Detection of A/H5N1 virus from asymptomatic native ducks in mid-summer in Egypt.

In spite of all the efforts to control H5N1 in Egypt, the virus still circulates endemically, causing significant economic losses in the poultry industry and endangering human health. This study aimed to elucidate the role of clinically healthy ducks in perpetuation of H5N1 virus in Egypt in mid-summer, when the disease prevalence is at its lowest level. A total of 927 cloacal swabs collected from 111 household and 71 commercial asymptomatic duck flocks were screened by using a real-time reverse transcription polymerase chain reaction. Only five scavenging ducks from a native breed in three flocks were found infected with H5N1 virus. This study indicates that H5N1 virus can persist in free-range ducks in hot weather, in contrast to their counterparts confined in household or commercial settings. Surveillance to identify other potential reservoirs is essential.

Effect of contrast media on coronary vascular resistance: contrast-induced coronary vasodilation.

STUDY OBJECTIVES: To determine if the vasodilatory response to the intracoronary injection of ionic and nonionic contrast media in intact pigs is dependent on nitric oxide (NO). The mechanisms responsible for inducing the increase in coronary blood flow in response to the intracoronary injection of contrast media during angiography are still not entirely understood. There is evidence to suggest that the response could be partially mediated by NO. PARTICIPANTS: We studied 14 anesthetized, open-chested pigs receiving ventilation. MEASUREMENTS AND RESULTS: Changes in coronary blood flow and coronary vascular resistance were measured in response to the coronary artery injection of saline solution (0.5 mol/L, isosmolar with plasma) and three different contrast agents: meglumine sodium ioxaglate (Hexabrix; Mallinckrodt Medical; Point-Claire, Quebec, Canada), a low osmolar ionic contrast agent; iohexol (Omnipaque 300; Sanofi Winthrop; Markham, Ontario, Canada), a nonionic contrast agent; and diatrizoate meglumine 66%, diatrizoate sodium 10% (MD-76; Mallinckrodt Medical), an ionic contrast agent. Measurements were made during three experimental conditions: the coronary artery infusion of (1) saline solution, control; (2) L-nitro-arginine (LNNA; 10(-3) mol/L and 10(-2) mol/L), a competitive inhibitor of NO synthase; and (3)L-arginine 10(-1) mol/L, a substrate for NO synthase. The infusion of LNNA produced an increase in baseline coronary vascular resistance (p < 0.001), but it did not attenuate the vasodilatory response to the infusion of the contrast agents. Both the high and low osmolar ionic and nonionic contrast media caused a decrease in baseline coronary vascular resistance. For all three conditions, MD-76, which has the highest osmolality, produced the greatest decrease in coronary vascular resistance. CONCLUSION: The vasodilatory response of the coronary vasculature to contrast agents is directly related to osmolality and is not mediated by NO.

Bronchopulmonary anastomotic and noncoronary collateral blood flow in humans during cardiopulmonary bypass.

The sole source of blood returning to the left atrium during cardiopulmonary bypass, while the aorta is cross-clamped, is the bronchopulmonary anastomotic blood flow. In addition, there is noncoronary collateral blood flow which returns to the right atrium. Routinely, the bronchopulmonary anastomotic flow is drained from the left ventricle by a cannula and returned to the main circuitry via a cardiotomy reservoir. The noncoronary collateral flow may be vented similarly by introducing a cannula into the right atrium. Both the anastomotic and the noncoronary collateral flow can be measured with no further surgical intervention. We measured bronchopulmonary anastomotic flow in 40 patients undergoing coronary artery bypass surgery and the noncoronary collateral blood flow in 27 of these patients. Results from this study show that the bronchopulmonary anastomotic flow for the 40 patients was 140 +/- 182 ml/min (range 8 to 1,043 ml/min), representing 3.23 +/- 4.15 percent of the pump flow (equivalent to the cardiac output), and the noncoronary collateral flow in the 27 patients was 48 +/- 74 ml/min (range 0 to 261 ml/min), representing 1.11 +/- 1.67 percent of the pump flow.

Phrenic nerve function and its relationship to atelectasis after coronary artery bypass surgery.

Atelectasis following coronary artery bypass surgery (CAB) occurs in the majority of patients. To determine the importance of operative variables in the development of postoperative atelectasis and the incidence of phrenic nerve injury caused by topical cold cardioplegic solution, we studied 57 patients (53 male, four female) undergoing CAB. Their mean age, +/- SD, was 58 +/- 13 years. Transcutaneous stimulation was used to evaluate phrenic nerve function preoperatively and postoperatively in 52 patients. An unequivocal paresis of the phrenic nerve was documented in five patients. In an additional 27 patients, the amplitude of the compound diaphragm action potential was reduced postoperatively. However, methodologic limitations did not allow the conclusion that this was secondary to a phrenic axonal degeneration. Discriminant analysis of intraoperative variables showed more severe atelectasis with a larger number of grafts, with a longer operative and bypass time, when the pleural space was entered, when a right atrial drain and a cardiac insulating pad were not used, and with a lower body temperature. It is concluded that phrenic paresis may occur after CAB and topical cold cardioplegia, but that other factors must explain the atelectasis found in the majority of patients.

Effect of autonomic blockade on tracheobronchial blood flow.

Tracheobronchial blood flow increases two to five times in response to cold and warm dry air hyperventilation in anesthetized tracheostomized dogs. In this series of experiments we have attempted to attenuate this increase by blockade of the autonomic nervous system. Four groups of anesthetized, tracheostomized, open-chest dogs were studied. Group 1 (n = 5) were hyperventilated for 30 min with 1) warm humid [approximately 26 degrees C, 100% relative humidity, (rh)] air followed by bilateral vagotomy, 2) warm humid air, 3) cold (-22 degrees C, 0% rh) dry air, and 4) warm humid air. Groups 2, 3, and 4 (n = 3/group) were hyperventilated for 30 min with 1) warm humid (approximately 41 degrees C, 100% rh) air, 2) warm dry (approximately 41 degrees C) air, 3) warm humid air, and 4) warm dry air. Group 2 were controls. Group 3 were given phentolamine, 0.6 mg/kg intravenously, as an alpha-blockade, and group 4 were given propranolol, 1 mg/kg, as a beta-blockade after warm dry air hyperventilation (period 2). Five minutes before the end of each 30-min period of hyperventilation, measurements of vascular pressures, cardiac output, arterial blood gases, and inspired, body, and tracheal temperatures were measured, and differently labeled radioactive microspheres were injected into the left atrium to make separate measurements of airway blood flow. After the last measurements had been made animals were killed and their lungs were excised. Blood flow to the airways and lung parenchyma was calculated.(ABSTRACT TRUNCATED AT 250 WORDS)

Tracheobronchial and upper airway blood flow in dogs during thermally induced panting.

Tracheobronchial blood flow increases two- to fivefold in response to isocapnic hyperventilation with warm dry or cold dry air in anesthetized, tracheostomized dogs. To determine whether this response is governed by central nervous system thermoregulatory control or is a local response to the drying and/or cooling of the airway mucosa, we studied eight anesthetized spontaneously breathing dogs in a thermally controlled chamber designed so that inspired air temperature, humidity, and body temperature could be separately regulated. Four dogs breathed through the nose and mouth (group 1), and four breathed through a short tracheostomy tube (group 2). Dogs were studied under the following conditions: 1) a normothermic control period and 2) two periods of hyperthermia in which the dogs panted with either warm 100% humidified air or warm dry (approximately 10% humidified) air. Radiolabeled microspheres (15 +/- 3 micron diam) were injected into the left ventricle as a marker of nasal, lingual, and tracheobronchial blood flow. After the final measurements, the dogs were killed and tissues of interest excised. Results showed that lingual and nasal blood flow (ml.min-1.g-1) increased during panting (P less than 0.01) in both groups and were not affected by the inspired air conditions. In group 1, tracheal mucosal blood flow barely doubled (P less than 0.01) and bronchial blood flow did not change during humid and dry air panting. In group 2, there was a sevenfold increase in tracheal mucosal and about a threefold increase in bronchial blood flow (P less than 0.01), which was only observed during dry air panting.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood flow to the trachea and bronchi: the pulmonary contribution.

It is generally assumed that when pulmonary vascular pressures are normal the pulmonary contribution to central airway blood flow (Qp) is negligible compared with systemic blood flow (Qs). However, it has been suggested in recent reports that a substantial portion of central airway blood flow is Qp. We have attempted to confirm whether there is a pulmonary contribution to central airway blood flow and to describe how it is anatomically distributed. Measurements of Qp were made using the radioactive microsphere technique in anesthetized ventilated dogs (n = 7) and sheep (n = 6). Qs to the central airways was also measured in another group of sheep (n = 10). At the end of each study, animals were killed and the lungs and trachea were excised. Qp to the upper and lower trachea, mainstem bronchi, and lobar bronchi was calculated, and the relative distribution of Qp and Qs to mucosa, cartilage, and adventitia was determined. Results showed a progressive increase (P < 0.01) in Qp (in ml.min-1 x 100 g-1) from upper trachea to lobar bronchi in both dogs and sheep. Qp and Qs supplied mainly the airway adventitia and the mucosa, respectively. Expressed as a percentage, 89 +/- 4% (SE) of Qp was to the adventitia and 0.1 +/- 0.07% was to the mucosa (P < 0.01), whereas 60 +/- 3.2% of Qs was to the mucosa and 22 +/- 4.6% was to the adventitia. In conclusion, in dogs and sheep there is a pulmonary contribution to central airway blood flow that increases from upper trachea to lobar bronchi and that supplies mainly the peritracheal adventitia.

Hypertonic aerosol inhalation does not alter central airway blood flow in dogs.

Tracheobronchial blood flow in dogs increases with cold or dry air hyperventilation, possibly as a result of airway drying leading to increased osmolarity of airway surface fluid. This study was designed to examine whether administration of aerosols of various tonicity to alter airway surface fluid osmolarity would induce similar blood flow changes. Tracheobronchial blood flow was measured by the radioactive microsphere technique in six anesthetized dogs ventilated with warm humid air (100% relative humidity) for 15 min (period 1), air containing ultrasonically nebulized saline aerosol (1,711 mosmol/kg) for 3 min (period 2) and 12 min (period 3), and the same aerosol at a higher nebulizer output for a further 3 min (period 4). Between periods 3 and 4, the dogs were ventilated with warm humid air for 30 min to reestablish base-line conditions. In another five dogs, measurements were made after 30 min of ventilation with 1) warm humid air, 2) isotonic saline aerosol, 3) warm humid air, 4) distilled water aerosol (3 dogs), and hypertonic saline aerosol (2 dogs). After the last measurement was made, each dog was killed, the trachea and major bronchi were excised, and blood flow was calculated. No change in blood flow was found during any period of aerosol inhalation. The osmolar load imposed on the airways was estimated and was similar to that occurring during cold or dry air hyperventilation. These data suggest that increasing osmolarity of airway surface fluid does not explain the blood flow changes seen during hyperventilation of cold or dry air.

Relationship between regional pulmonary edema and blood flow.

We studied the effect of edema on the regional distribution of pulmonary blood flow in 12 anesthetized dogs. Two were controls, six had low-pressure pulmonary edema, and four had high-pressure pulmonary edema. All were ventilated with 100% O2. The physiological shunt fraction (Qs/QT), as an indicator of the degree of venous admixture, was determined by measuring the arterial and venous blood gases and the hemoglobin at different times during the experiment. Cardiac output (QT) was modestly increased by opening the femoral arteriovenous shunts. The initial regional blood flow (Qi) and final regional blood flow (Qf) were marked before and after the shunts were opened, using two differently labeled macroaggregates. The dogs were then killed, and the lungs were removed and sampled completely so that Qi and Qf and the amount of regional extravascular lung water (Wdl) in each regional sample could be measured (sample size: wet wt = 5.9 +/- 2.9 g, n = 833; Wdl ranged from 5.15 +/- 1.18 to 14.42 +/- 2.34 g). The data show that QS/QT increased as QT increased in the three conditions studied. However, there was no correlation between Wdl and Qi, Qf, or the relative change in regional blood flow. The data also show that gravity affects regional blood flow more than it affects regional edema. We conclude that the increased Qs/QT seen with increased pulmonary blood flow cannot be explained by a preferential increase of blood flow to the more edematous regions.

Distribution of blood flow and neutrophil kinetics in bronchial vasculature of sheep.

The bronchial circulation, as opposed to the pulmonary circulation, is the likely source of the edema and inflammatory cells that contribute to airflow obstruction and airway narrowing associated with asthma and pulmonary edema. The purpose of this study was to understand the mechanism of edema formation and inflammation in airway walls. Therefore, we sought first to determine the normal bronchial venous drainage pathways. In anesthetized, ventilated, open-chest sheep we measured the relative distribution of 51Cr-labeled red blood cells to the right and left ventricles after injection into the bronchial artery (n = 7). Using this information, we then studied the kinetics of leukocytes in the bronchial vascular bed. We measured the extraction of 111In-labeled neutrophils during their first pass through the microvasculature after injection into the bronchial artery or right ventricle (n = 6). In the first set of experiments, we found > 85% of the systemic blood flow to the lung returns to the left ventricle. In the second set of experiments, we found that extraction of neutrophils in the bronchial vasculature (50-60%) was less (P < 0.05) than that in the pulmonary vasculature (80%). This finding may be explained by differences in the anatomy and/or hydrodynamic dispersal forces between the pulmonary and bronchial vascular beds or may reflect sequestration of neutrophils within the pulmonary microvasculature while traversing bronchial-to-pulmonary anastomotic pathways.

Mechanism for increase in tracheobronchial blood flow induced by hyperventilation of dry air in dogs.

To test whether the consistent increase in tracheal and bronchial blood flow observed in dogs during hyperventilation of dry air might be the result of release of mediators such as vasodilatory prostaglandins or neuropeptides, we studied two groups of anesthetized mechanically ventilated dogs. Group 1 (n = 6) was hyperventilated for four 30-min periods with 1) warm humid air (38-40 degrees C, 100% relative humidity), 2) warm dry air (38-40 degrees C, 0% relative humidity), 3) warm humid air, and 4) warm dry air. After period 2, a loading dose of indomethacin (4 mg/kg iv) was given over 15 min followed by a constant infusion (4 mg.kg-1.h-1). Group 2 (n = 10) was hyperventilated for four 15- to 20-min periods by use of the protocol described above. After period 3 (group 2a) or period 2 (group 2b), topical 4% lidocaine hydrochloride solution was instilled into the trachea and main stem bronchi. Five minutes before the end of each period of hyperventilation, cardiac output and vascular pressures were measured. To determine airway blood flow, differently labeled radioactive microspheres were injected into the left atrium. After the last measurements, dogs were killed and the lungs excised. Blood flow to the trachea, main stem bronchi, and parenchyma (group 1 only) was calculated. Results showed that hyperventilation of dry air produced a significant increase in blood flow to the trachea and bronchi (period 2). In group 1, this increase was attenuated (P less than 0.02) after administration of indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchial vasodilatory response to ionic and nonionic contrast media.

It has recently been shown that bronchial arterial injection of conventional contrast medium causes a significant increase in bronchial blood flow (Qbr) and that this response is partially attenuated after infusion of N omega-nitro-L-arginine (L-NNA). However, the precise mechanism for this increase in Qbr is unknown. In this study we examined the effect of bronchial arterial injection of conventional ionic as well as nonionic contrast media. We measured Qbr in nine anesthetized, ventilated, open-chest sheep. Qbr was recorded before (baseline) and at the peak response to injection of 0.5 ml of either 0.9% saline (control; isosmolar with plasma), Omnipaque 300 (iohexol; nonionic), Conray 66 (sodium iothalamate; ionic), or 50% dextrose (viscous control). Measurements were made during a control period, after infusion of the alpha-agonist phenylephrine (5 x 10(-6) to 5 x 10(-7) M), and after bronchial arterial infusion of L-NNA (10(-2) M). The results were as follows: bronchial arterial injection of saline, Omnipaque, Conray, and dextrose caused an increase in Qbr (P < 0.05). During the control period, increases in peak Qbr on injection of saline, Omnipaque, Conray, and dextrose were 55 +/- 29, 112 +/- 62, 280 +/- 99, and 388 +/- 125% of baseline, respectively. Bronchial arterial infusion of L-NNA lowered baseline Qbr and partially attenuated the response to injection of saline, Omnipaque, and Conray (P < 0.05). Phenylephrine, in doses that decreased baseline Qbr to the same extent as did L-NNA, did not attenuate the bronchial vasodilation. There was a linear relationship between osmolality and the percentage increase in bronchial blood flow. We conclude that an osmolar stress is the trigger for the contrast-induced bronchial vasodilation and that the response is partially mediated by endothelial release of nitric oxide.

Blood flow distribution to upper airway muscles.

Radiolabeled (15-microns) microspheres were used to measure blood flow to upper airway muscles [alae nasi (AN), intrinsic laryngeal, tongue, cervical strap, and hyoid musculature], diaphragm (DI), and parasternals (PS) during spontaneous breathing in 24 anesthetized tracheotomized supine dogs. Six dogs were also studied while -28 +/- 3 (SE) cmH2O tracheal airway pressure was generated against an inspiratory resistance (IR) (upper airway bypassed). Blood flow to posterior cricoarytenoid muscle (PCA) [24.0 +/- 2.1 (SE) ml.min-1.100 g-1] was greater than that to DI (18.0 +/- 2.3 ml.min-1.100 g-1) and comparable to that to PS (21.4 +/- 2.9 ml.min-1.100 g-1). Blood flow per unit weight did not differ between AN, tongue muscles, laryngeal adductors, cervical strap muscles, and cricothyroid (CT). Average blood flow to these muscles was only 8.0 +/- 0.8 ml.min-1.100 g-1. With the exception of CT, blood flow to these upper airway muscles was less than that to DI and PCA. Relative to blood flow during spontaneous breathing, IR loading increased blood flow to AN by a factor of 7.5, to PCA by 3.4, to DI by 3.2 and to PS by 1.9. There was no change in blood flow in the other muscles during loading. Our results show that at rest blood flow to main glottic dilator (PCA) is similar to that to main inspiratory muscles. Furthermore, in response to an IR load, blood flow to PCA and AN increased by an equivalent or greater amount than that to DI.(ABSTRACT TRUNCATED AT 250 WORDS)

Endogenous nitric oxide influences acetylcholine-induced bronchovascular dilation in sheep.

To test whether endogenous endothelial nitric oxide (NO) influences baseline bronchial vascular tone and mediates acetylcholine (ACh)-induced bronchial vascular dilation and/or modulates bronchoconstriction in ovine airways, we studied anesthetized ventilated open-chest sheep and measured bronchial blood flow (Qbr) and pulmonary resistance (RL). In six sheep we measured the response of Qbr and RL to the dose of ACh required to produce 50% of the maximal increase in Qbr at baseline during infusion of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA; 10(-2) M). Infusion of L-NNA decreased both the baseline Qbr (28 +/- 13 to 8 +/- 2 ml/min, P < 0.01) and the change in Qbr (delta Qbr) from the baseline value (84 +/- 42 to 33 +/- 18 ml/min, P < 0.05). There was no difference in baseline RL or in the response of RL to ACh at any time. In another six sheep, phenylephrine (5 x 10(-6) to 5 x 10(-7) M) decreased baseline Qbr (22 +/- 6 to 10 +/- 3 ml/min, P < 0.05) but not delta Qbr (62 +/- 13 to 66 +/- 21 ml/min, not significant). Infusion of L-NNA in these sheep decreased the baseline Qbr to a similar extent (11 +/- 5 ml/min) and also decreased delta Qbr (42 +/- 16 ml/min, P < 0.05). We conclude that endogenous endothelial NO influences baseline vascular tone and ACh-induced vasodilation of the ovine bronchial vasculature but has no effect on baseline RL or ACh-induced bronchoconstriction.

Bronchial vascular occlusion does not attenuate or accentuate oleic acid lung injury in anesthetized sheep.

To determine if bronchial blood flow affects the consequences of acute pulmonary vascular injury, we studied oleic acid lung injury in 12 anesthetized sheep. In six sheep (group 1), we injected 2 ml of ethanol directly into the bronchoesophageal artery to decrease bronchial blood flow. In the control sheep (group 2), we injected 2 ml of normal saline. One hour later, oleic acid (0.1 ml/kg) was injected into the right ventricle in both groups. We measured hemodynamics and lung mechanics at baseline, 1 h after injection into the bronchoesophageal artery but just before the injection of oleic acid, and 3 h after injection of oleic acid. We measured bronchial blood flow at baseline and 3 h after injection of oleic acid and extravascular lung water at 3 h after injection of oleic acid. One hour after injection of ethanol or saline into the bronchoesophageal artery, hemodynamics and lung mechanics did not change. Three hours after injection of oleic acid, systemic arterial pressure decreased, pulmonary arterial pressure increased, cardiac output decreased, dynamic compliance decreased, pulmonary resistance increased, arterial oxygen tension decreased, and extravascular lung water was greater than normal. There were no differences in these measurements between the two groups. However, bronchial blood flow decreased only in group 1. We conclude that decreasing bronchial blood flow does not attenuate or accentuate the consequences of oleic acid lung injury.

A method for estimating the Young's modulus of complete tracheal cartilage rings.

Cartilage is primarily responsible for maintaining the stability of the large airways; yet very little is known about the mechanical properties of airway cartilage. This work establishes a technique whereby average values for the equilibrium modulus of excised tracheal cartilage rings can be obtained. An apparatus was designed to apply preset deformations to a tracheal segment and to monitor the deforming force. Segments of four human tracheae obtained postmortem and containing three rings were mounted in the apparatus after being stripped of posterior membrane. The load-deformation behavior was analyzed with a model on the basis of thin curved beam theory. Agreement between predicted deformed shapes and those observed was good in three of the four cases and in the case of a short length of longitudinally split rubber tube. The technique is suitable for comparing mechanical properties of cartilage before and after an intervention.

Measurement of airway wall blood flow in sheep by laser-Doppler flowmetry: interpretation and problems.

We have used laser-Doppler flowmetry (LDF), a technique that detects movement of erythrocytes, to measure tracheal and bronchial wall blood flow in anesthetized open-chest sheep. LDF derives continuous measurements noninvasively, although fiber-optic bronchoscopy is necessary to introduce the LDF probe into the airways. The response of the LDF flow signals at four regions of the airway walls to varying bronchial arterial flow rates was examined in both live and dead sheep by cannulation and subsequent perfusion of the common bronchial artery at different flow rates by use of a roller pump. In the live sheep, variations in bronchial arterial blood flow resulted in variations in LDF signals in the principal bronchus and in lobar and segmental bronchi but not in the trachea. In the dead sheep, variations in bronchial arterial blood flow resulted in variations in LDF signals in all four regions. Within regions, the average response of the LDF signals to varying bronchial blood flow rates was approximately linear in both live and dead sheep, but considerable site-to-site variation in response was observed. In the live sheep, significant LDF signals were observed when the bronchial arterial flow was set to zero and when the bronchial artery was perfused with dextran solution, which would in theory be expected to produce no LDF signal. A small LDF signal was also detected under zero flow conditions in the dead sheep. These observations suggest that the LDF technique, in addition to detecting blood flow from the bronchial artery also detects background noise and/or collateral circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of cold and warm dry air hyperventilation on canine airway blood flow.

Tracheobronchial blood flow increases with cold air hyperventilation in the dog. The present study was designed to determine whether the cooling or the drying of the airway mucosa was the principal stimulus for this response. Six anesthetized dogs (group 1) were subjected to four periods of eucapnic hyperventilation for 30 min with warm humid air [100% relative humidity (rh)], cold dry air (-12 degrees C, 0% rh), warm humid air, and warm dry air (43 degrees C, 0% rh). Five minutes before the end of each period of hyperventilation, tracheal and central airway blood flow was determined using four differently labeled 15-micron diam radioactive microspheres. We studied another three dogs (group 2) in which 15- and 50-micron microspheres were injected simultaneously to determine whether there were any arteriovenous communications in the bronchovasculature greater than 15 micron diam. After the last measurements had been made, all dogs were killed, and the lungs, including the trachea, were excised and blood flow to the trachea, left lung bronchi, and parenchyma was calculated. Warm dry air hyperventilation produced a consistently greater increase in tracheobronchial blood flow (P less than 0.01) than cold dry air hyperventilation, despite the fact that there was a smaller fall (6 degrees C) in tracheal tissue temperature during warm dry air hyperventilation than during cold dry air hyperventilation (11 degrees C), suggesting that drying may be a more important stimulus than cold for increasing airway blood flow. In group 2, the 15-micron microspheres accurately reflected the distribution of airway blood flow but did not always give reliable measurements of parenchymal blood flow.

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.

Airway blood flow response to eucapnic dry air hyperventilation in sheep.

Eucapnic hyperventilation, breathing dry air, produces a two- to fivefold increase in airway blood flow in the dog. To determine whether airway blood flow responds similarly in the sheep we studied 16 anesthetized sheep. Seven sheep (1-7) were subjected to two 30-min periods of eucapnic hyperventilation breathing 1) warm humid air [100% relative humidity (rh)] followed by 2) warm dry air [0% rh] at 40 breaths/min. To determine whether there was a dose-response effect on blood flow of increasing levels of hyperventilation of dry air, another nine sheep (8-16) were subjected to four 30-min periods of eucapnic hyperventilation breathing warm humid O2 followed by warm dry O2 at 20 or 40 breaths/min in random sequence. Five minutes before the end of each period of hyperventilation, hemodynamics, blood gases, and tracheal mucosal temperature were measured, and tracheal and bronchial blood flows were determined by injection of 15- or 50-micron-diam radiolabeled microspheres. After the last measurements had been made, all sheep were killed, and the lungs and trachea were removed for determination of blood flow to trachea, bronchi, and parenchyma. In sheep 1-7, warm dry air hyperventilation at 40 breaths/min produced an increase in blood flow to trachea (7.6 +/- 3.5 to 17.0 +/- 6.2 ml/min, P less than 0.05) and bronchi (9.0 +/- 5.4 to 18.2 +/- 8.2 ml/min, P less than 0.05) but not to the parenchyma. When blood flow was compared with the two ventilatory rates (sheep 8-16), tracheal blood flow increased (9.1 +/- 3.3 to 18.2 +/- 6.1 ml/min, P less than 0.05) at a rate of 40 breaths/min but not at 20 breaths/min.(ABSTRACT TRUNCATED AT 250 WORDS)