Metrics of progress in the understanding and management of threats to Australian birds.

Although evidence-based approaches have become commonplace for determining the success of conservation measures for the management of threatened taxa, there are no standard metrics for assessing progress in research or management. We developed 5 metrics to meet this need for threatened taxa and to quantify the need for further action and effective alleviation of threats. These metrics (research need, research achievement, management need, management achievement, and percent threat reduction) can be aggregated to examine trends for an individual taxon or for threats across multiple taxa. We tested the utility of these metrics by applying them to Australian threatened birds, which appears to be the first time that progress in research and management of threats has been assessed for all threatened taxa in a faunal group at a continental scale. Some research has been conducted on nearly three-quarters of known threats to taxa, and there is a clear understanding of how to alleviate nearly half of the threats with the highest impact. Some management has been attempted on nearly half the threats. Management outcomes ranged from successful trials to complete mitigation of the threat, including for one-third of high-impact threats. Progress in both research and management tended to be greater for taxa that were monitored or occurred on oceanic islands. Predation by cats had the highest potential threat score. However, there has been some success reducing the impact of cat predation, so climate change (particularly drought), now poses the greatest threat to Australian threatened birds. Our results demonstrate the potential for the proposed metrics to encapsulate the major trends in research and management of both threats and threatened taxa and provide a basis for international comparisons of evidence-based conservation science.

Medidas de Progreso en el Entendimiento y el Manejo de las Amenazas que Enfrentan las Aves Australianas Resumen Aunque los métodos basados en evidencias se han vuelto muy comunes para la determinación del éxito de las medidas de conservación del manejo de los taxones amenazados, hoy en día no existen medidas estandarizadas para la evaluación del progreso de la investigación o el manejo. Desarrollamos cinco medidas para cumplir con esta necesidad que tienen los taxones amenazados y para cuantificar la necesidad de una mayor acción y un alivio efectivo de las amenazas. Estas medidas (falta de investigación, éxito de la investigación, falta de manejo, éxito del manejo y porcentaje de reducción de amenazas) pueden agregarse para examinar las tendencias de un taxón individual o las tendencias de las amenazas para múltiples taxones. Probamos la utilidad de estas medidas por medio de su aplicación en aves australianas amenazadas, que parece ser la primera vez que se evalúa el progreso en la investigación y en el manejo de amenazas para el caso de varios taxones amenazados dentro de un grupo faunístico a escala continental. Se ha realizado algún tipo de investigación sobre casi tres cuartas partes de las amenazas conocidas para los taxones, y hay un claro entendimiento de cómo aliviar casi la mitad de las amenazas con el impacto más alto. Se ha intentado algún tipo de manejo con casi la mitad de las amenazas. Los resultados del manejo variaron desde ensayos exitosos hasta la mitigación completa de la amenaza, incluso para un tercio de las amenazas de alto impacto. Tanto el progreso en la investigación como en el manejo tendió a ser mayor para los taxones que estaban siendo monitoreados, o que ocurrían en islas oceánicas. La depredación por gatos tuvo el puntaje más como amenaza potencial. Sin embargo, ha habido poco de éxito en la reducción del impacto de la depredación por gatos, así que ahora el cambio climático (particularmente la sequía) es la mayor amenaza para las aves amenazadas en Australia. Nuestros resultados demuestran el potencial que tienen las medidas propuestas de encapsular las tendencias más importantes en la investigación y en el manejo tanto de las amenazas como de los taxones amenazados y de proporcionar una base para comparaciones internacionales de la ciencia de la conservación basada en evidencias.

How humans drive speciation as well as extinction.

A central topic for conservation science is evaluating how human activities influence global species diversity. Humanity exacerbates extinction rates. But by what mechanisms does humanity drive the emergence of new species? We review human-mediated speciation, compare speciation and known extinctions, and discuss the challenges of using net species diversity as a conservation objective. Humans drive rapid evolution through relocation, domestication, hunting and novel ecosystem creation-and emerging technologies could eventually provide additional mechanisms. The number of species relocated, domesticated and hunted during the Holocene is of comparable magnitude to the number of observed extinctions. While instances of human-mediated speciation are known, the overall effect these mechanisms have upon speciation rates has not yet been quantified. We also explore the importance of anthropogenic influence upon divergence in microorganisms. Even if human activities resulted in no net loss of species diversity by balancing speciation and extinction rates, this would probably be deemed unacceptable. We discuss why, based upon 'no net loss' conservation literature-considering phylogenetic diversity and other metrics, risk aversion, taboo trade-offs and spatial heterogeneity. We conclude that evaluating speciation alongside extinction could result in more nuanced understanding of biosphere trends, clarifying what it is we actually value about biodiversity.

[Sudden Cardiac Death in Patients With Hypertrophic Cardiomyopathy].

This literature review is devoted to the problem of studying sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM). It covers prevalence of SCD and its structure among young individuals and trained athletes, contains discussion of relation of SCD to sex, age, and hypertrophic response of myocardium to physical exercise. Modern views on arrhythmogenic substrate underlying SCD in HCM as well as pathophysiologic cascade of life-threatening ventricular tachyarrhythmia are presented in detail. Approaches to identification of individuals at high risk of SCD are described and main and supplemental clinical criteria are discussed from the point of view of SCD risk stratification. The review also contains results of large trials assessing the role of implantable cardioverter-defibrillators (ICD) in primary and secondary prevention of SCD in HCM patients, and recommendations on appropriateness of ICD implantation taking into account efficiency of these devices and rate of complications.

Assessing blue wildebeests' vigilance, grouping and foraging responses to perceived predation risk using playback experiments.

Two aspects of reactive antipredator behaviour are still unclear for ungulates. First, when there is a direct predation threat, how do prey balance antipredator and social vigilance to learn a predator's location and assess the risk? Second, how do an individual's group and environment affect its responses? We tested the responses of adult females in 101 groups of wildebeest to playbacks of lion roars or car noises in Etosha National Park, Namibia. We analysed how the times they spent in different types categories of vigilance, and their within-group density, were affected by the playbacks and how a range of social and environmental variables affected those responses. Females increased their antipredator vigilance but not their social vigilance, after lion roars but not car noises, suggesting that they mostly relied on their own vigilance rather than social information to try to find the source of the lion roars. Females' antipredator vigilance increased more when they were further from cover and with other prey species, suggesting that both circumstances increased their perception of risk. They 'bunched' more after lion roars than car noises and their bite rates decreased as they bunched. Animals' use of social information about threats is likely to be context-dependent.

beta(2)-adrenergic receptor overexpression increases alveolar fluid clearance and responsiveness to endogenous catecholamines in rats.

beta-Adrenergic agonists accelerate the clearance of alveolar fluid by increasing the expression and activity of epithelial solute transport proteins such as amiloride-sensitive epithelial Na(+) channels (ENaC) and Na,K-ATPases. Here we report that adenoviral-mediated overexpression of a human beta(2)-adrenergic receptor (beta(2)AR) cDNA increases beta(2)AR mRNA, membrane-bound receptor protein expression, and receptor function (procaterol-induced cAMP production) in human lung epithelial cells (A549). Receptor overexpression was associated with increased catecholamine (procaterol)-responsive active Na(+) transport and increased abundance of Na,K-ATPases in the basolateral cell membrane. beta(2)AR gene transfer to the alveolar epithelium of normal rats improved membrane-bound beta(2)AR expression and function and increased levels of ENaC (alpha subunit) abundance and Na,K-ATPases activity in apical and basolateral cell membrane fractions isolated from the peripheral lung, respectively. Alveolar fluid clearance (AFC), an index of active Na(+) transport, in beta(2)AR overexpressing rats was up to 100% greater than sham-infected controls and rats infected with an adenovirus that expresses no cDNA. The addition of the beta(2)AR-specific agonist procaterol to beta(2)AR overexpressing lungs did not increase AFC further. AFC in beta(2)AR overexpressing lungs from adrenalectomized or propranolol-treated rats revealed clearance rates that were the same or less than normal, untreated, sham-infected controls. These experiments indicate that alveolar beta(2)AR overexpression improves beta(2)AR function and maximally upregulates beta-agonist-responsive active Na(+) transport by improving responsiveness to endogenous catecholamines. These studies suggest that upregulation of beta(2)AR function may someday prove useful for the treatment of pulmonary edema.

Inactivation of one copy of the mouse neurotrophin-3 gene induces cardiac sympathetic deficits.

Whether two copies of the neurotrophin-3 (NT3) gene are necessary for proper development of cardiac sympathetic innervation was investigated in mice carrying a targeted inactivation of the NT3 gene. Heterozygous (+/-) and null (-/-) mutant mice had fewer stellate ganglion neurons than did wild-type (+/+) mice at postnatal day 0 (P0 or birth), and this deficit was maintained between adult (P60) +/- and +/+ mice. The sympathetic innervation of the heart matured postnatally in +/+ and +/- mice. Tyrosine hydroxylase (TH)-positive axons were restricted largely to the epicardium at P0, were concentrated around large blood vessels in the myocardium at P21, and were present among cardiac myocytes at P60. Cardiac norepinephrine (NE) concentrations paralleled the growth of the sympathetic axons into the heart. NE concentrations were equivalent among +/+, +/-, and -/- mice at birth, but differences between +/- and +/+ mice increased with age. Adult +/- mice also exhibited lower resting heart rates and sympathetic tonus than +/+ mice. Thus deletion of one copy of the NT3 gene translates into anatomical, biochemical, and functional deficits in cardiac sympathetic innervation of postnatal mice, thereby indicating a gene-dosage effect for the NT3 gene.

Carbamazepine in the treatment of neuroleptic malignant syndrome.

BACKGROUND: Neuroleptic malignant syndrome (NMS) is a potentially lethal adverse effect to neuroleptic drugs. METHODS: We report on 2 cases where NMS dramatically improved with carbamazepine. Incidental removal and reapplication of carbamazepine attests to its effectiveness for this condition. RESULTS: A 34-year-old woman treated for a major depressive disorder experienced NMS with a phenothiazine. Her condition dramatically improved in 8 hours after she was administered carbamazepine. Since carbamazepine was discontinued, NMS recurred in 10 hours and remitted anew within less than 24 hours after reintroduction. A 31-year-old woman experiencing a schizoaffective disorder displayed NMS with aphenothiazine and a butyrophenone. NMS completely resolved within 8 hours after she was administered carbamazepine. NMS recurred within 12 hours after carbamazepine discontinuation. CONCLUSIONS: These data thus account for a cause-effect relationship between carbamazepine administration and NMS relief, and argue against the neuroleptic withdrawal to be responsible by itself for NMS relief.

Role of prostaglandins in blood-induced vasoconstriction of canine cerebral arteries.

We tested the hypothesis that the vasoconstriction produced by the application of blood to the adventitial surfaces of the vessels of an isolated perfused canine circle of Willis preparation was mediated by products of prostaglandin metabolism. In this preparation (perfused at constant flow and outflow pressure), topical application of blood produced an average 16.6 +/- 1.8 (SE) mm Hg increase in inflow pressure. This response could be prevented with four structurally dissimilar cyclooxygenase inhibitors (aspirin, indomethacin, ibuprofen, and meclofenamate), suggesting that the blood-induced increase in vascular resistance was mediated by prostaglandins. Imidazole, an inhibitor of thromboxane synthetase, had no effect on the blood response. Further support for the involvement of prostaglandins in this response was provided by additional experiments in which either arachidonic acid, prostaglandin E2 (PGE2), or PGF2 alpha were administered. All three treatments produced vasoconstriction. These results suggest that the vessels of this preparation are capable of synthesizing vasoconstrictor prostaglandins and indicate that they are reactive to known vasoactive prostaglandins.

Prevalence of hypertrophic cardiomyopathy in an outpatient population referred for echocardiographic study.

Although hypertrophic cardiomyopathy (HC) is believed to be a relatively uncommon cardiac disease, the frequency with which it occurs in the general or cardiac population has not been defined. To address this issue, the patient population of a community-based echocardiography laboratory was used to assess the prevalence of HC in 714 consecutively studied outpatients with (or suspected of having) heart disease. The most common cardiac disease identified was mitral valve prolapse (73 patients [10%]), and HC was present in 4 patients (0.5%). Ages were 50 to 69 years. Maximal left ventricular wall thicknessess were 15 to 22 mm (mean 19); only 1 had evidence of obstruction to left ventricular outflow by virtue of marked mitral valve systolic anterior motion. Before echocardiographic study, each of the 4 patients with HC had signs or symptoms of cardiac disease, but the correct diagnosis had not been suspected. Of 11 other patients who were referred for echocardiographic study because of a clinical suspicion of HC, none proved to have this disease. The present study demonstrates that HC is a particularly uncommon disease entity occurring in about 0.5% of an unselected outpatient population referred for echocardiographic study.

Assessment of QT dispersion as a prognostic marker for sudden death in a regional nonreferred hypertrophic cardiomyopathy cohort.

In a consecutive, prospectively assessed and unselected hypertrophic cardiomyopathy (HC) cohort closely resembling the true disease state, QTc dispersion (and QTc) on the 12-lead electrocardiogram did not prove to be a reliable predictor of HC-related sudden death. Therefore, QT dispersion would not appear to be useful in devising future risk stratification strategies for predicting sudden death in HC.

A canine model of neurogenic pulmonary edema.

The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40-60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic arterial, pulmonary arterial, and left ventricular end-diastolic (LVEDP) pressures were followed for 1 h. Eleven animals developed alveolar edema. In these animals, systemic arterial pressure increased to 273 +/- 9 (SE) Torr, pulmonary arterial pressure to 74.5 +/- 4.9 Torr, and LVEDP to 42.8 +/- 4.5 Torr, and large amounts of pink frothy fluid, with protein concentrations ranging from 48 to 93% of plasma, appeared in the airways. Postmortem extravascular lung water content (Qwl/dQl) averaged 7.30 +/- 0.46 g H2O/g dry lung wt. Six animals escaped developing this massive degree of edema after veratrine (Qwl/dQl = 4.45 +/- 0.24). These animals exhibited similar elevated systemic arterial pressures (268 +/- 15 Torr), but did not develop the degree of pulmonary hypertension (pulmonary arterial pressure = 52.5 +/- 6.7 Torr, LVEDP = 24.8 +/- 4.0 Torr) observed in the other group. These results suggest that both hemodynamic and permeability mechanisms may play a role in the development of this form of edema and that veratrine administration may provide a useful model of NPE.

Pulmonary vasoconstriction in a canine model of neurogenic pulmonary edema.

The intracisternal administration of veratrine to the chloralose-anesthetized dog produces pulmonary hypertension (PH) and neurogenic pulmonary edema (NPE). To determine whether pulmonary vasoconstriction, mediated by a circulating agent, contributes to the PH, the left lower lung lobe (LLL) perfusion of seven splenectomized (to keep hematocrit and blood viscosity constant) dogs was isolated so the LLL could be perfused at constant flow and outflow pressure with blood pumped from the pulmonary artery. The LLL was denervated by removing it from the dog. Veratrine (40-160 micrograms/kg) increased LLL arterial pressure by 39.2% and produced large increases in plasma catecholamine concentrations. The double-occlusion technique indicated that 74% of the increase in the LLL arteriovenous pressure gradient was due to an increase in venous tone. This pattern of vasoconstriction was similar to that previously observed during the infusion of exogenous catecholamines and suggested that catecholamines mediated the LLL response. The more severe degree of PH observed in the intact animal in NPE, however, suggests that passive rather than active changes in pulmonary hemodynamics are predominantly responsible for the development of PH in this disorder.

Analysis of airway fluid protein concentration in neurogenic pulmonary edema.

Intracisternal administration of veratrine (40 micrograms/kg) in the alpha-chloralose-anesthetized dog produces fulminant neurogenic pulmonary edema (NPE). To determine whether the edema resulted from increased microvascular pressure or from increased permeability, the airway fluid-to-plasma protein (A/P) concentration ratios were compared for both total proteins and endogenous protein fractions of known molecular radii (37-114 A) from dogs with edema produced by either veratrine, alloxan (permeability edema), or combined left atrial pressure and volume overload (hemodynamic edema). High A/P ratios (0.98 +/- 0.05) were observed after alloxan administration, whereas lower values (0.54 +/- 0.04) were observed in hemodynamic edema. A/P ratios were observed after veratrine administration that formed a continuum (0.48-0.84) between these extremes. Veratrine animals with high overall A/P ratios exhibited elevated A/P ratios for all protein fractions, whereas animals with lower overall A/P ratios exhibited A/P protein fraction ratios similar to those observed in the hemodynamic group. These data indicate that both hemodynamic and increased permeability mechanisms may play a role to varying degrees in the development of this form of NPE.

Effect of elevated vascular pressure transients on protein permeability in the lung.

Neurogenic pulmonary edema (NPE) may develop in individuals with head trauma or seizures and is generally thought to have a hydrostatic basis in the severe degree of pulmonary hypertension that occurs. Recently, it has been suggested that vascular pressures may rise to levels that damage the vessels, leaving the patient at risk for further edema development. The objective of this study was to determine if pulmonary vascular protein permeability is increased in a canine isolated perfused left lower lung lobe (LLL) preparation by pressure transients that may occur in NPE. Venous pressure (Pv) was transiently raised to values ranging from 8 to 102 Torr in 19 LLL. One Pv transient was studied per LLL. After Pv was returned to normal, the osmotic reflection coefficient (sigma d) for total proteins was determined by the hematocrit-protein double indicator technique. No reduction in sigma d was observed until microvascular pressure exceeded 70 Torr. The average sigma d for the 11 LLL in which the peak microvascular pressure was less than 70 Torr was 0.74 +/- 0.03 (SE). Above this level sigma d fell linearly with increasing Pv, with a value of 0.26 being observed after the highest Pv transient. These results suggest that protein permeability may increase in patients with NPE who develop very large increases in pulmonary vascular pressures but may not be a universal occurrence in this disorder.

Dose-response relationship between plasma epinephrine concentration and alveolar liquid clearance in dogs.

Previously, alveolar liquid clearance (ALC) was observed to increase in a canine model of neurogenic pulmonary edema (NPE) by adrenal epinephrine (S. M. Lane, K. C. Maender, N. E. Awender, and M. B. Maron. Am. J. Respir. Crit. Care Med. 158: 760-768, 1998). In this study the dose-response relationship between plasma epinephrine concentration and ALC was determined in anesthetized dogs by infusing epinephrine to produce plasma concentrations of 256 +/- 37, 1,387 +/- 51, 15,737 +/- 2,161, and 363,997 +/- 66,984 (SE) pg/ml (n = 6 for each concentration) for 4 h and measuring the resultant ALC. The latter was determined by mass balance after instillation of autologous plasma into a lower lung lobe. These plasma concentrations produced ALCs of 14.3 +/- 1.2, 20.5 +/- 1.9, 30.1 +/- 1.5, and 37.9 +/- 2.7% of the instilled volume, respectively. ALC after the lowest infusion rate was not different from that previously observed under baseline conditions (14.1 +/- 2.1%), whereas in a previous study of NPE, plasma epinephrine concentration increased to 7,683 +/- 687 pg/ml and ALC was 30.4 +/- 1.6%. These data indicate that, during recovery from canine NPE, ALC is not maximally stimulated and suggest that it might be possible to pharmacologically produce further increases in the rate of resolution of this form of edema.

Effect of papaverine on pulmonary vascular permeability to proteins.

Previous studies have suggested that papaverine, a drug commonly used in studies of transvascular fluid and solute exchange to eliminate confounding effects of changes in vascular tone, may itself increase vascular permeability. In this study, we determined the ability of papaverine to alter pulmonary vascular protein permeability by measuring the osmotic reflection coefficient (sigma) for total proteins in a canine isolated perfused left lower lung lobe (LLL) preparation. The reflection coefficient, determined by the hematocrit-protein double-indicator technique, for control LLL's was 0.83 +/- 0.04 (SE) (n = 7). In separate groups of LLL's, blood papaverine HCl concentrations of 10(-5), 10(-4), and 10(-3) M resulted in sigma's of 0.84 +/- 0.02 (n = 6), 0.73 +/- 0.04 (n = 7), and 0.53 +/- 0.04 (n = 6), respectively. When two LLL's from the 10(-4) M group with sigma's of 0.56 and 0.57 were excluded from the analysis, the average sigma for this group was 0.79 +/- 0.02. We conclude that papaverine increases protein permeability at a concentration of 10(-3) M but does so in only some lobes at 10(-4) M. These results suggest that caution be taken when using high concentrations of papaverine in fluid balance studies.

Calculation of the reflection coefficient from measurements of endogenous vascular indicators.

The solvent drag reflection coefficient (sigma) for total proteins can be estimated by comparing the relative degrees of concentration of erythrocytes and plasma proteins that occur during fluid filtration in an isolated perfused organ. In this analysis, we evaluated the accuracy of equations proposed by Pilati and Maron [Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H1-H7, 1984] and Wolf et al. [Am. J. Physiol. 253 (Heart Circ. Physiol. 22): H194-H204, 1987] to calculate sigma from these concentration changes. We calculated sigma with each equation using data generated from a mathematical model of fluid and solute flux in membranes with known sigma's. We found that the equation of Wolf et al. provided the closest approximation to the true sigma over the entire range of filtration fractions tested (0.1-0.6), with the differences between the two equations increasing with filtration fraction. At low filtration fractions, the difference in sigma obtained using either approach was found to be inconsequential. At larger filtration fractions, a closer approximation of the true sigma can be obtained using the equation of Wolf et al.

Pulmonary hemodynamics and lung water content during splanchnic ischemic shock.

Pulmonary hemodynamics and lung water content were evaluated in open-chest dogs during splanchnic arterial occlusion (SAO) shock. Mean pulmonary arterial pressure [Ppa = 13.0 +/- 0.6 (SE) mmHg] and pulmonary venous pressure (4.1 +/- 0.2 mmHg) were measured by direct cannulation and the capillary pressure (Ppc = 9.0 +/- 0.6 mmHg) estimated by the double-occlusion technique. SAO shock did not produce a significant change in Ppa or Ppc despite a 90% decrease in cardiac output. An 18-fold increase in pulmonary vascular resistance occurred, and most of this increase (70%) was on the venous side of the circulation. No differences in lung water content between shocked and sham-operated dogs were observed. The effect of SAO shock was further evaluated in the isolated canine left lower lobe (LLL) perfused at constant flow and outflow pressure. The addition of venous blood from shock dogs to the LLL perfusion circuit caused a transient (10-15 min) increase in LLL arterial pressure (51%) that could be reversed rapidly with papaverine. In this preparation, shock blood produced either a predominantly arterioconstriction or a predominantly venoconstriction. These results indicate that both arterial and venous vasoactive agents are released during SAO shock. The consistently observed venoconstriction in the intact shocked lung suggests that other factors, in addition to circulating vasoactive agents, contribute to the pulmonary hemodynamic response of the open-chest shocked dog.

Hemodynamic basis for cocaine-induced pulmonary edema in dogs.

We tested the hypothesis that cocaine-induced impairment of left ventricular function results in cardiogenic pulmonary edema. Mongrel dogs, anesthetized with alpha-chloralose, were injected with two doses of cocaine (5 mg/kg iv) 27 min apart. Cocaine produced transient decreases in aortic and left ventricular systolic pressures that were followed by increases exceeding control. As aortic pressure recovered, left ventricular end-diastolic, left atrial (Pla), pulmonary arterial (Ppa), and central venous pressures rose. Cardiac output and stroke volume were reduced when measured 4-5 min after cocaine administration. Peak Ppa and Pla were 31 +/- 5 (SE) mmHg (range 17-51 mmHg) and 26 +/- 5 mmHg (range 12-47 mmHg), respectively. Increases in extravascular lung water content (4.10 to 6.24 g H2O/g dry lung wt) developed in four animals in which Pla exceeded 30 mmHg. Analysis of left ventricular function curves revealed that cocaine depressed the inotropic state of the left ventricle. Cocaine-induced changes in hemodynamics spontaneously recovered and could be elicited again by the second dose of the drug. Our results show that cocaine-induced pulmonary hypertension, associated with decreased left ventricular function, produces pulmonary edema if pulmonary vascular pressures rise sufficiently.

Time course of blood volume changes in an isolated lung lobe after venous pressure elevation.

The elevation of venous pressure (Pv) in isolated perfused organs causes organ weight to increase in a biphasic manner. The initial rapid phase results primarily from an increase in blood volume (BV), whereas the second slower phase is generally considered to reflect fluid filtration. Recent studies have suggested, however, that BV may continue to increase during the slow weight gain phase. To address this question, we made serial measurements of circulating BV by indicator dilution with indocyanine green dye in a canine isolated perfused left lower lung lobe (LLL) preparation during 40 min of Pv elevation. Pv was raised to approximately 18 Torr in six LLLs beginning an average of 28 min after the start of perfusion. After an initial rapid increase, BV continued to increase at a slower rate for approximately 30 min. The increase in BV observed between 3 and 40 min of Pv elevation [4.3 +/- 0.3 (SE) ml] was 47.9 +/- 9.1% of the weight gain that occurred during this period. In six additional LLLs, Pv elevation was delayed until approximately 70 min after the perfusion was started. In these LLLs, BV generally achieved constancy 3 min after Pv was elevated. These data indicate that the dynamics of the BV response of this preparation to Pv elevation is time dependent and that gravimetric determinations of the rate of fluid filtration may substantially overestimate the true filtration rate in the presence of continuing increases in BV. The increases in BV observed in the first group of LLLs appear to be due to vascular recruitment rather than stress relaxation.