Mapping the twist-angle disorder and Landau levels in magic-angle graphene.

The recently discovered flat electronic bands and strongly correlated and superconducting phases in magic-angle twisted bilayer graphene (MATBG)1,2 crucially depend on the interlayer twist angle, θ. Although control of the global θ with a precision of about 0.1 degrees has been demonstrated1-7, little information is available on the distribution of the local twist angles. Here we use a nanoscale on-tip scanning superconducting quantum interference device (SQUID-on-tip)8 to obtain tomographic images of the Landau levels in the quantum Hall state9 and to map the local θ variations in hexagonal boron nitride (hBN)-encapsulated MATBG devices with relative precision better than 0.002 degrees and a spatial resolution of a few moiré periods. We find a correlation between the degree of θ disorder and the quality of the MATBG transport characteristics and show that even state-of-the-art devices-which exhibit correlated states, Landau fans and superconductivity-display considerable local variation in θ of up to 0.1 degrees, exhibiting substantial gradients and networks of jumps, and may contain areas with no local MATBG behaviour. We observe that the correlated states in MATBG are particularly fragile with respect to the twist-angle disorder. We also show that the gradients of θ generate large gate-tunable in-plane electric fields, unscreened even in the metallic regions, which profoundly alter the quantum Hall state by forming edge channels in the bulk of the sample and may affect the phase diagram of the correlated and superconducting states. We thus establish the importance of θ disorder as an unconventional type of disorder enabling the use of twist-angle gradients for bandstructure engineering, for realization of correlated phenomena and for gate-tunable built-in planar electric fields for device applications.

Hofstadter's butterfly and the fractal quantum Hall effect in moiré superlattices.

Electrons moving through a spatially periodic lattice potential develop a quantized energy spectrum consisting of discrete Bloch bands. In two dimensions, electrons moving through a magnetic field also develop a quantized energy spectrum, consisting of highly degenerate Landau energy levels. When subject to both a magnetic field and a periodic electrostatic potential, two-dimensional systems of electrons exhibit a self-similar recursive energy spectrum. Known as Hofstadter's butterfly, this complex spectrum results from an interplay between the characteristic lengths associated with the two quantizing fields, and is one of the first quantum fractals discovered in physics. In the decades since its prediction, experimental attempts to study this effect have been limited by difficulties in reconciling the two length scales. Typical atomic lattices (with periodicities of less than one nanometre) require unfeasibly large magnetic fields to reach the commensurability condition, and in artificially engineered structures (with periodicities greater than about 100 nanometres) the corresponding fields are too small to overcome disorder completely. Here we demonstrate that moiré superlattices arising in bilayer graphene coupled to hexagonal boron nitride provide a periodic modulation with ideal length scales of the order of ten nanometres, enabling unprecedented experimental access to the fractal spectrum. We confirm that quantum Hall features associated with the fractal gaps are described by two integer topological quantum numbers, and report evidence of their recursive structure. Observation of a Hofstadter spectrum in bilayer graphene means that it is possible to investigate emergent behaviour within a fractal energy landscape in a system with tunable internal degrees of freedom.

Src-type tyrosine kinase p56lck is critical for thymic stromal lymphopoietin-induced allergic rhinitis.

BACKGROUND: Thymic stromal lymphopoietin (TSLP) is a regulator of mast cell-mediated allergic inflammatory reactions, but the manner in which TSLP contributes to allergic rhinitis (AR) remains unclear. OBJECTIVE: Here, we sought to determine that TSLP plays a crucial role in AR by interacting with Src-type tyrosine kinase p56lck and STAT6 and promoting mast cells degranulation. METHODS: The effects of TSLP on mast cell degranulation and AR were analysed in human mast cell line (HMC-1 cells), ovalbumin (OVA)-induced AR animal model, and human subjects. Small interfering RNA experiments were performed in HMC-1 cells and OVA-induced AR model. Immune responses were analysed by enzyme-linked immunosorbent assay, Western blotting, immunoprecipitation, and histological studies. RESULTS: Thymic stromal lymphopoietin levels and mast cell-derived p56lck activation were elevated in human subjects with AR, and in AR mice, exogenous TSLP accelerated TH2-allergic inflammatory reactions by up-regulating p56lck and STAT6. On the other hand, depletion of TSLP, p56lck, and STAT6 ameliorated clinical symptoms in AR mice. The selective inhibitor of p56lck, damnacanthal, inhibits AR reactions. CONCLUSION: Collectively, these observations suggest a role for TSLP/p56lck/STAT6 in AR and offer insight into potential therapeutic strategies.

Global Deletion of Pannexin 3 Resulting in Accelerated Development of Aging-Induced Osteoarthritis in Mice.

OBJECTIVE: Osteoarthritis (OA) results in pathologic changes in the joint tissue. The mechanisms driving disease progression remain largely unclear, and thus disease-modifying treatments are lacking. Pannexin 3 (Panx3) was identified as a potential mediator of cartilage degeneration in OA, and our previous study in mice indicated that deletion of the Panx3 gene delayed surgically induced cartilage degeneration. This study was undertaken to examine the role of Panx3 in other OA subtypes, particularly primary OA during aging, in a mouse model of aging-induced OA. METHODS: Wild-type (WT) and Panx3-/- C57BL/6J (Black-6) mice, ages 18-24 months, were analyzed by micro-computed tomography to investigate bone mineral density and body composition. Joints were harvested from the mice, and histopathologic analysis of the joint tissue for OA development was conducted with a specific focus on changes in articular cartilage, subchondral bone, and synovial tissue. RESULTS: Global loss of Panx3 in aging mice was not associated with increased mortality or changes in body composition. Mice lacking Panx3 had shorter appendicular skeletons than WT mice, but overall the body compositions appeared quite similar. Panx3 deletion dramatically accelerated cartilage degeneration and subchondral bone thickening with aging in both 18-month-old and 24-month-old mice, while promoting synovitis in 18-month-old mice. CONCLUSION: These observations in a mouse model of OA suggest that Panx3 has a protective role against the development of primary aging-associated OA. It appears that Panx3 has opposing context-specific roles in joint health following traumatic injury versus that associated with aging. These data strongly suggest that there are differences in the molecular pathways driving different subtypes of OA, and therefore a detailed understanding of these pathways could directly improve strategies for OA diagnosis, therapy, and research.

Activation of hypoxia-inducible factor-1 regulates human histidine decarboxylase expression.

Histidine decarboxylase (HDC) catalyzes the formation of histamine from histidine. Histamine has various effects in physiological and pathological reactions, such as inflammation, cell growth, and neuro-transmission. We investigated the role of hypoxia-inducible factor (HIF)-1 on hypoxia-induced HDC expression in human mast cell line, HMC-1 cells and mouse bone marrow-derived mast cells (BMMCs). Hypoxia significantly increased histamine production. HDC expression and activity were induced by hypoxia. Additionally, when cells were transfected with a native form of HIF-1alpha, hypoxia could induce higher HDC expression than in the nontransfected cell. HIF-1 binding activity for HDC 5' flanking region (HFR) was similar to that for the hypoxia-responsive element. Using HDC promoter deletion analysis, we also demonstrated that HFR was regulated by HIF-1 activation. In addition, depletion of HIF-1alpha prevents hypoxic induction of HDC in BMMCs. In conclusion, these results demonstrate that hypoxia induces HDC expression by transcriptional mechanisms dependent upon HIF-1.

Unilateral thalamic stroke does not decrease ipsilateral sleep spindles.

STUDY OBJECTIVES: To measure the sleep spindle characteristics in patients with unilateral thalamic stroke. DESIGN: A prospective study of patients with thalamic stroke and age-matched healthy controls. SETTING: Department of Neurology of a University Hospital. PARTICIPANTS: Thirteen patients (mean age: 67 years, SD: 13,44) with an isolated, unilateral acute thalamic stroke and 18 healthy age-matched volunteers. INTERVENTIONS: A polysomnogram recording from 14 scalp EEG electrodes performed during 2 consecutive nights, the second or third week after the stroke. Only the sleep of the second night was analyzed. MEASUREMENTS AND RESULTS: Sleep spindles were counted during two separate 10-minute epochs of stage II. Spindles appearing synchronously in both sides with similar amplitude were called "bilateral." Spindles with twice the amplitude in one side than the other were "right" or "left-side predominant". There were 8 patients with posterolateral, 3 with global and 2 with anterior lesions. Eight were right and 5 left-sided. The number of spindles was similar in patients (39.8 +/- 23.4 in 20 minutes) than controls (26.07 +/- 29.07; p=0.173). Spindles with a centroparietal (34%) and centroparieto-occipital localization (22%) were the most frequent. In controls approximately 66% of the spindles had a bilateral and symmetric distribution over the scalp, 23% of the spindles were predominantly left-sided and 5% were predominantly right-sided. In patients, bilateral spindles decreased (p<0.0001) but asymmetric spindles did not change. CONCLUSION: Unilateral acute thalamic stroke does not decrease sleep spindles ipsilaterally; rather, it seems to produce a bilateral diminution in their number.

Effects of isotonic crystalloid resuscitation on fluid compartments in hemorrhaged rats.

Redistribution of fluid after isotonic crystalloid resuscitation from hemorrhage may result not only in interstitial edema but also in cellular edema. We measured the extent to which shock and resuscitation altered fluid compartments in different organs. Nephrectomized, anesthetized rats were randomly divided into a Control group (n = 10) and a Hemorrhage plus Resuscitation group (H/R, n = 10). Rats were subjected to 60 min hemorrhagic hypotension (50 mmHg) followed by a 60 min resuscitation period with .9% NaCl infused as needed to maintain mean arterial pressure at 80% of baseline. A 2 h 51Cr-EDTA distribution space was used to estimate extracellular fluid volume (ECFV) and a 5 min 125I-albumin distribution space was used to measure plasma volume (PV). After euthanasia, total tissue water was measured by wet/dry weight analysis and interstitial fluid volume (ISFV) and cell water were calculated for selected organs. Resuscitation volume was two times the shed blood volume, but resulted in a PV equal to that of the Controls. There were no significant differences in whole animal ECFV or ISFV, although the mean values in the H/R group were greater than that of the Control group. The mean values for total tissue water for each tissue in the H/R group were larger than the respective means of the Control tissues but was significantly greater for only the heart (3639 +/- 56 microL/g vs. 3493 +/- 24 microL/g, mean +/- S.E., p < .05). In all H/R tissues, mean values for ISFV were also larger; this difference was significant for only the liver and small intestines (744 +/- 62 vs. 518 +/- 29 microL/g and 1117 +/- 155 vs. 706 +/- 58 microL/g, respectively). Heart cell water was significantly larger in H/R than Controls (2900 +/- 60 microL/g vs. 2738 +/- 27 microL/g). These data suggest that resuscitation of hemorrhage using isotonic crystalloid normalizes overall PV and ECFV but also causes interstitial expansion in selected gut tissues and cellular edema in the heart.

Kindling with rapidly recurring hippocampal seizures.

Bipolar electrodes, stereotactically implanted in the hippocampus of adult rats, were used to deliver 10 s trains of suprathreshold tetanic electrical stimuli every few minutes. As indices of seizure intensity, durations of the afterdischarges triggered by these stimuli were measured, and the accompanying behaviors were scored on a 5-point scale. After 2-3 h, prolonged afterdischarges appeared in conjunction with severe limbic seizures, separated by periods of approximately 60 min. After 3-9 h, the stimulation was withheld until the following day. Upon reinstitution of the stimuli, intense seizures were seen at the onset, and the cycle time between them was shortened. Enhanced responsiveness to a fixed stimulus persisted for several months, the longest period tested. In addition, the enhanced epileptogenicity showed transference and was not stimulus-specific. These studies, using stimuli with low intertrain frequency and short interstimulus intervals, establish a robust and rapidly-developing model of epileptogenesis in the hippocampus that is comparable to traditional kindling.

Effects of retinoic acid treatment on release of arachidonic acid by chondrogenic cells in response to ionophore A23187.

Chondrogenic differentiation in mouse limb bud mesenchymal cells cultured at high density was suppressed by supplementation of the medium with retinoic acid in a dose-dependent fashion. Cells prelabeled with (3H) arachidonic acid were treated with 0.3 microgram/ml retinoic acid. Treatment with retinoic acid increased the (3H) fatty acid in the triglyceride fraction. Furthermore, treatment with retinoic acid enhanced the release of (3H) fatty acid upon stimulation of these cells with the divalent ionophore A23187. These data permit the suggestion that there may be a correlation between altered lipid metabolism and retinoic acid's ability to disrupt chondrogenic differentiation.

Regeneration of Ceratozamia euryphyllidia (Cycadales, Gymnospermae) plants from embryogenic leaf cultures derived from mature-phase trees.

Embryogenic cultures were induced from pinnae removed from young leaf flushes of mature-phase trees of the endangered cycad species, Ceratozamia euryphyllidia. Induction media consisted of B5 major salts, Murashige and Skoog minor salts and organics, 400 mg l-1 glutamine, 100 mg l-1 asparagine, 100 mg l-1 arginine, 60 g l-1 sucrose, 2 g l-1 gellan gum, 4.65-13.94 µM kinetin and 4.52-9.05 µM 2,4-dichlorophenoxyacetic acid. Cultures were maintained in darkness. Embryogenic cultures were comprised of precotyledonary somatic embryos that proliferated by somatic polyembryogenesis following subculture onto medium without plant growth regulators. Somatic embryo development and maturation occurred spontaneously from proliferating cultures on medium without plant growth regulators. Somatic embryos were monocotyledonous and mature somatic embryos germinated on semisolid medium without growth regulators. Subsequent development, which included the elongation of the first leaves, occurred only after subculture onto semisolid medium without plant growth regulators containing 0.5% (wt/vol) activated charcoal and under low light intensity. The time period from explanting to plant recovery was approximately 3 years.

Evaluation of setting properties and retention characteristics of mineral trioxide aggregate when used as a furcation perforation repair material.

Furcation perforations were created in 32 extracted maxillary and mandibular molars. The perforations were prepared in the center of the pulp chamber floor parallel to the long axis of each tooth and a saline-moistened Gelfoam matrix was placed below the perforation to simulate a clinical condition. The teeth were randomly divided into four groups, and the perforations were all repaired with mineral trioxide aggregate (MTA) and then covered with either a wet or dry cotton pellet for 24 or 72 h. Instron testing was used to measure the force required to displace the material from the perforation. The force measurements showed that MTA resisted displacement at 72 h to a significantly greater level than at 24 h (p < 0.05). When slight displacement occurred at 24 h the material demonstrated the ability to re-establish resistance to dislodgement from the dentin wall. The presence of some moisture in the perforation during placement was advantageous in aiding adaptation of MTA to the walls of the perforation, but there was no significant difference in MTA retention when a wet or dry cotton pellet was placed in the pulp chamber during the setting time (p > 0.05).

The stem of sinomenium acutum inhibits mast cell-mediated anaphylactic reactions and tumor necrosis factor-alpha production from rat peritoneal mast cells.

The aqueous extract of Sinomenium acutum stem (SSAE) (0.1-1000 mg/kg) dose-dependently inhibited systemic anaphylactic reaction induced by compound 48/80 in mice. In particular, SSAE reduced compound 48/80-induced anaphylactic reaction with 50% at the dose of 1000 mg/kg. SSAE (100-1000 mg/kg) also significantly inhibited local anaphylactic reaction activated by anti-dinitrophenyl (DNP) IgE. When mice were pretreated with SSAE at a concentration ranging from 0.1 to 1000 mg/kg, the plasma histamine levels were reduced in a dose-dependent manner. SSAE (1-1000 microg/ml) dose-dependently inhibited histamine release from the rat peritoneal mast cells (RPMCs) activated by compound 48/80 or anti-DNP IgE. In addition, SSAE (0.1 microg/ml) had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis factor-alpha (TNF-alpha) production. These results indicate that SSAE inhibits mast cell-mediated anaphylactic reactions and TNF-alpha production from mast cells.

Paravertebral thoracolumbar anaesthesia in 10 horses.

The caudal border of the last rib was used as a reliable point of orientation while performing paravertebral thoracolumbar anaesthesia (PTLA) on 10 horses undergoing standing flank laparotomy. The local anaesthetic in all horses was 2% lidocaine. The PTLA procedure was completed in 9.8 +/- 1.8 mins (mean +/- sd). Sedation was provided by a combination of intravenous morphine with xylazine or detomidine. Overall analgesia, provided by the combination of PTLA and sedation, was rated as excellent in 2 horses and good in 6 horses. In the remaining 2 horses, overall analgesia was rated as fair because of incomplete analgesia at the ventral portion of the incision. Total time, from start of PTLA to end of surgery was 143.5 +/- 24.2 mins. Five horses responded mildly to suturing of the ventral portion of the incision. Apart from 1 horse which developed transient, unilateral hindlimb weakness intraoperatively, no other complications were noticed. We conclude that PTLA can easily be performed in the horse and, combined with systemic sedation, is an effective and safe method of providing analgesia for standing flank laparotomy.

The influence of proximal retention grooves on the retention and resistance of class II preparations for amalgams.

The addition of proximal retention grooves to various designs of the Class II cavity preparation considerably improves the retention and resistance characteristics of amalgam restorations. The incorporation of proximal grooves should reduce the necessity for gross outline form as a means of gaining adequate retention adn resistance in the Class II preparation.

Allergic contact stomatitis from a gold alloy--fixed partial denture.

Allergic contact stomatitis to gold is rare. To our knowledge, seven cases caused by dental restorations have been previously reported. Each of the patients was female. This report documents an allergic reaction to gold in a fixed prosthesis. A female patient, previously sensitized to gold earrings, experienced an itching and burning pain sensation and ulceration of the oral tissues adjacent to the gold restoration. Patch tests confirmed the allergy to gold. The dentist needs to be aware of the symptoms that are characteristic of the allergic manifestations of gold. Inquiries about allergies to metals and jewelry should be a part of the medical history. Any patient experiencing pain, itching, burning, and ulceration of the mucosa adjacent to a cast gold restoration should be suspected of an allergic contact stomatitis.

Cortisol suppression in cats after induction of anesthesia with etomidate, compared with ketamine-diazepam combination.

OBJECTIVE: To evaluate duration and magnitude of adrenocortical function suppression after administration of etomidate to cats. ANIMALS: 15 purpose-bred, healthy cats. PROCEDURE: Cats were allotted to 2 groups. Anesthesia was induced with etomidate (ET, 2 mg/kg of body weight, i.v.; n = 8) or a mixture (KD, n = 7) of ketamine (5 mg/kg; i.v) and diazepam (0.25 mg/kg, i.v.). Anesthesia was maintained with halothane in all cats for 2 hours. ACTH gel (2.2 U/kg, i.m.) was administered 30 minutes after anesthesia induction. Blood samples for cortisol assay were taken before anesthesia induction (T -30), and before (T0) and at 30, 60, 120, 180, 300, and 420 minutes after ACTH administration. Anesthesia was discontinued after the T120 sample was obtained. RESULTS: After anesthesia induction, median (interquartile range [Q1-Q3]) cortisol values were significantly lower in the ET group (4 [3 to 4] micrograms/dl) at T0, compared with T -30 values and with T0 values in the KD group (5 [3 to 9] micrograms/dl). After ACTH administration, cortisol values in the ET group continued to decrease two- to threefold below T -30 values and remained decreased over the 2-hour anesthesia period. After ACTH administration, cortisol values increased twofold for 2 hours in the KD group, compared with T -30 values. One hour after anesthesia recovery, cortisol values in the ET group (3 [2 to 3] micrograms/dl) remained significantly lower than values in the KD group (9 [7 to 11] micrograms/dl) and preanesthesia values. By T300, both groups had cortisol concentration near 7 micrograms/dl, similar to preanesthesia values. CONCLUSION: Induction of anesthesia with etomidate caused suppression of adrenocortical function during 2 hours of halothane anesthesia and 1 hour of recovery in cats. Cortisol concentration did not return to baseline until after 2 additional hours. CLINICAL RELEVANCE: Results from these healthy cats suggest profound suppression of important stress hormones after anesthesia induction with etomidate, use of which could put critically ill cats at further risk.

Evaluation of quantitative acid-base balance and determination of unidentified anions in swine.

Arterial blood samples were collected from 19 anesthetized pigs before and after hemorrhage was induced. Blood gas tensions and concentrations of sodium, potassium, chloride, lactate, and total protein were measured. Results indicated that hydrogen ion (H+) concentration calculated from a specific formula was a biased and imprecise estimate of measured H+ concentration. The bias was 5.45 nEq/L, with limits of agreement from -7.92 to 18.83 nEq/L. Because albumin is the fraction of plasma protein most important in acid-base balance, the agreement between predicted and measured H+ concentration was reevaluated, using an albumin charge estimate and a reference swine albumin-to-globulin ratio. This improved the ability of the formula to predict H+ concentration; the bias decreased to 1.33 nEq/L with limits of agreement from -12.16 to 9.49 nEq/L. The formula and a simplified approach for clinical application were biased and unacceptably imprecise estimators of lactate (L-) concentration. The formula approach underestimated L- concentration by 2.8 (-12.4, 6.7) mEq/L, whereas the simplified method overestimated L- concentration by 5.0 (-3.8, 13.9) mEq/L.

Effects of tromethamine buffer on coagulation variables and ionized calcium concentration in dogs.

OBJECTIVE: To evaluate coagulation variables in 2 groups of dogs after tromethamine administration. ANIMALS: 13 Beagles. PROCEDURES: Both groups of dogs received a 30-minute IV infusion of 10 ml of 0.3M tromethamine/kg of body weight. In unsedated dogs (group 1, n = 8), prothrombin time, activated partial thromboplastin time, normalized ionized calcium concentration, platelet numbers, and platelet function were measured prior to treatment, at the end of the infusion, and 1 hour after the infusion. In xylazine-sedated dogs (group 2, n = 5), buccal mucosal bleeding time and plasma percentage of von Willebrand factor antigen were measured before and 1 hour after infusion, and fibrin degradation products concentration was measured 1 hour after infusion. Platelet function was assessed by determining platelet aggregation and by measuring ATP release from the aggregating platelets over 6 minutes, using a whole blood aggregometer, with 20, 10, and 5 microM ADP and 5 and 10 micrograms of collagen/ml as platelet activation agonists. RESULTS: There was no significant change in any of the variables measured in either group of dogs, compared with baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: When administered to healthy dogs, tromethamine does not change the coagulation indices measured.

Acid-base, metabolic, and hemodynamic effects of sodium bicarbonate or tromethamine administration in anesthetized dogs with experimentally induced metabolic acidosis.

OBJECTIVE: To evaluate buffering capacity and side effects of equivalent doses of tromethamine (THAM) and sodium bicarbonate (BIC). ANIMALS: 18 purebred dogs. PROCEDURE: Acidosis was induced by having dogs breathe a hypoxic gas mixture (FIO2 = 0.10) until arterial base balance < or = -7.5 mEq/L was reached. Dogs then received a 30-minute infusion of 5% BIC (n = 6) or 0.3M THAM (n = 8), and FIO2 increased to 0.30. Drug doses were calculated to correct base balance to zero. RESULTS: During hypoxia, for BIC- and THAM-treated groups, median (interquartile range [Q1, Q3]) pHa and arterial base balance decreased to 7.16 (7.07, 7.38) and 7.19 (7.11, 7.31), -14 (-16, 9) and -12 (-16, -11) mEq/L, respectively, and mixed venous lactate concentration increased to 7 (2, 15) and 6 (3, 13) mmol/L, respectively. Immediately after each infusion, acid-base and cardiopulmonary variables returned toward baseline. For respective BIC- and THAM-treated groups, pHa increased to 7.37 (7.26, 7.44) and 7.40 (7.33, 7.49) and base balance increased to 0 (-4, 7) and 0 (-4, 2) mEq/L. Lactate concentration decreased only slightly to 5 (2, 6) and 5 (2, 9) mmol/L, but continued to decrease throughout the study. The only significant (P < or = 0.05) difference between groups was hypernatremia after BIC administration that persisted for 60 minutes. The PaCO2 in BIC-treated dogs increased immediately after infusion, compared with values during hypoxia. Standardized ionized calcium values initially decreased in both groups, but returned to baseline by 60 minutes. CONCLUSION: The buffering capacity of THAM is equal to that of BIC, although THAM does not cause the transient hypernatremia or hypercapnia observed after BIC administration. Hypocalcemia may be transient after administration of either solution. Thus, THAM is an acceptable alternative to BIC for treatment of metabolic acidosis in selected anesthetized dogs.

Effects of a highly concentrated hypertonic saline-dextran volume expander on cardiopulmonary function in anesthetized normovolemic horses.

Conventional fluid resuscitation is unsatisfactory in a small percentage of equine emergency surgical cases because the large volumes of fluids required cannot be given rapidly enough to adequately stabilize the horse. In anesthetized horses, the volume expansion and cardiopulmonary effects of a small volume of highly concentrated hypertonic saline-dextran solution were evaluated as an alternative initial fluid choice. Seven halothane-anesthetized, laterally recumbent, spontaneously ventilating, normovolemic horses were treated with a 25% NaCl-24% dextran 70 solution (HSD) at a dosage of 1.0 ml/kg of body weight, IV, infused over 10 minutes, and the effects were measured for 120 minutes after infusion. Plasma volume expansion was rapid and significant (from 36.6 +/- 4.6 ml/kg to 44.9 +/- 4.8 ml/kg), and remained significantly expanded for the duration of the experiment. Packed cell volume, total blood hemoglobin, and plasma protein concentrations significantly decreased, confirming rapid and sustained volume expansion with hemodilution. Cardiac index and stroke index immediately increased and remained high for the entire study (from 69.6 +/- 15.3 ml/min/kg to 106.6 +/- 28.4 ml/min/kg, and from 1.88 +/- 0.49 ml/beat/kg to 2.50 +/- 0.72 ml/beat/kg, respectively). Systemic vascular resistance significantly decreased immediately after HSD infusion and remained decreased for the duration of the study (from 1.41 +/- 0.45 mm of Hg/ml/min/kg to 0.88 +/- 0.22 mm of Hg/ml/min/kg). Arterial and venous blood oxygen content decreased significantly because of hemodilution, but actual oxygen transport transiently increased at the 10-minute measurement before returning toward baseline.(ABSTRACT TRUNCATED AT 250 WORDS)