Spatial Abilities and Performance in Anatomy for Occupational Therapy and Physical Therapy Doctoral Students.

Spatial ability is the capacity to comprehend three-dimensional structures and positional relationships and to mentally manipulate these structures and relationships to predict the outcome correctly. Spatial ability, which requires extensive knowledge of three-dimensional relationships, contributes to success in endeavors such as studying human anatomy, a foundational component of rehabilitation science curricula. This investigation explored relationships between anatomy course grades, learning preferences, and spatial abilities of graduate healthcare students from two fields of rehabilitation science. We administered the Mental Rotation Test to 95 Doctor of Physical Therapy students and 66 Occupational Therapy students at the start of the anatomy course in the first semester of their professional programs. The spatial abilities of doctoral students in physical therapy and occupational therapy programs reflect consistently reported trends for gender and anatomy performance. Physical therapy students demonstrated higher spatial ability scores than occupational therapy students, which could result from differences in life experience or academic preparation. Awareness of students' spatial abilities, the factors that influence them, and their relationships to student success have important implications for teaching, learning, advising, and retention.

Predicting First-Time National Physical Therapy Examination Performance for Graduates of an Entry-Level Physical Therapist Education Program.

INTRODUCTION: The National Physical Therapy Examination (NPTE) is a standardized examination designed to assess competence after graduation from an entry-level physical therapist education program. REVIEW OF LITERATURE: Previous studies have identified applicant and student variables that are related to NPTE performance, with applicant variables reflecting performance before admission and student variables reflecting performance after admission. However, there are very few articles describing how these variables can be combined to predict NPTE performance. The purpose of this study was to develop, evaluate, and describe models to predict first-time NPTE scores and NPTE outcomes (pass vs fail), based on various applicant and student variables related to academic performance. SUBJECTS: Pre- and postadmission data and NPTE scores were recorded for 185 individuals who graduated from an entry-level physical therapist education program. METHODS: Multiple linear regression was used to develop a model to predict NPTE scores, and binary logistic regression was used to develop a model to predict NPTE outcomes (pass vs fail). RESULTS: A model including undergraduate prerequisite grade point average, grade point average in basic science courses taken during the program, and comprehensive examination scores combined to explain 30.9% of the variance in NPTE scores and accurately predicted NPTE outcomes (pass vs fail) 81.1% of the time. DISCUSSION: In general, our findings support the notion that prediction of NPTE performance should be based on a combination of applicant and student variables. The models described in this article could be used to identify students who may be likely to struggle on the NPTE, making it possible to provide additional support to these students. CONCLUSION: Various applicant and student variables related to academic performance can be combined to predict NPTE performance. The results of this study provide a framework for programs interested in applying models to predict NPTE performance.

Evolutionary and comparative aspects of nitric oxide, carbon monoxide and hydrogen sulfide.

The concept that non-respiratory gases, such as nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H(2)S) functioned as signaling moieties is a relatively recent development, due in part to their ephemeral existence in biological tissues. However, from an evolutionary perspective these gases dominated the prebiotic and anoxic Earth and were major contributors to the origin of life and the advent of eukaryotic animals. As Earth's oxygen levels rose, NO, CO and H(2)S disappeared from the environment and cells began to utilize their now well-developed metabolic pathways to compartmentalize and regulate these three gases for signaling purposes. Ironically, many of the signaling pathways have become now intimately involved in regulating oxygen delivery and their evolution has continued well into the vertebrates. This review examines the role NO, CO and H(2)S played in early life and their regulatory roles in oxygen delivery during the course of vertebrate evolution.

Hydrogen sulfide (H2S) and hypoxia inhibit salmonid gastrointestinal motility: evidence for H2S as an oxygen sensor.

Hydrogen sulfide (H(2)S) has been shown to affect gastrointestinal (GI) motility and signaling in mammals and O(2)-dependent H(2)S metabolism has been proposed to serve as an O(2) 'sensor' that couples hypoxic stimuli to effector responses in a variety of other O(2)-sensing tissues. The low P(O2) values and high H(2)S concentrations routinely encountered in the GI tract suggest that H(2)S might also be involved in hypoxic responses in these tissues. In the present study we examined the effect of H(2)S on stomach, esophagus, gallbladder and intestinal motility in the rainbow trout (Oncorhynchus mykiss) and coho salmon (Oncorhynchus kisutch) and we evaluated the potential for H(2)S in oxygen sensing by examining GI responses to hypoxia in the presence of known inhibitors of H(2)S biosynthesis and by adding the sulfide donor cysteine (Cys). We also measured H(2)S production by intestinal tissue in real time and in the presence and absence of oxygen. In tissues exhibiting spontaneous contractions, H(2)S inhibited contraction magnitude (area under the curve and amplitude) and frequency, and in all tissues it reduced baseline tension in a concentration-dependent relationship. Longitudinal intestinal smooth muscle was significantly more sensitive to H(2)S than other tissues, exhibiting significant inhibitory responses at 1-10 µmol l(-1) H(2)S. The effects of hypoxia were essentially identical to those of H(2)S in longitudinal and circular intestinal smooth muscle; of special note was a unique transient stimulatory effect upon application of both hypoxia and H(2)S. Inhibitors of enzymes implicated in H(2)S biosynthesis (cystathionine ß-synthase and cystathionine γ-lyase) partially inhibited the effects of hypoxia whereas the hypoxic effects were augmented by the sulfide donor Cys. Furthermore, tissue production of H(2)S was inversely related to O(2); addition of Cys to intestinal tissue homogenate stimulated H(2)S production when the tissue was gassed with 100% nitrogen (~0% O(2)), whereas addition of oxygen (~10% O(2)) reversed this to net H(2)S consumption. This study shows that the inhibitory effects of H(2)S on the GI tract of a non-mammalian vertebrate are identical to those reported in mammals and they provide further evidence that H(2)S is a key mediator of the hypoxic response in a variety of O(2)-sensitive tissues.

Effects of carbon monoxide on trout and lamprey vessels.

Carbon monoxide (CO) is endogenously produced by heme oxygenase (HO) and is involved in vascular, neural, and inflammatory responses in mammals. However, the biological activities of CO in nonmammalian vertebrates is unknown. To this extent, we used smooth muscle myography to investigate the effects of exogenously applied CO (delivered via a water-soluble CO-releasing molecule, CORM-3) on isolated lamprey (Petromyzon marinus) dorsal aortas and examined its mechanisms of action on trout (Oncorhynchus mykiss) efferent branchial (EBA) and celiacomesenteric (CMA) arteries. CORM-3 dose-dependently relaxed all vessels examined. Trout EBA were twofold more sensitive to CORM-3 when precontracted with norepinephrine (NE) than KCl and CORM-3 relaxed five-fold more of the NE- than KCl-induced tension. Glybenclamide (10 microM), an ATP-sensitive potassium channel inhibitor, inhibited NE-induced contraction, but did not affect CORM-3-induced relaxation. NS-2028 (10 microM), a soluble guanylyl cyclase inhibitor, had no effect on a NE-contraction, but inhibited a subsequent CORM-3-induced relaxation. Zinc protopophyrin-IX (ZnPP-IX, 0.3-30 microM), a HO inhibitor, elicited a small, yet dose-dependent and significant, increase in baseline tension but did not have any effect on subsequent NE-induced contractions or a nitric oxide-induced relaxation (via sodium nitroprusside). [ZnPP-IX] greater than 3 microM, however, significantly reduced the predominant vasodilatory response of trout EBA to hydrogen sulfide. These results implicate an active HO/CO pathway in trout vessels having an impact on resting vessel tone and CO-induced vasoactivity that is at least partially mediated by soluble guanylyl cyclase.

Oxygen dependency of hydrogen sulfide-mediated vasoconstriction in cyclostome aortas.

Hydrogen sulfide (H(2)S) has been proposed to mediate hypoxic vasoconstriction (HVC), however, other studies suggest the vasoconstrictory effect indirectly results from an oxidation product of H(2)S. Here we examined the relationship between H(2)S and O(2) in isolated hagfish and lamprey vessels that exhibit profound hypoxic vasoconstriction. In myographic studies, H(2)S (Na(2)S) dose-dependently constricted dorsal aortas (DA) and efferent branchial arteries (EBA) but did not affect ventral aortas or afferent branchial arteries; effects similar to those produced by hypoxia. Sensitivity of H(2)S-mediated contraction in hagfish and lamprey DA was enhanced by hypoxia. HVC in hagfish DA was enhanced by the H(2)S precursor cysteine and inhibited by amino-oxyacetate, an inhibitor of the H(2)S-synthesizing enzyme, cystathionine beta-synthase. HVC was unaffected by propargyl glycine, an inhibitor of cystathionine lambda-lyase. Oxygen consumption (M(O(2))) of hagfish DA was constant between 15 and 115 mmHg P(O(2)) (1 mmHg=0.133 kPa), decreased when P(O(2)) <15 mmHg, and increased after P(O(2)) exceeded 115 mmHg. 10 micromol l(-1) H(2)S increased and > or =100 micromol l(-1) H(2)S decreased M(O(2)). Consistent with the effects on HVC, cysteine increased and amino-oxyacetate decreased M(O(2)). These results show that H(2)S is a monophasic vasoconstrictor of specific cyclostome vessels and because hagfish lack vascular NO, and vascular sensitivity to H(2)S was enhanced at low P(O(2)), it is unlikely that H(2)S contractions are mediated by either H(2)S-NO interaction or an oxidation product of H(2)S. These experiments also provide additional support for the hypothesis that the metabolism of H(2)S is involved in oxygen sensing/signal transduction in vertebrate vascular smooth muscle.

Effects of hypoxia on vertebrate blood vessels.

Hypoxia contracts mammalian respiratory vessels and increases vascular resistance in respiratory tissues of many vertebrates. In systemic vessels these responses vary, hypoxia relaxes mammalian vessels and contracts systemic arteries from cyclostomes. It has been proposed that hypoxic vasoconstriction in cyclostome systemic arteries is the antecedent to mammalian hypoxic pulmonary vasoconstriction, however, phylogenetic characterization of hypoxic responses is lacking. In this study, we characterized the hypoxic response of isolated systemic and respiratory vessels from a variety of vertebrates using standard myography. Pre-gill/respiratory (ventral aorta, afferent branchial artery, pulmonary artery) and post-gill/systemic (dorsal and thoracic aortas, efferent branchial artery) from lamprey (Petromyzon marinus), sandbar shark (Carcharhinus plumbeus), yellowfin tuna (Thunnus albacares), American bullfrog (Rana catesbeiana), American alligator (Alligator mississippiensis), Pekin duck (Anas platyrhynchos domesticus), chicken (Gallus domesticus) and rat (Rattus norvegicus) were exposed to hypoxia at rest or during pre-stimulation (elevated extracellular potassium, epinephrine or norepinephrine). Hypoxia produced a relaxation or transient contraction followed by relaxation in all pre-gill vessels, except for contraction in lamprey, and vasoconstriction or tri-phasic constriction-dilation-constriction in all pulmonary vessels. Hypoxia contracted systemic vessels from all animals except shark and rat and in pre-contracted rat aortas it produced a transient contraction followed by relaxation. These results show that while the classic "systemic hypoxic vasodilation and pulmonary hypoxic vasoconstriction" may occur in the microcirculation, the hypoxic response of the vertebrate macrocirculation is quite variable. These findings also suggest that hypoxic vasoconstriction is a phylogenetically ancient response.

The effects of salt-induced hypertension on alpha1-adrenoreceptor expression and cardiovascular physiology in the rainbow trout (Oncorhynchus mykiss).

Experiments were conducted on rainbow trout to determine the impact of dietary salt on arterial blood pressure. After 4-6 wk, fish fed a salt-enriched diet exhibited a 37% elevation of dorsal aortic pressure (from 23.8 +/- 1.2 to 32.6 +/- 1.4 mmHg) and an 18% increase in ventral aortic pressure (from 33.0 +/- 1.5 to 38.9 +/- 1.3 mmHg). The hypertension presumably reflected the increase in cardiac output (from 31.0 +/- 0.8 to 36.4 +/- 2.2 ml.min(-1).kg(-1)) because systemic and branchial resistances were statistically unaltered by salt feeding. The chronic hypertension was associated with a decrease in the pressor responses of the systemic vasculature to catecholamines and hypercapnia in the salt-fed fish. The reduction in alpha-adrenergic responsiveness of the systemic vasculature is consistent with desensitization or loss of functional alpha-adrenoceptors (alpha-ARs). In support of this idea, the salt-fed fish exhibited significantly decreased levels of alpha(1D)-AR mRNA in the dorsal aorta and the afferent (ABA) and efferent branchial arteries (EBA). In contrast, however, the results obtained from norepinephrine dose-response curves for EBA and ABA vascular rings in vitro did not provide evidence for loss of function of branchial artery alpha(1)-ARs in the salt-fed fish. Indeed, the EC(50) for the EBA norepinephrine dose-response curve was significantly reduced (from 3.75 x 10(-7) to 2.12 x 10(-7) M) in the salt-fed fish, indicating an increase in the binding affinity of the alpha(1)-ARs.

Hydrogen sulfide as an oxygen sensor/transducer in vertebrate hypoxic vasoconstriction and hypoxic vasodilation.

How vertebrate blood vessels sense acute hypoxia and respond either by constricting (hypoxic vasoconstriction) or dilating (hypoxic vasodilation) has not been resolved. In the present study we compared the mechanical and electrical responses of select blood vessels to hypoxia and H2S, measured vascular H2S production, and evaluated the effects of inhibitors of H2S synthesis and addition of the H2S precursor, cysteine, on hypoxic vasoconstriction and hypoxic vasodilation. We found that: (1) in all vertebrate vessels examined to date, hypoxia and H2S produce temporally and quantitatively identical responses even though the responses vary from constriction (lamprey dorsal aorta; lDA), to dilation (rat aorta; rA), to multi-phasic (rat and bovine pulmonary arteries; rPA and bPA, respectively). (2) The responses of lDA, rA and bPA to hypoxia and H2S appear competitive; in the presence of one stimulus, the response to the other stimulus is substantially or completely eliminated. (3) Hypoxia and H2S produce the same degree of cell depolarization in bPA. (4) H2S is constitutively synthesized by lDA and bPA vascular smooth muscle. (5) Inhibition of H2S synthesis inhibits the hypoxic response of lDA, rA, rPA and bPA. (6) Addition of the H2S precursor, cysteine, doubles hypoxic contraction in lDA, prolongs contraction in bPA and alters the re-oxygenation response of rA. These studies suggest that H2S may serve as an O2 sensor/transducer in the vascular responses to hypoxia. In this model, the concentration of vasoactive H2S in the vessel is governed by the balance between endogenous H2S production and its oxidation by available O2.

Hydrogen sulfide mediates hypoxia-induced relaxation of trout urinary bladder smooth muscle.

Hydrogen sulfide (H2S) is a recently identified gasotransmitter that may mediate hypoxic responses in vascular smooth muscle. H2S also appears to be a signaling molecule in mammalian non-vascular smooth muscle, but its existence and function in non-mammalian non-vascular smooth muscle have not been examined. In the present study we examined H2S production and its physiological effects in urinary bladder from steelhead and rainbow trout (Oncorhynchus mykiss) and evaluated the relationship between H2S and hypoxia. H2S was produced by trout bladders, and its production was sensitive to inhibitors of cystathionine beta-synthase and cystathionine gamma-lyase. H2S produced a dose-dependent relaxation in unstimulated and carbachol pre-contracted bladders and inhibited spontaneous contractions. Bladders pre-contracted with 80 mmol l(-1) KCl were less sensitive to H2S than bladders contracted with either 80 mmol l(-1) KC2H3O2 (KAc) or carbachol, suggesting that some of the H2S effects are mediated through an ion channel. However, H2S relaxation of bladders was not affected by the potassium channel inhibitors, apamin, charybdotoxin, 4-aminopyridine, and glybenclamide, or by chloride channel/exchange inhibitors 4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt, tamoxifen and glybenclamide, or by the presence or absence of extracellular HCO3-. Inhibitors of neuronal mechanisms, tetrodotoxin, strychnine and N-vanillylnonanamide were likewise ineffective. Hypoxia (aeration with N2) also relaxed bladders, was competitive with H2S for relaxation, and it was equally sensitive to KCl, and unaffected by neuronal blockade or the presence of extracellular HCO3-. Inhibitors of H2S synthesis also inhibited hypoxic relaxation. These experiments suggest that H2S is a phylogenetically ancient gasotransmitter in non-mammalian non-vascular smooth muscle and that it serves as an oxygen sensor/transducer, mediating the effects of hypoxia.

Effect of pH on trout blood vessels and gill vascular resistance.

pH is recognized as a modulator of vascular smooth muscle (VSM) tone in mammalian vessels, but little is known about its effects on fish VSM. We investigated the effects of extracellular and intracellular pH (pH(o) and pH(i), respectively) on isolated vessels from steelhead and rainbow trout (Oncorhynchus mykiss, Skamania and Kamloops strains, respectively) and of pH(o) on perfused gills from rainbow trout. In otherwise unstimulated (resting) efferent branchial (EBA) and coeliaco-mesenteric arteries (CMA), anterior cardinal veins (ACV) and perfused gills, increasing pH(o) from 6.8 to 8.8-9.0 produced a dose-dependent contraction or increase in gill resistance (R(GILL)) with an estimated half-maximal response of 8.0-8.2. pH(o) interactions with other contractile stimuli were agonist specific; more force was developed at low pH(o) in ligand-mediated (arginine vasotocin) contractions, whereas depolarization-mediated (40-80 mmol l(-1) KCl) contractions were greatest at high pH(o). Increasing pH(i) by application of 40 mmol l(-1) NH4Cl produced sustained contraction in afferent branchial arteries (ABA) suggesting that these vessels could not readily restore pH(i). NH(4)Cl application only transiently contracted EBA and CMA in Hepes buffer, whereas it produced a slight, but prolonged, relaxation of EBA and CMA in Cortland buffer. The buffer effect was due to the presence of Hepes and in this environment EBA and CMA appeared to readily restore pH(i). Increasing pH(i) in KCl-contracted EBA in Hepes produced an additional contraction, whereas ligand-contracted (thromboxane A2 analog, U-46619) EBA relaxed. Reducing pH(i) (NH(4)Cl washout) transiently contracted resting EBA and CMA in both Hepes and Cortland buffer. NH4Cl washout produced an additional, transient contraction of both KCl- and U-46619-contracted EBA in Hepes. EBA contractions produced by increased pH(i) depend primarily on intracellular Ca2+, whereas both intracellular and extracellular Ca2+ contributed to the response to decreased pH(i). Three cycles of perfusate acidification (pH(o) 7.8 to 6.2 and back to 7.8) reproducibly halved, then restored R(GILL) with no adverse effects, indicating that this was not a pathophysiological response. These studies show that the general effects of pH on VSM are phylogenetically conserved from fish to mammals but even within a species there are vessel-specific differences. Furthermore, as fish are exposed to substantial fluctuations in environmental (and therefore plasma) pH, the obligatory response of fish VSM to these changes may have substantial impact on cardiovascular homeostasis.

Vertebrate phylogeny of hydrogen sulfide vasoactivity.

Hydrogen sulfide (H(2)S) is a recently identified endogenous vasodilator in mammals. In steelhead/rainbow trout (Oncorhynchus mykiss, Osteichthyes), H(2)S produces both dose-dependent dilation and a unique dose-dependent constriction. In this study, we examined H(2)S vasoactivity in all vertebrate classes to determine whether H(2)S is universally vasoactive and to identify phylogenetic and/or environmental trends. H(2)S was generated from NaHS and examined in unstimulated and precontracted systemic and, when applicable, pulmonary arteries (PA) from Pacific hagfish (Eptatretus stouti, Agnatha), sea lamprey (Petromyzon marinus, Agnatha), sandbar shark (Carcharhinus milberti, Chondrichthyes), marine toad (Bufo marinus, Amphibia), American alligator (Alligator mississippiensis, Reptilia), Pekin duck (Anas platyrhynchos domesticus, Aves), and white rat (Rattus rattus, Mammalia). In otherwise unstimulated vessels, NaHS produced 1) a dose-dependent relaxation in Pacific hagfish dorsal aorta; 2) a dose-dependent contraction in sea lamprey dorsal aorta, marine toad aorta, alligator aorta and PA, duck aorta, and rat thoracic aorta; 3) a threshold relaxation in shark ventral aorta, dorsal aorta, and afferent branchial artery; and 4) a multiphasic contraction-relaxation-contraction in the marine toad PA, duck PA, and rat PA. Precontraction of these vessels with another agonist did not affect the general pattern of NaHS vasoactivity with the exception of the rat aorta, where relaxation was now dominant. These results show that H(2)S is a phylogenetically ancient and versatile vasoregulatory molecule that appears to have been opportunistically engaged to suit both organ-specific and species-specific homeostatic requirements.

Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout.

Hydrogen sulfide (H(2)S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H(2)S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H(2)S concentration was measured colorimetrically (CM) and with ion-selective electrodes (ISE) in rainbow trout plasma. NaHS produced a triphasic response consisting of a relaxation (phase 1), constriction (phase 2), and relaxation (phase 3) in both unstimulated vessels and in stEBA precontracted with carbachol (Carb). Phase 1 and phase 3 in stEBA were decreased and phase 2 increased in unstimulated vessels by K(+)(ATP) channel inhibition (glibenclamide), or a cocktail of inhibitors of cyclooxygenase, lipoxygenase, and cytochrome P-450 (indomethacin, esculetin, and clotrimazole). Inhibition of soluble guanylate cyclase with ODQ o NS-2028 inhibited phase 3 in stEBA, although NaHS decreased cGMP production by tEBA. stEBA phase 2 contractions were partially inhibited by the myosin light chain kinase inhibitor, ML-9, but unaffected by L-type calcium channel inhibition (methoxyverapamil), whereas contraction in tEBA was partially inhibited by nifedipine or removal of extracellular calcium. Phase 3 relaxations were more pronounced in stEBA precontracted with Carb and no epinephrine (NE) than those cont acted by KCl or K(2)SO(4). stEBA phase 2 and phase 3 responses were dose dependent (EC(50) = 1.1 +/- 1.2 x 10(-3) M and 6.7 +/- 0.9 x 10(-5) M, respectively; n = 7). NaHS was also vasoactive in steelhead bulbus arteriosus, celiac mesenteric arteries, and anterior cardinal veins. Rainbow trout plasma sulfide concentration was 4.0 +/- 0.3 x 10(-5) M, n = 4 (CM) and 3.8 +/- 0.4 x 10(-5) M, n = 9 (ISE); similar to phase 3 EC(50). Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H(2)S, is a tonically active endogenous vasoregulator in trout.

Transvascular and intravascular fluid transport in the rainbow trout: revisiting Starling's forces, the secondary circulation and interstitial compliance.

The kinetics of transvascular fluid transport across fish capillaries and redistribution of fluids between intravascular compartments in intact fish are unknown. Cannulae were placed in the dorsal aorta (DA) and caudal vein (CV) of rainbow trout Oncorhynchus mykiss (mass 0.45-0.85 kg) and the fish spleenectomized. The following day a peristaltic pump was fitted to complete the extracorporeal arterio-venous circulation. Hematocrit (Hct) was monitored in unanesthetized fish either manually, by collecting blood from the extracorporeal loop at 5 min intervals for a period of 1 h (groups 1 and 2), or continuously (instantaneously) with an impedance flow-cell inserted in the aortic cannula (group 3). Fish in group 1 were volume expanded by injecting a volume of saline (0.9 g% NaCl; SI) or trout plasma (PI) equivalent to 40% of the plasma volume. In group 2, 20% or 35% of the blood volume was removed, and in group 3, 35% of the blood volume was removed. Plasma volume (Vp) was calculated from an assumed blood volume of 35 ml kg(-1) and the Hct. Vp declined mono-exponentially after SI with a half-time of 6.8 min and Vp reached a new steady state at 28.1 ml kg(-1); 30% of the injected volume remained in the vasculature. Volume recovery after PI was also mono-exponential, but slower (half-time=15.4 min) than SI, whereas the steady-state Vp (27.3 ml kg(-1)) was similar and 30% of the injected volume remained in the vasculature. Thus the presence of plasma proteins delayed fluid efflux from the vasculature, but did not affect the volume lost. Transvascular fluid filtration coefficients calculated from this data were 5.5 (SI) and 4.5 ml mmHg(-1) kg(-1) min(-1) (PI), and interstitial compliance was 11.8 (SI) and 9.7 ml mmHg(-1) kg(-1) (PI). The rate of volume recovery after 20% or 35% hemorrhage was independent of the hemorrhage volume (half-time=13.3 and 15.1 min, respectively) and similar to the half-time of PI, indicating that protein-rich interstitial fluid is returned to the vasculature. There is a nearly instantaneous change in Hct that occurs during the hemorrhage period; it is dependent on hemorrhage duration and volume and not associated with the subsequent mono-exponential recovery. This initial response is best explained by a rapid fluid shift from a large-volume (approximately 40% of total blood volume), low-hematocrit (less than half of systemic Hct) microcirculation into the higher-hematocrit macrocirculation. These studies are consistent with transcapillary fluid flux across a barrier that is highly permeable to protein, and cannot be explained by fluid shift between primary and secondary circulations, or by transcapilllary flux across a capillary bed that is impermeable to plasma proteins. The results support the hypothesis that whole-body reflection coefficients in trout are very low and that plasma oncotic pressure is not a determinant of transcapillary fluid balance. They also show that both transvascular and intravascular fluid movements are important effectors of central volume homeostasis.