Recognition of child maltreatment in emergency departments in Europe: Should we do better?

OBJECTIVES: To evaluate the different policies to recognize child maltreatment in emergency departments (EDs) in Europe in order to define areas of improvement. METHODS: A survey was conducted on the recognition of child maltreatment in EDs in European countries with a focus on screening methods, parental risk factors, training and hospital policies. The survey was distributed through different key members from the EUSEM, REPEM and the EuSEN. A summary score based on the NICE guideline (4 questions on child characteristics, 4 questions on parental characteristics and 5 questions on hospital policy) was calculated. RESULTS: We analysed 185 completed surveys, representing 148 hospitals from 29 European countries. Of the respondents, 28.6% used a screening tool, and 31.8% had guidelines on parental risk factors. A total of 42.2% did not follow training based on child characteristics, and 57.6% did not follow training on parental characteristics. A total of 71.9% indicated that there was a need for training. 50.8% of the respondents reported a standardized policy for the detection of child maltreatment. Translating the survey results to NICE summary scores of the EDs in Europe, we found that 25.6% (34/133) met most, 22.6% (30/133) met some and 51.9% (69/133) met few of the NICE guideline recommendations. More specifically, with respect to hospital policies, 33.8% (45/133) met most, 15.0% (20/133) met some and 51.1% (68/133) met few of the NICE guideline recommendations. CONCLUSION: There is high variability regarding policies for child maltreatment detection and only a quarter of the EDs met most of the NICE guideline recommendations for child maltreatment. There is a need for the use of screening tools, training of ED staff and implementation of local hospital policies.

Control of pulmonary surfactant secretion: an evolutionary perspective.

Pulmonary surfactant, a mixture consisting of phospholipids (PL) and proteins, is secreted by type II cells in the lungs of all air-breathing vertebrates. Virtually nothing is known about the factors that control the secretion of pulmonary surfactant in nonmammalian vertebrates. With the use of type II cell cultures from Australian lungfish, North American bullfrogs, and fat-tailed dunnarts, we describe the autonomic regulation of surfactant secretion among the vertebrates. ACh, but not epinephrine (Epi), stimulated total PL and disaturated PL (DSP) secretion from type II cells isolated from Australian lungfish. Both Epi and ACh stimulated PL and DSP secretion from type II cells of bullfrogs and fat-tailed dunnarts. Neither Epi nor ACh affected the secretion of cholesterol from type II cell cultures of bullfrogs or dunnarts. Pulmonary surfactant secretion may be predominantly controlled by the autonomic nervous system in nonmammalian vertebrates. The parasympathetic nervous system may predominate at lower body temperatures, stimulating surfactant secretion without elevating metabolic rate. Adrenergic influences on the surfactant system may have developed subsequent to the radiation of the tetrapods. Furthermore, ventilatory influences on the surfactant system may have arisen at the time of the evolution of the mammalian bronchoalveolar lung. Further studies using other carefully chosen species from each of the vertebrate groups are required to confirm this hypothesis.

The ventilatory responses of the caecilian Typhlonectes natans to hypoxia and hypercapnia.

Typhlonectes natans empty their lungs in a single extended exhalation and subsequently fill their lungs by using a series of 10-20 inspiratory buccal oscillations. These animals always use this breathing pattern, which effectively separates inspiratory and expiratory airflows, unlike most urodele and anuran amphibians that may use one to many buccal oscillations for lung inflation and typically mix expired and inspired gases. Aquatic hypoxia had no significant effect on the breathing pattern or mechanics in these animals. Aerial hypoxia stimulated ventilatory frequency and increased the number of inspiratory oscillations but had little effect on inspiratory and expiratory tidal volume. Aquatic hypercapnia elicited a large significant increase in air-breathing frequency and minute ventilation compared to the small stimulation of minute ventilation seen during aerial hypercapnia. Some animals responded to aquatic hypercapnia with a series of three or four closely spaced breaths separated by long nonventilatory periods. Overall, T. natans showed little capacity to modulate expiratory or inspiratory tidal volumes and depended heavily on changing air-breathing frequency to meet hypoxic and hypercapnic challenges. These responses are different from those of anurans or urodeles studied to date, which modulate both the number of ventilatory oscillations in lung-inflation cycles and the degree of lung inflation when challenged with peripheral or central chemoreceptor stimulation.

Developmental changes in in vivo cardiac performance in the moth Manduca sexta.

While an extensive literature on cardiovascular development exists for insects, almost all studies focus on in vitro preparations, and very few report on more than a single developmental stage. The present study examines in vivo cardiac performance in the intact, unanesthetized larvae, pupae and adults of the tobacco hornworm Manduca sexta. For all three stages, electrode pairs of fine steel wire were inserted subcuticularly at two dorsal abdominal locations. Impedance signals produced by contraction of the dorsal abdominal vessel (tube heart) were amplified and recorded. In addition to providing heart rate, a comparison of the relative timing of the signal from each electrode pair allowed the calculation of the propagation velocity and direction of heart contraction. Experimental treatments of intact animals included exposure to hypoxia and hyperoxia (21 %, 15 %, 10 %, 5 %, 0 % and 100 % O(2)), to hypercapnia (0 %, 4 %, 8 %, 16 %, 20 % and 24 % CO(2)), to temperature variation (10, 20 and 30 degrees C) and to 2 min periods of forced activity. The pattern of contraction of the dorsal abdominal vessel of M. sexta changed substantially with developmental stage. Larvae showed a relatively simple, invariably posterior-to-anterior pattern (mean rate 34.8+/-1.16 beats min(-)(1)). The heart rate pattern in pupal M. sexta displayed great variability in rate, amplitude and direction. Periods of regular heart beats (21.5+/-1.09 beats min(-)(1)) were frequently and irregularly interrupted by periods of cardiac arrests ranging from a few seconds to over 20 min. Adults showed a highly stereotypic but complex pattern, with periods of 'fast forward' (FF; rate 47.6+/-2.6 beats min(-)(1)), 'slow forward' (SL; 32.8+/-3.0 beats min(-)(1)) and 'reversed' (R; 32.2+/-2.4 beats min(-)(1)) beating. The contraction propagation velocity in larvae and pupae averaged 5. 52+/-0.36 and 2.03+/-0.11 cm s(-)(1), respectively. The SF, R and FF phases of the adults had average propagation velocities of 5.52+/-0. 51, 5.05+/-0.52 and 5.43+/-0.37 cm s(-)(1), respectively. Heart rate and contraction propagation velocity were remarkably resistant to ambient hypoxia and hypercapnia at all developmental stages, decreasing significantly only at 0 % O(2) or 24 % CO(2). As expected, the heart rates of all three developmental stages increased significantly with increasing temperature, with heart rate Q(10) values for larvae, pupae and adults of 2.33, 3.14 and 1.61, respectively, between 10 and 20 degrees C. Corresponding Q(10) values for these stages between 20 and 30 degrees C were 2.22, 2.03 and 2.29. Larval heart rates showed no significant response to forced activity induced by prodding. In contrast, adult heart rate increased nearly fivefold from 50.1 beats min(-)(1) during rest to 223.5 beats min(-)(1) after 1 min of prodding. The activity-induced tachycardia in adults ceased within 10-12 min. Patterns of cardiac contraction in larval, pupal and adult M. sexta were as dissimilar as their morphological appearances and revealed a gradation from simple to complex. These developmentally based distinctive cardiac patterns are undoubtedly related to developmental differences in both morphology and life-style. Larvae are anatomically 'homogeneous' compared with other stages, with no distinct head, thorax and abdominal region (or wings) that might require selective perfusion or drainage. The far more complex pattern of heart activity seen in pupae probably relates to the dramatic changes in internal morphology during this stage. Simultaneous degradation and synthesis of tissues throughout the body may expose the heart to numerous peptides or neurohormones that affect cardiac activity. In adult moths, the complex and repetitive pattern of cardiac activity is reflected in the previously described complexity of hemolymph movement, together with thermoregulatory capabilities in this species that depend on well-regulated hemolymph movements between the thorax, wings and abdomen.

Whole-body composition of Xenopus laevis larvae: implications for lean body mass during development.

Body composition in developing animals has been extensively investigated in fish larvae and bird embryos. However, no studies to date have attempted to determine whole-animal body composition or lean body mass (MLB) in developing amphibians. The present study investigates how body composition changes during development in Xenopus laevis and the potential implications of MLB for substrate turnover, energy stores, oxygen consumption and other physiological measures. Whole-animal composition was determined during development from eggs (NF stage 1) to 2 weeks post-feeding (NF 50-51), which represents two-thirds of the developmental period. Wet and dry masses were found to be highly correlated, with water content remaining constant at 93 % of wet mass. Whole-animal nucleic acid content was linearly correlated with both wet and dry masses, and declined relative to mass as development progressed. Similarly, total protein content was linearly correlated with wet and dry masses; however, total protein content increased with developmental stage. Amounts of individual neutral lipids were variable although, overall, total neutral lipid content declined progressively with development. The stoichiometric energy balance paralleled the changes seen in mass-specific .MO2, with the energy primarily from lipids fueling respiration up to NF 44-45. Quantification of total body composition revealed that lipid stores greatly influenced the calculations of MLB and therefore had profound underestimating effects on the mass-specific expression of numerous physiological measures through development.

The effects of artificial lung inflation on pulmonary blood flow and heart rate in the turtle Trachemys scripta.

As for most ectothermic vertebrates, the breathing pattern of turtles is episodic, and pulmonary blood flow (Qpul) and heart rate (fH) normally increase several-fold during spontaneous ventilation. While some previous studies suggest that these cardiovascular changes are caused by stimulation of pulmonary stretch receptors (PSRs) during ventilation, it has been noted in other studies that blood flows often change prior to the initiation of breathing. Given the uncertainty regarding the role of PSRs in the regulation of central vascular blood flows, we examined the effect of manipulating lung volume (and therefore PSR stimulation) on blood flows and heart rate in the freshwater turtle Trachemys scripta. Turtles were instrumented with blood flow probes on the left aortic arch and the left pulmonary artery for measurements of blood flow, and catheters were inserted into both lungs for manipulation of lung volume. In both anaesthetized and fully recovered animals, reductions or increases in lung volume by withdrawal of lung gas or injection of air, N2, O2 or 10% CO2 (in room air) had no effect on blood flows. Furthermore, simulations of normal breathing bouts by withdrawal and injection of lung gas did not alter Qpul or fH. We conclude that stimulation of PSRs is not sufficient to elicit cardiovascular changes and that the large increase in Qpul and fH normally observed during spontaneous ventilation are probably caused by a simultaneous feedforward control of central origin.

Surfactant regulates pulmonary fluid balance in reptiles.

Reptilian lungs are potentially susceptible to fluid disturbances because they have very high pulmonary fluid filtration rates. In mammals, pulmonary surfactant protects the lung from developing alveolar edema. Reptiles also have an order of magnitude more surfactant per square centimeter of respiratory surface area compared with mammals. We investigated the role of reptilian surfactant 1) in the entry of vascularly derived fluid into the alveolar space of the isolated perfused lizard (Pogona vitticeps) lung and 2) in the removal of accumulated fluid from the alveolar space of the isolated perfused turtle (Trachemys scripta) lung by both the pulmonary venous and lymphatic circulations. The flux of fluorescent (fluorescein isothiocyanate) inulin from the vasculature into the alveolar compartment increased 60% after the removal of surfactant, but capillary fluid filtration over a 10-min period was not affected. Surfactant removal decreased alveolar inulin clearance by both the pulmonary venous circulation and the pulmonary lymphatic system approximately 1.5- and 3-fold, respectively. In reptiles, fluid flux from capillary to air space must occur indirectly via the interstitium. In the absence of surfactant, this may result in interstitial drying, which affects both pulmonary venous and pulmonary lymphatic clearance of alveolar fluid.

The influence of temperature, phylogeny, and lung structure on the lipid composition of reptilian pulmonary surfactant.

The lungs of all air-breathing vertebrates contain a form of pulmonary surfactant that lines the alveolar air-water interface where it modifies the interfacial surface tension. These pulmonary surfactants all consist of varying amounts of phospholipids (saturated and unsaturated) and cholesterol. The extent of variation between vertebrate groups and between species within a vertebrate group has been attributed to differences in factors such as phylogeny, body temperature, habitat, and lung structure. The influence of these factors on amphibian surfactant composition and function has been studied, but the reptiles, which comprise a polyphyletic group of vertebrates, have never been critically examined. The surfactant lipid composition from species belonging to the three groups of reptiles, the Archosauria (crocodiles), Lepidosauria (snakes and lizards), and Anapsida (turtles), has been determined. New data is presented in conjunction with already published data to create an evolutionary framework that concentrates particularly on the influence of phylogeny, body temperature, and lung structure on the composition of the surfactant lipids. Large amounts of pulmonary surfactant were found in all species of reptiles. All species lavaged at 23 degrees C (except C. atrox) demonstrated DSP/PL ratios of 23-33%. Animals with multicameral lungs exhibited an elevated CHOL/DSP ratio compared with species with unicameral lungs. In all groups, phosphatidylcholine (PC) was the dominant (60-80%) phospholipid. Phosphatidylserine and phosphatidylinositol (PS/PI) and sphingomyelin (S) represented the other phospholipids, while phosphatidylglycerol (PG), lysophosphatidylcholine (LPC), and phosphatidylethanolamine (PE) were occasionally observed. In two species of lizards (C. nuchalis and P. vitticeps), the saturated fatty acid, palmitic acid (16:0), was the dominant tail group on the phospholipids. Oleic acid (18:1) was the dominant monounsaturated fatty acid, whereas polyunsaturates comprised about a fifth of the total fatty acid profile. Short-term (4 h) changes in temperature did not affect the relative proportions of the fatty acids in either species. Comparison of the current data with previously published literature suggests that phylogeny and habitat do not significantly influence surfactant lipid composition, but body temperature and to a lesser extent lung structure are important determinants of reptilian surfactant lipid composition.

The composition and function of reptilian pulmonary surfactant.

In mammals, the surface tension of the fluid lining the inner lung greatly contributes to the work of breathing. Surface tension is modified by the secretion of a mixture of surface active lipids and proteins (termed pulmonary surfactant). A disaturated phospholipid (DSP), predominantly dipalmitoylphosphatidylcholine (DPPC), can eliminate surface tension under high dynamic compression. Cholesterol (CHOL) and unsaturated phospholipids (USP) promote respreading upon inflation by converting DPPC to the disordered liquid-crystalline state. It appeared to us that a surfactant rich in DPPC, which has a high phase transition temperature of 41 degrees C, is likely to be of only limited use in the lungs of reptiles, many of which have preferred body temperatures between 20 and 30 degrees C. We review here the presence and composition of surfactant in species from the three subclasses of the Reptilia and relate these to lung structure and function, phylogeny and environmental selection pressures such as body temperature. We also discuss the function of reptilian surfactant and the factors which control surfactant turnover. Large amounts of pulmonary surfactant have been found in all reptiles so far examined. In general, warmer reptiles have greater amounts of surfactant which is also relatively enriched in DSP. Cold lizards (18 degrees C) have significantly elevated levels of surfactant cholesterol. As in all vertebrates, PC is always the dominant phospholipid (60-80%). Unlike mammals, phosphatidylglycerol (PG) is absent, with the exception of one species. The remaining phospholipid groups are present to varying degrees. The saturated fatty acid, palmitic acid (16:0) is the dominant acyl group, oleic acid (18:1) is the dominant mono-unsaturated fatty acid, and polyunsaturates comprise only about 20% of the total fatty acid profile. For two species of dragon lizards, short term changes in temperature do not affect the fatty acids, but protracted periods of cold significantly decrease the presence of 16:0 in turtle lavage (Lau and Keough, Can.J. Biochem. 59: 208-219, 1981). Surfactant appears to function as an antiglue in most reptiles, serving to lower opening pressure, and decrease the work of breathing. However, surface tension forces generally do not influence reptilian lung compliance, suggesting that the primary functions of mammalian surfactant are not necessarily relevant to reptiles.

Lack of edema in toad lungs after pulmonary hypertension.

Pulmonary hypertension and hyperperfusion were experimentally induced in conscious toads (Bufo marinus) to test whether excessive transcapillary filtration might result in pulmonary edema. Elimination of pulmocutaneous baroreceptor afferent input by bilateral sectioning of recurrent laryngeal nerves caused mean pulmonary arterial pressure to increase by nearly 25 mmHg and pulmonary blood flow to increase fourfold. Left lungs of control (normotensive) and hypertensive toads were isolated by snares at the hilus and excised for compartmental lung fluid analysis. Total lung water was significantly elevated in hypertensive toads (8.44 +/- 0.30 ml/g dry mass) compared with control animals (7.15 +/- 0.22 ml/g dry mass), but this increase was apparently not due to an accumulation of transcapillary filtrate (extravascular fluid volumes = 4.57 +/- 0.21 and 4.35 +/- 0.17 ml/g dry mass, respectively). Instead, significant increases in pulmonary intravascular fluid volume accounted for 83% of the increase in total lung water. Such absence of pulmonary edema under these extreme cardiovascular states suggests that mobilization of pulmonary lymph is unusually effective in these animals.

Surfactant composition and function in lungs of air-breathing fishes.

Examination of lung washings from primitive air-breathing fishes (ropefish, bichirs, and gar) revealed a lipid-based surfactant with an average disaturated phospholipid-to-total phospholipid ratio five times lower than in mammals. The lung lavage of fishes was exceptionally rich in cholesterol, resulting in average cholesterol-to-phospholipid ratios three times higher, and cholesterol-to-disaturated phospholipid ratios nearly 15 times higher, than those of mammals. Removal of lung surfactant doubled the pressures necessary to initially open the anterior regions of collapsed lungs in all three fish species but had little or no effect on pressures required to fill the lung (i.e., compliance) after the initial opening. The elevated cholesterol content found in pulmonary surfactant of these fishes is consistent with such findings in other ectotherms, suggesting that the proportional elevation of cholesterol may serve to stabilize the fluidity of the lung surfactant over broader temperature ranges. The influence of surfactant on lung opening pressures rather than on compliance contrasts with that seen in mammals and supports an "antiglue" role of pulmonary surfactant in the simpler open-design lungs of lower vertebrates.

The composition and function of the pulmonary surfactant system during metamorphosis in the tiger salamander Ambystoma tigrinum.

Mammalian lungs secrete a mixture of surface-active lipids (surfactant), which greatly reduces the surface tension of the fluid coating the inner lung surface, thereby reducing the risk of collapse upon deflation and increasing compliance upon inflation. During foetal lung maturation, these lipids become enriched in the primary and active ingredient, a disaturated phospholipid. However, disaturated phospholipids exist in their inactive gel-like form at temperatures below 37 degrees C and thus are inappropriate for controlling surface tension in the lungs of many ectotherms. We examined the development of the composition and function of the surfactant system of the tiger salamander (Ambystoma tigrinum) during metamorphosis from the fully aquatic larva (termed stage I) through an intermediate air-breathing larval form (stage IV) to the terrestrial adult (stage VII). Biochemical analysis of lung washings from these three life stages revealed a decrease in the percentage of disaturated phospholipid per total phospholipid (23.03 versus 15.92%) with lung maturity. The relative cholesterol content remained constant. The increased level of phospholipid saturation in the fully aquatic larvae may reflect their generally higher body temperature and the higher external hydrostatic compression forces exerted on the lungs, compared to the terrestrial adults. Opening pressure (pressure required for initial lung opening) prior to lavage decreased from larval to adult salamanders (7.96 versus 4.69 cm H2O), indicating a decrease in resistance to opening with lung development.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of acute hemoconcentration in bullfrogs in response to hypoxemia.

Three general mechanisms have been proposed to explain rapid increases in red blood cell concentration in vertebrates in response to hypoxia: spleen emptying, red blood cell swelling, and decreases in plasma volume. We have experimentally tested these potential mechanisms for the hemoconcentration of red blood cells associated with hypoxemia in cold (10 degrees C), submerged bullfrogs. The mean increase of hematocrit was approximately 1.4-fold (the increase was highly variable between individual frogs) when arterial oxygen saturation was reduced from 80% to 8% by lowering ambient O2 partial pressure (PO2). The largest response was seen when arterial oxygen saturation was below 33% (a saturation that is not unusual in submerged amphibians). There was no difference between hematocrit increases during hypoxemia in spleen-ligated compared with sham-operated frogs submerged in hyperoxic, normoxic, and hypoxic water, suggesting that spleen emptying is not the primary mechanism. Increased hematocrit was not due to red blood cell swelling: mean corpuscular hemoglobin concentration increased slightly as hematocrit increased, indicating that red blood cells shrank slightly rather than swelling. Plasma volume, measured in a separate group of animals by dilution of 51Cr-labeled autologous red blood cells, decreased almost 50% during hypoxemia, closely correlated with a mean increase of 1.76-fold of hematocrit. We thus conclude that the hematocrit increase seen during hypoxemia in bullfrogs is caused by a loss of plasma volume. This has important implications for cardiovascular function, since blood viscosity, oxygen carrying capacity, and cardiac output are all affected by changes in plasma volume.

Effects of central and peripheral chemoreceptor stimulation on ventilation in the marine toad, Bufo marinus.

The contributions of central and peripheral chemoreceptors to respiratory control in lightly anesthetized Bufo marinus, were assessed by measuring the ventilatory responses to unidirectional ventilation (UDV) of the lungs at several concentrations of CO2 or O2, during intracranial perfusion (ICP) with hypercapnic acidic (5% CO2, pH 7.2) or hypocapnic alkaline (0% CO2, pH 8.3) mock CSF solutions. Peripheral chemoreceptor stimulation alone (hypoxia or hypercapnia during ICP with hypocapnic alkaline CSF) significantly increased breathing frequency and amplitude. ICP with hypercapnic acidic CSF further stimulated ventilation, primarily by significantly increasing the number of breaths/bout of breathing and decreasing the non-ventilatory time at all levels of peripheral ventilatory drive. When peripheral and central chemoreceptor stimulation was low toads were apneic. Stimulation of either central or peripheral chemoreceptors was sufficient to reinitiate breathing. Responses to ICP were greatest when perfusion was directed to the ventral medullary surface (VMS). These results suggest that the initiation of breathing and overall levels of breathing are functions of the combined afferent input from peripheral chemoreceptors and central CO2/pH sensitive chemoreceptors, located near the VMS. Stimulation of central chemoreceptors, however, produced longer duration bouts of rhythmic breathing than did peripheral chemoreceptor stimulation.

Factors terminating nonventilatory periods in the turtle, Chelydra serpentina.

PaO2, PaCO2 and pHa were measured via an extracorporeal loop in conscious snapping turtles (Chelydra serpentina) breathing air or hypoxic (10, 15% O2), hyperoxic (30% O2), or hypercapnic (2% CO2) gases. Turtles breathed into an inverted funnel ventilated with the test gas. Breathing was recorded with a differential pressure transducer. In all turtles, nonventilatory periods were interrupted by breathing episodes containing multiple breaths. In normoxia, PaO2 at the end of nonventilatory periods ranged from 22-128 mm Hg, although PaCO2 showed a less than 5 mm Hg variation about the mean. There was a positive correlation between PaCO2 at the end of the nonventilatory period and the number of breaths in the succeeding period of ventilation. PaCO2 at the end of nonventilatory periods did not change significantly in hyperoxia, although mean PaO2 was significantly increased. In hypoxia, on the other hand, mean PaO2 was significantly reduced and PaCO2 at the end of the nonventilatory period was slightly, but significantly lower. Nonventilatory periods were shorter when turtles breathed 15% O2 (9.3 +/- 1.2 min) or 10% O2 (5.5 +/- 0.3 min) than when they breathed air (17.6 +/- 3.4 min). The results indicate that, in undisturbed turtles, the most important stimulus triggering a breathing episode is the rise in PaCO2 to a critical value during the preceding nonventilatory period. An increase in hypoxic drive shortens the nonventilatory period. However, in normoxia, PaO2 at the end of many nonventilatory periods probably does not fall sufficiently to stimulate O2-sensitive chemoreceptors.

Pulmonary fluid balance following pulmocutaneous baroreceptor denervation in the toad.

Pulmonary hemodynamics and net transcapillary fluid flux (NTFF) were measured in conscious toads before and following bilateral denervation of the recurrent laryngeal nerves (rLN), which contain afferents from baroreceptors located in the pulmocutaneous arteries. Denervation caused an acute doubling of the arterial-venous pressure gradient across the lung and a threefold increase in pulmonary blood flow. Calculated pulmonary vascular resistance fell and remained below control values through the period of experimentation. NTFF increased by an order of magnitude (0.74-7.77 ml X kg-1 X min-1), as filtration increased in response to the hemodynamic changes caused by rLN denervation. There was a better correlation between NTFF and pulmonary blood flow than between NTFF and pulmonary driving pressure. Our results support the view that tonic neural input from pulmocutaneous baroreceptors protects the anuran lung from edema by restraining pulmonary driving pressure and blood flow and perhaps by reflexly maintaining vascular tone in the extrinsic pulmonary artery, therefore tending to increase the pre-to-postpulmonary capillary resistance ratio and biasing the Starling relationship in the pulmonary capillaries against filtration.

Accessory lymph sacs and body fluid partitioning in the lizard, Sauromalus hispidus.

Chuckwalla lizards (genus Sauromalus) may accumulate substantial quantities of body fluid in extracoelomic, lateral abdominal spaces called accessory lymph sacs. The lymph sac fluid (LSF) of S. hispidus is similar to that of serum in Na+, K+ and Cl- concentrations, but the total protein content (3.58 +/- 0.20 g dl-1) is only half that measured in serum (7.05 +/- 0.26 g dl-1). These analyses confirm that LSF is an extravascular form of extracellular fluid, similar in composition to true lymph. Measurements of body fluid partitioning by dilution analysis indicate that Sauromalus hispidus Stejnejer possesses a comparatively large (38.9% body mass) and labile extracellular fluid volume (ECFV), and that the volume of LSF is dependent on the ECFV. Expansion of the ECFV (and subsequent accumulation of LSF) is observed following large, intercompartmental fluid shifts from intracellular to extracellular locations when lizards are kept inactive in simulated hibernation, are injected with KCl in amounts similar to those found in their field diet, and are hydrated with NaCl that is isotonic to their body fluids. These data collectively suggest that the lymph sacs of chuckwallas facilitate expansion of the ECFV, and may be adaptive not only as a means to store body water, but to accommodate transient shifts in body fluid from intracellular to extracellular locations.

Partitioning of body fluids and cardiovascular responses to circulatory hypovolaemia in the turtle, Pseudemys scripta elegans.

Investigations were conducted (1) to measure the steady state compartmentation of body fluids and (2) to assess the efficacy of blood volume and pressure maintenance during haemorrhage-induced hypovolaemia in the pond turtle, Pseudemys scripta elegans. The pre-haemorrhage blood volume, as determined by tracer dilution of 51Cr-labelled erythrocytes, averaged 6.89 +/- 0.33% of the body mass, and was part of comparatively large extracellular (40.2 +/- 0.70%) and total body fluid volumes (75.25 +/- 1.48%). Turtles exhibited progressive reductions in systemic arterial pressure throughout a cumulative haemorrhage of -48% of their original blood volume, despite dramatic increases in heart rate and comparatively large magnitudes of transcapillary fluid transfer from interstitial to intravascular spaces. Arterial blood pressure returned to pre-haemorrhage values 2h after experimental haemorrhage ceased, concomitant with the restoration of the original blood volume. Our results support arguments made in previous studies that the resistance to fluid movement between vascular and extravascular locations in reptiles is comparatively low. Furthermore, the haemodynamic responses of turtles to experimental hypovolaemia suggest that barostasis through adjustments in vascular tone is less effective than that observed in other reptiles.

Maintenance of blood volume in snakes: transcapillary shifts of extravascular fluids during acute hemorrhage.

Tracer dilution analysis (D2O, 51Cr, and NaS14CN) was used to investigate the steady-state compartmentation of body fluids and the extent of fluid transfer from extravascular to vascular spaces during hemorrhage-induced hypovolemia in two species of snakes, Elaphe obsoleta and Crotalus viridis. Fluid spaces of the two species are not significantly different (means, blood volume 6.1, 5.4; extracellular fluid 42.2, 41.9; total body water 77.2, 77.2% body mass, respectively), but values for extracellular fluid exceed those reported for other reptiles. Both species of snake withstand graded hemorrhage where 4% of the initial blood volume is withdrawn every 10 min until the cumulative deficit is 32%. Some snakes are able to maintain their initial blood volume throughout hemorrhage, while others restore 90% of deficits within 2 h after hemorrhage ceases. Typically, 50-60% of the hemorrhaged deficit is transferred from the interstitium to the circulation throughout hemorrhage (Fig. 2). The source of fluid entering the vascular space is entirely extracellular during hemorrhage, the blood within 2 h after hemorrhage ceases. Snakes are able to maintain arterial pressure during these experiments (Fig. 3). The ability of snakes to maintain hemodynamic stability despite substantial losses of blood can be explained in terms of a large interstitial fluid volume that may shift rapidly to the vascular space. Shifts in the opposite direction also occur in response to hemodynamic factors, implying a low resistance to fluid movement across the capillary wall.