Hypoxia and hypercarbia increase bronchial blood flow through bronchopulmonary anastomoses in anesthetized dogs

We studied the effect of systemic hypoxemia and hypercarbia on the bronchial blood flow in open-chested, anesthetized dogs. The pulmonary artery and vein of the left lower lobe (LLL) were isolated with cannulas and connected to reservoirs set at atmospheric pressure relative to the base of the LLL. That fraction of the bronchial arterial flow (Qbr) to the LLL, which flowed through the bronchopulmonary anastomoses into these reservoirs, was continuously measured. The LLL was inflated continuously with 6% CO2 and air at a constant alveolar pressure of 10 cm H2O. Systemic arterial O2 tension (PaO2) and arterial CO2 tension (PaCO2) were varied by separately ventilating the right lung through a bifurcated endotracheal tube. A 10-min period was allowed for stabilization after each change in experimental condition. Anastomotic Qbr was measured for 5 min during each experiment. In separate animals, similar studies were performed before and 30 min after intravenously administered indomethacin (6 mg/kg body weight). During normoxic conditions when PaO2 was 79 +/- 8 torr (mean +/- SEM), the mean anastomotic Qbr was 5.7 +/- 2.0 ml/min (n = 9). This flow increased to 8.3 +/- 2.5 ml/min (p less than 0.05) during hypoxemic conditions (PaO2, 38 +/- 3). The anastomotic Qbr increased from 5.8 +/- 1 to 9.0 +/- 2 ml/min (p less than 0.005) when PaCO2 was increased from 23 +/- 1 to 47 +/- 2 torr (n = 11). Pretreatment with intravenously administered indomethacin blocked both the hypoxemia-induced (n = 4) and hypercarbia-induced (n = 4) increases in anastomotic Qbr. We conclude that both hypoxemia and hypercarbia increased the anastomotic Qbr through a mechanism involving cyclooxygenase products of arachidonic acid.     

The effect of bronchial venous pressure on pulmonary edema in the dog

We examined the effect of elevating systemic venous pressure on the rate of edema formation in the left lower lobes (LLL) of anesthetized, open-chested dogs. The pulmonary circulation of the LLL was isolated using cannulae in the artery and vein which were attached to blood-filled reservoirs. The LLL was distended to an alveolar pressure of 25 cm H2O with 5% CO2 and air, and suspended from a strain gauge which allowed continuous weight recording. The pulmonary vascular pressures were raised so all of the LLL was in zone III. The rate of weight change occurring over the last 4 minutes of a 6 minute period of this pulmonary vascular pressure rise was taken to represent the control transvascular fluid flux. The rate of weight gain of the LLL was then determined with the same pulmonary vascular pressure elevation only when downstream bronchial venous pressure alone, downstream lymphatic pressure alone, or when both downstream lymphatic and bronchial venous pressures were elevated. The transvascular fluid flux was increased when downstream bronchial venous pressure was elevated. When only downstream lymphatic pressure was elevated there was no augmentation of transvascular fluid flux. These findings suggest that when a lung is already subjected to raised pulmonary vascular pressure sufficient to cause edema, acute elevation of bronchial systemic venous pressure augments the net rate of outward fluid flux, while downstream lymphatic pressure elevation does not.     

Vagal cooling and positive end-expiratory pressure reduce systemic to pulmonary bronchial blood flow in dogs

Positive end-expiratory pressure (PEEP) reduces systemic to pulmonary bronchial blood flow [Qbr(s-p)] presumably because it increases bronchial vascular resistance. Since PEEP increases lung volume and thus could stimulate pulmonary stretch receptors, we investigated the hypothesis that the PEEP-related decrease in bronchial blood flow was due to a reflex mediated by the vagus. In open-chest dogs the left lower lobe (LLL) was isolated, independently ventilated, perfused in situ with a closed pulmonary vascular circuit and weighed continuously. Qbr(s-p) was measured as LLL vascular circuit overflow and changes in LLL weight. When LLL PEEP was increased from 5 to 15 cm H2O in a group of 11 dogs Qbr(s-p) was reduced by half from 60.8 +/- 10.5 to 31.6 +/- 6.1 ml/min/100 g dry lobe weight. In another group of 7 dogs Qbr(s-p) was 46.5 +/- 6.9 with PEEP = 5 cm H2O; it decreased to 28.3 +/- 6.8 with bilateral cervical vagal cooling (0-1.5 degrees C) and did not decrease further after increasing PEEP to 15 cm H2O. We conclude that the effect of resting vagal tone is to increase Qbr(s-p) and that the effect of PEEP on Qbr(s-p) may be mediated at least partially by vagal influences.     

Pulmonary artery infusion of prostacyclin increases lobar bronchial blood flow

Intrapulmonary systemic to pulmonary bronchial blood flow [Qbr (s-p)] decreases with administration of cyclooxygenase inhibitors. This effect may be due to a decrease in the production of vasodilating prostaglandins and reflect either a decrease in the total intrapulmonary bronchial blood flow (Qbr), or a redistribution of the intrapulmonary systemic venous return. In nine open chested dogs the left lower lobe (LLL) was isolated and perfused in situ. Blood flow to the extrapulmonary airways (Qep), and Qbr were measured by the reference flow technique. Qbr (s-p) was measured as the overflow from the closed LLL perfusion circuit. After ibuprofen, PG-I2 was infused into the LLL PA and the Qbr (s-p) was continuously monitored. Qbr, and Qep were measured before and after ibuprofen, and during and after the PG-I2 infusion. The upstream pressure for Qbr (s-p) was estimated with and without PG-I2 infusion. After ibuprofen the Qep, Qbr, and Qbr (s-p) fell to 45, 22, and 17%, respectively, of the pre-ibuprofen values (P less than 0.05). PG-I2 increased the Qbr (s-p) and Qbr (P less than 0.05), while Qep was unchanged. During all experimental conditions the simultaneous measurements of Qbr and Qbr (s-p) were not different from each other (P less than 0.001). The upstream pressure for Qbr (s-p) increased from 30 to 50 cm H2O (P less than 0.05). Intralobar bronchial blood flow is drained almost entirely through the pulmonary circulation, and PG-I2 in the LLL pulmonary circulation increases systemic blood flow to the LLL, probably acting at the level of a systemic arteriole.     

Temperature dependence of intraparenchymal bronchial blood flow

Previous studies suggested that bronchial vascular resistance, like that of the skin, changes with the temperature of the surrounding tissue. To investigate this phenomenon, we recorded anastomotic (systemic to pulmonary) (Qbrs-p) and total (Qbr) bronchial blood flow over a temperature range centered on normal. In 7 open-chested dogs the in situ left lower lobe (LLL) was separately ventilated (30 degrees C, 5% CO2 in humidified air) and was suspended in a fabric net from a strain gauge for continuous recording of weight. The pulmonary circulation of the LLL was pump-perfused at 255 +/- 69 ml/min in a closed circuit with temperature set at 30, 33, 36, 39 and 42 degrees C. Qbrs-p was measured as overflow from the LLL vascular circuit corrected for LLL weight changes. Qbr, tracheal, mid-esophageal and coronary flow were measured with 15 mu radiolabelled microspheres injected in the left atrium. The animal's core temperature and that of the humidified air around the LLL were held constant. Qbr and Qbrs-p were equal and reached a peak at 36 degrees C with lower levels of flow at higher and lower temperatures. Esophageal, tracheal and coronary flow and cardiac output did not change nor did pressures in the systemic and LLL pulmonary artery and in the LLL airways. An intralobar change in temperature above or below 36 degrees C decreases only the lobar bronchial blood flow and does not influence blood flow to other nearby tissues including those vascularized by the bronchial circulation.     

Relationship of ultrafiltration and anastomotic flow in isolated rat lungs.

OBJECTIVE: When arterial and venous pressures are increased to equal values in "stop-flow" studies, perfusate continues to enter the pulmonary vasculature from the arterial and venous reservoirs. Losses of fluid from the pulmonary vasculature are due to ultrafiltration and flow through disrupted anastomotic (bronchial) vessels. This study compared the relative sites of ultrafiltration and anastomotic flows at low and high intravascular pressures. METHODS: Isolated rat lungs were perfused for 10 minutes with FITC-dextran, which was used to detect ultrafiltration. Arterial and venous catheters were then connected to reservoirs containing radioactively labeled dextrans at 20 or 30 cm H2O for 10 minutes. The vasculature was subsequently flushed into serial vials, and ultrafiltration and vascular filling during the equal-pressure interval were calculated. RESULTS: Ultrafiltration equaled 0.43 +/- 0.11 mL at 20 cm H2O and was similar to the volume of fresh arterial and venous perfusate which entered and remained in the pulmonary vasculature during the equal-pressure interval (0.45 +/- 0.10 mL). At 30 cm H2O, 0.80 +/- 0.23 mL entered and remained in the vasculature during the equal-pressure interval, replacing the original perfusate, and calculated transudation (0.56 +/- 0.09 mL) was not significantly more than at 20 cm H2O. Fluid also entered the airspaces at 30 cm H2O but not at 20 cm H2O. CONCLUSIONS: At 20 cm H2O, flow through anastomotic vessels occurs at sites that are at the arterial and venous ends of the microcirculation. Flow in exchange vessels remains minimal, permitting measurements of ultrafiltration and exchange. Losses of perfusate from the pulmonary vessels complicate measurements of ultrafiltration at 30 cm H2O.     

Functional anatomy of bronchial veins

The amount of bronchial arterial blood that drains into the systemic venous system is not known. Therefore, in this study we further delineated the functional anatomy of the bronchial venous system in six adult, anesthetized, and mechanically ventilated sheep. Through a left thoracotomy, the left azygos vein was dissected and the insertion of the bronchial vein into the azygos vein was identified. A pouch was created by ligating the azygos vein on either side of the insertion of the bronchial vein. A catheter was inserted into this pouch for the measurement of bronchial venous occlusion pressure and bronchial venous blood flow. An ultrasonic flow probe was placed around the common bronchial branch of the bronchoesophageal artery to monitor the bronchial arterial blood flow. Catheters were also placed into the carotid artery and the pulmonary artery. The mean bronchial blood flow was 20.6+/-4.2mlmin(-1) (mean+/-SEM) and, of this, only about 13% of the blood flow drained into the azygos vein. The mean systemic artery pressure was 72.4+/-4.1mmHg whereas the mean bronchial venous occlusion pressure was 38.1+/-2.1mmHg. The mean values for blood gas analysis were as follows: bronchial venous blood pH=7.54+/-0.02, PCO(2)=35+/-2.6, PO(2)=95+/-5.7mmHg; systemic venous blood-pH=7.43+/-0.02, PCO(2)=48+/-3.2, PO(2)=42+/-2.0mmHg; systemic arterial blood-pH=7.51+/-0.03, PCO(2)=39+/-2.1, PO(2)=169+/-9.8mmHg. We conclude that the major portion of the bronchial arterial blood flow normally drains into the pulmonary circulation and only about 13% drains into the bronchial venous system. In addition, the oxygen content of the bronchial venous blood is similar to that in the systemic arterial blood.     

Endobronchial changes in chronic pulmonary venous hypertension

The bronchial venous system closely communicates with the pulmonary circulation. To assess the changes in the bronchial circulation in chronic pulmonary venous hypertension, fiberoptic bronchoscopy and right heart catheterization were performed in 31 patients with mitral stenosis. Nonpulsatile submucosal vessel dilatation, consistently seen in all patients and called the vessel dilatation score, was assessed visually by three independent bronchoscopists. The vessel dilatation score was correlated more closely with pulmonary artery wedge pressure (r = 0.687) (p less than 0.001) than to mean pulmonary artery pressure (r = 0.531) (p less than 0.01) and right atrial pressure (r = 0.178) (NS). The vessel dilatation score decreased after reduction of the left atrial load by surgery. These results suggest that the dilated vessels observed in patients with mitral stenosis are bronchial veins that are engorged secondary to increased blood flow via bronchopulmonary anastomoses.     

Effect of edema on segmental vascular resistance in isolated lamb lungs determined by micropuncture

We have studied the mechanical effects of fluid accumulation on the pulmonary vasculature in 28 isolated blood perfused lungs of newborn lambs. Vascular resistance in the pulmonary arteries, microvessels, and veins was determined by micropuncture measurement of microvascular pressures, and regional distribution of blood flow in the lungs was determined using radiolabelled microspheres both before and after the development of varying degrees of hydrostatic edema. Edema was induced by raising venous pressure. During measurements, alveolar and venous pressures were kept constant at 7 and 8 cm H2O, respectively, as well as lung blood flow (540 +/- 107 ml/min). All vascular pressures were referenced to the superior surface of the lung, site of all micropunctures. Active vasomotor changes were eliminated by addition of papaverine to the perfusate. Under baseline nonedematous conditions in the absence of vasomotor tone, 17% of the total pressure drop was in arteries, 41% was in microvessels, and 42% was in veins. With the development of alveolar edema (80 +/- 13% weight gain), there was no change in total or segmental vascular resistance, but after 148 +/- 97% weight gain, total pulmonary vascular resistance increased by 74%. Segmental pressure drop increased in arteries by 172% and in microvessels by 132% but decreased by 22% in the venous segment. Regional distribution of blood flow remained unchanged. Possible mechanisms for increased resistance to blood flow may be compression of small arterioles and venules (less than 20 micron diameter) by liquid cuffs and/or occlusion of microvessels by the weight of alveolar liquid.     

Effect of lung surface tension on pulmonary vascular mechanics in excised dog lungs

We measured pulmonary vascular pressure (Pvas)-volume (Vvas) relationships in excised air and oil-filled dog lungs. First, pulmonary vessels were perfused with dextran and Pvas-Vvas curves of the total pulmonary circulation were measured. Second, air was perfused into the artery or vein, and the arterial or venous extra-alveolar Pvas-Vvas curves were measured. Alveolar vessel Pvas-Vvas curve was obtained by the substraction of both the arterial and venous extra-alveolar Pvas-Vvas curves from the total vascular Pvas-Vvas curves. When lung recoil pressure (PL) was reduced by filling the lung with oil at a given lung volume (VL), the determinants of pulmonary vascular dimensions and compliances were compared in terms of PL and VL. The arterial vascular area (Avas) was correlated with PL, while venous Avas was correlated with both PL and VL. Alveolar vessel Vvas at high Pvas reached its peak at PL 5 cm H2O. Compliance of arteries, veins, and alveolar vessels were correlated with PL. We concluded that lung surface tension contributes to the lung parenchyma's radial traction to the extra-alveolar vessels and that it also contributes to the stabilization of the alveolar vessels.     

Systemic to pulmonary bronchial blood flow in mitral stenosis

We measured systemic to pulmonary bronchial blood flow [Qbr(s-p)] during total cardiopulmonary bypass in 15 patients with mitral stenosis and elevated pulmonary venous pressure (group A, mean pulmonary wedge pressure = 22.2 +/- 5.4 mm Hg, mean +/- SD) and in 15 patients with coronary artery diseases and normal pulmonary venous pressure (group B). Qbr(s-p) is the volume of blood accumulating in the left side of the heart in the absence of pulmonary and coronary flows. This blood was vented through a cannula introduced into the left atrium and measured. Qbr(s-p) was 76.3 +/- 13.9 ml/min (2.18 +/- 0.37 percent of extracorporeal circulation pump flow) and 22.3 +/- 2.1 (0.63 +/- 0.15) in group A and B, respectively (p less than 0.01). During total cardiopulmonary bypass, pulmonary venous pressure is approximately atmospheric pressure, and no differences in systemic blood pressure, extracorporeal circulation pump flow, and airways pressure were observed between group A and B. Therefore, vascular resistance through the bronchial vessels draining into the pulmonary circulation is reduced in patients with mitral stenosis and elevated pulmonary venous pressure.     

Inspired gas relative humidity affects systemic to pulmonary bronchial blood flow in humans

To our knowledge, the effects of humidity of inspired air on bronchial blood flow in humans are unknown. During total cardiopulmonary bypass, we measured systemic to pulmonary bronchial blood flow (Qbr[s-p]) which is the volume of blood accumulating into the left side of the heart in the absence of pulmonary and coronary flow. A cannula was introduced into the right upper pulmonary vein and advanced into the lowermost portion of the left side of the heart. From this cannula Qbr(s-p) was vented by gravity and measured. Inspired gas (10 L/min, endotracheal tube, 50 percent O2 + 50 percent N2O) relative humidity was less than 20 percent and greater than 85 percent in group A (n = 25) and in group B (n = 25), respectively. Mean (+/- SE) Qbr(s-p) was 40.7 +/- 0.06 ml/min or 1.32 +/- 0.12 ml/min (percent cardiac output) in group A and 21.7 +/- 1.8 ml/min or 0.68 +/- 0.06 ml/min in group B. These data indicate that under these conditions Qbr(s-p) is increased by dry gas lung inflation in humans.     

Left atrial pressure can be accurately transmitted to the pulmonary artery despite zone 1 conditions

Pulmonary arterial occlusion pressure is not thought to reflect left atrial pressure (Pla) when alveolar pressure (PA) exceeds pulmonary venous pressure because alveolar capillaries collapse and the required continuous fluid column between the pulmonary artery and left atrium is interrupted. However, arterial-to-venous flow can occur when PA exceeds both the pulmonary arterial pressure (Ppa) and pulmonary venous pressure (i.e., in Zone 1 conditions), indicating the existence of a continuous patent vascular channel. Accordingly, Ppa should reflect Pla under these conditions. To investigate this connection cannulas were placed in the pulmonary arteries and left atria of eight excised rabbit lungs. Ppa and Pla were set 5 cm H2O above PA, which ranged from 0 to 25 cm H2O. Pla was then reduced in 2 to 4 cm H2O decrements while recording Ppa when arterial-to-venous flow ceased. At all PAs greater than 0 cm H2O, Pla was accurately reflected by the Ppa when both were exceeded by PA. The greater the PA, the lower the Ppa could track Pla below PA. Pla can be accurately measured by a pulmonary arterial catheter under Zone 1 conditions.     

Drainage routes of bronchial blood flow in anaesthetized sheep

The systemic circulation to the lung supplies the trachea and airway walls and may be important in the pathophysiology of asthma and pulmonary oedema. An understanding of the venous drainage pathways of this bronchial blood flow may be therapeutically important. The purpose of this study was to understand the normal drainage pathways in sheep. In seven anaesthetized, ventilated sheep we injected echo contrast agents into a systemic vein or into the bronchial artery while performing echocardiography to determine whether the drainage could be observed to the right heart and/or to the left heart. During transoesophageal echo (n=5) or heart surface echo (n=2), cephalic vein injection of <8 microm diameter gelatin microballoons promptly opacified the right but never the left-sided circulation. Air in agitated saline in the seven animals showed the same result. By contrast, injection into the bronchial artery promptly opacified the left atrium, left ventricle, and aorta but not the right-sided circulation in all seven microballoon injections and all but one of the air in agitated saline injections. The failure of the echo agents to pass through the pulmonary circulation may be related to sheep pulmonary intravascular macrophages or the surface forces on air bubbles of small size promoting collapse. The main conclusion is that there are bronchopulmonary anastomoses that connect the bronchial circulation to the pulmonary venous circulation connecting distal to the pulmonary capillaries. Any bronchial venous drainage to the right-sided circulation must have been below the detection level of the instruments and would in any case appear to be much less that the post-pulmonary capillary anastomoses noted. Pulmonary venous hypertension would be expected to have a direct effect on the bronchial circulation.     

Calculation of lung flow differential after single-lung transplantation: a transesophageal echocardiographic study

Single-lung transplantation (SLT) is a viable option for patients with end-stage pulmonary disease. After successful SLT, pulmonary blood flow is preferentially shifted to the transplanted lung, creating a flow differential. Lack of flow differential may be indicative of potential vascular complications such as anastomotic stenosis or thrombosis. To assess the ability of transesophageal echocardiography (TEE) in estimating lung flow differential in patients undergoing SLT, biplane TEE was prospectively performed in 18 consecutive patients undergoing SLT early (24 to 72 hours), and in 10 of them late (3 to 6 months) after surgery. Right and left pulmonary vein flow were calculated as Qnu=A. VTI, where A, the pulmonary vein area, was derived as pi.(D/2)(2) and VTI is the velocity time integral of the pulmonary vein spectral display. Lung flow differential was calculated as the ratio of right (RQnu) or left (LQnu) pulmonary vein flow to total pulmonary venous flow (RQnu + LQnu). Lung perfusion imaging scintigraphy (technetium-99m) was used for comparison. Pulmonary vein velocity time integral of transplanted lung was significantly greater than that of native lung (34 +/- 9 vs 18 +/- 8 cm, p <0.001). Percent differential lung flow derived by perfusion imaging scintigraphy and by TEE showed a good correlation (r = 0.67, p <0.001). Pulmonary artery anastomoses were seen in all 12 right-lung recipients, and in 4 of the 6 left-lung recipients; no significant stenosis was noted in the arteries visualized. The pulmonary venous anastomoses were imaged in all patients. Small, nonocclusive pulmonary vein thrombi were seen in 1 patient. In conclusion, TEE is a useful method for calculating lung flow differential in patients undergoing SLT. In addition, TEE provides superb direct visualization of the venous and arterial anastomoses in most patients. Contrary to previous reports, the overall incidence of anastomotic complications is relatively low.     

Bronchopulmonary arterial shunting without anatomic anastomosis in the dog.

The effects of bronchial arterial administration of vasoactive substances on the pulmonary circulation were studied by a new technique for selective catheterization of a bronchial artery in intact dogs. In most experiments, this technique permitted pressor agents to be distributed mainly to one lung with smaller amounts to the other lung. The intercostal arteries were avoided, and in all but 2 of 23 experiments only microscopic quantities of injected India ink could be identified in the distribution of the esophageal and mediastinal branches. These studies indicate that serotonin, angiotensin, histamine, and norepinephrine injected selectively into a bronchial artery increase lobar arterial pressure. Since blood flow was constant and left atrial pressure did not change, the increase in pressure suggests active pulmonary vasoconstriction. Additionally, the responses to bronchial and lobar arterial injections of pressor agents were similar. The contribution of bronchopulmonary shunt flow to pulmonary flow was small, since, under conditions of controlled lobar blood flow, changes in bronchial flow elicited by 65-75-mm Hg changes in bronchial arterial pressure produced little if any change in pressure in the perfused lobar artery or small vein. Bronchoconstriction contributed little to the response to bronchial administration of pressor agents, since responses were similar in the ventilated and the collapsed lobe. Injection of vasoflavine dyes into the bronchial artery showed the close proximity of bronchial and pulmonary arteries and confirmed the bronchial arterial origin of the vasa vasorum of pulmonary arteries. No vasa venorum were identified. Although no direct anatomic bronchial artery-pulmonary artery shunt was identified, ascorbic acid and 5-hydroxydopamine diffused rapidly into intrapulmonary arteries from the bronchial artery. These data suggest that the pulmonary pressor response results from passage of the vasoactive agents from the bronchial artery to the lobar artery through the vasa vasorum and by diffusion. Since no vasa venorum were found, pulmonary venoconstriction probably resulted from pressor agents reaching the veins by way of bronchopulmonary shunt flow. These results suggest a mechanism by which pressor substances present or liberated in the bronchial vascular bed can affect tone in the pulmonary vascular bed.     

The Effects of Endoscopic Sclerotherapy Combined with Transhepatic Variceal Obliteration on Portal Hemodynamics

We studied the effects of endoscopic sclerotherapy with transhepatic variceal obliteration on portal hemodynamics in 20 patients with cirrhosis (six with a spontaneous splenorenal shunt and 14 without it). Portal venous flow 1 month after combined therapy (measured by pulsed Doppler flowmeter) was significantly increased compared with that before therapy (n = 20, 843 +/- 339 vs. 669 +/- 253 ml/min, p less than 0.001). Portal vein catheterization and portal venous flow measurement were repeated 18 months after therapy in eight patients without a splenorenal shunt before therapy and in two patients with a splenorenal shunt before therapy. Two of the former developed a splenorenal shunt. In these 10 patients, portal venous flow before, one month, and 18 months after therapy was 617 +/- 219, 784 +/- 227, and 720 +/- 224 ml/min, respectively, and in 8 of 10 patients the portal venous flow at 18 months remained similar to the values at one month. Portal vein pressures were not significantly elevated 18 months after therapy (35.4 +/- 6.4 vs. 33.6 +/- 5.1 cm H2O) and the mean portal vein pressure change was 2.75 cm H2O (range -6 to +7.5 cm H2O). To summarize, portal venous flow was significantly increased one month after combined sclerotherapy in cirrhotics, the portal venous flow at 18 months remained similar to the values at 1 month in most patients, and the change in portal vein pressure after therapy was small.     

Acute ozone exposure increases bronchial blood flow in conscious sheep

This study was initiated to determine the effects of ozone (O3) on sheep airway blood flow. Twenty-three nasally intubated sheep were exposed to filtered air (n = 5), 1 ppm O3 (n = 4), 2 ppm O3 (n = 5), 3 ppm O3 (n = 5), and 4 ppm O3 (n = 4) for 3 h. Bronchial artery flow (Qbr) was measured using a chronically implanted 20 MHz pulsed Doppler flow probe. Qbr, mean aortic pressure, cardiac output, pulmonary artery pressure, arterial blood gases, and core temperature were monitored during the period of the exposures. Exposure to 3 and 4 ppm O3 resulted in a significant increase in Qbr (103 and 204% change, respectively) without affecting any of the other cardiopulmonary parameters measured. These results indicate that O3 induces a dose dependent increase in Qbr which is the result of a vasodilation of the bronchial vasculature which is not dependent upon changes in blood gases or upstream driving pressure.     

Shifts in external iliac venous pressure under local and general anaesthesia. Their impact on the tactics of venous thrombectomy in iliofemoral thrombosis

The authors measured the venous pressure in the iliofemoral segment in 12 patients in good general conditions, with a normal patency of the inferior caval vein, profound pelvic veins, and lower limb veins. Examination was performed with Claudy manometer. The resting venous pressure in the external iliac vein was 40--75 mm H2O = 3--5.5 mmHg. During Valsalva's manoeuvre the patients achieved an overpressure 250--1 100 mm H2O = 18--81 mmHg for 20 s. After induction of general anaesthesia and intubation, the anaesthesiologist produced an overpressure of 50 cm H2O in the patient's respiratory circuit for 20 s, but the venous pressure rose only to 90--175 mm H2O = 7-- mmHg. This rise is lesser with a high statistical significance than the overpressure produced in the Valsalva's manoeuvre. In the light of these results the authors discuss the tactics of venous thrombectomy. As a safe prevention of peroperative uplmonary embolism they regard either Valsalva's manoeuvre, carried out under local anaesthesia, or a tourniquet fixation of the clot head during the surgical intervention under general anaesthesia. The anaesthesiologist cannot prevent embolism by restriction of the venous return by producing an overpressure in the respiratory circuit of a patient under general anaesthesia.     

PEEP and "reverse mismatch". A case where less PEEP is best

A V/Q lung scan was obtained in a patient with LLL collapse who was receiving IPPV and PEEP. This revealed absent ventilation and hyperperfusion to the collapsed lobe. After a reduction in PEEP from 12 to 5 cm H2O, a repeat V/Q scan showed a more even distribution of pulmonary perfusion. Arterial hypoxemia improved.