanced and arterial spin-labeling techniques for measuring perfusion, hyperpolarized gas techniques for measuring regional ventilation, and apparent diffusion coefficient and multiecho and gradient echo techniques for measuring proton density and lung water. Some of the major advantages and disadvantages of each technique are discussed. In addition, some of the physiological issues associated with making measurements are discussed, along with strategies for understanding large and complex data sets.