Structural and oxidative enzyme characteristics of the diaphragm.

During exercise, the horse can achieve oxygen uptakes and ventilations in excess of 200 ml/kg/min and 1800 l/min, respectively. Whether the diaphragm has the capacity to contribute substantially to inspiratory effort in the exercising horse is not known. To investigate the potential for the horse diaphragm to generate tension, lung displacement and sustain ventilatory function, we measured diaphragm thickness, muscle length and oxidative enzyme activity (citrate synthase) within the ventral, medial and dorsal costal and crural diaphragm. In the diaphragms of 6 mature horses (5 Thoroughbreds, one Quarter Horse; body mass (mean +/- s.e.) 475 +/- 14 kg, age 4 +/- 1 years), the mass of the freshly-excised diaphragm was 4.54 +/- 0.19 kg of which 79% was the costal diaphragm, 17% the crural diaphragm and 4% the central tendon. The medial costal region (2.1 +/- 0.1 cm) was significantly thicker (P<0.05) than either the ventral (1.4 +/- 0.1 cm) or dorsal (1.2 +/- 0.2 cm) costal regions and the crural diaphragm was significantly thicker (>3.2 +/- 0.3 cm, P<0.05) than any costal diaphragm region. With respect to the costal diaphragm, excised muscle length was greatest (P<0.05) in the medial costal (17.2 +/- 1.0 cm) than either the ventral costal (<12.6 +/- 1.5 cm) or dorsal costal (<13.9 +/- 1.8 cm) regions and therefore the medial region would be expected to exhibit the greatest absolute length change on inspiration. Citrate synthase activity was high throughout the diaphragm (40.8 +/- 113 to 55.3 +/- 9.7 micromol/g/min), but was not significantly different among regions. These structural characteristics and the oxidative potential of the horse diaphragm are consistent with the diaphragm providing a significant and substantial contribution to the inspiratory effort during exercise in the horse. Consequently, clinical and physiological investigations of exercise performance should not ignore the potentially crucial importance of the diaphragm.

Ventilatory sensitivity to changes in inspired and arterial carbon dioxide partial pressures in the chicken.

To determine if intrapulmonary chemoreceptors could be the sole peripheral chemoreceptors responsible for ventilatory responses to inhaled CO2, we studied the relationships of minute ventilation, tidal volume, and respiratory frequency to inspired and arterial partial pressure of CO2 (P(I)CO2 and PaCO2) in decerebrate upright chickens when the birds inspired gases containing four low partial pressures of CO2 (0.02, 5.0, 8.2, and 11.4 torr). Because of variability in the measured variables from time to time in the same birds, as well as between birds, and because of the limited precision in measuring PaCO2, a 4 x 4 Latin square design and four statistical methods of data analyses (modified reduced major axis estimator, maximum likelihood estimator, average slope method, and summary slope method) were used. Tidal volume, minute ventilation, and PaCO2 increased, but respiratory frequency remained unchanged, as gases containing increased partial pressures of CO2 were inhaled. The results indicate that intrapulmonary chemoreceptors are not the sole receptors stimulated by inhaling gas containing even low partial pressures of CO2 and that stimulation of arterial and central chemoreceptors also occurs. Stimulation of these latter chemoreceptors may account for the increase in ventilation. Further, the results demonstrate the importance of maintaining a low level of environmental CO2 in poultry houses to minimize its influence on ventilation.

Cardiorespiratory impact of the nitric oxide synthase inhibitor L-NAME in the exercising horse.

To investigate the role of nitric oxide, NO, in facilitating cardiorespiratory function during exercise, five horses ran on a treadmill at speeds that yielded 50, 80 and 100% of peak pulmonary oxygen uptake (V(O(2)) peak) as determined on a maximal incremental test. Each horse underwent one control (C) and one (NO-synthase inhibitor; N(G)-L-nitro-arginine methyl ester (L-NAME), 20 mg/kg) trial in randomized order. Pulmonary gas exchange (open flow system), arterial and mixed-venous blood gases, cardiac output (Fick Principle), and pulmonary and systemic conductances were determined. L-NAME reduced exercise tolerance, as well as cardiac output (C, 291+/-34; L-NAME, 246+/-38 L/min), body O(2) delivery (C, 74.4+/-5. 5; L-NAME, 62.1+/-5.6 L/min), and both pulmonary (C, 3.07+/-0.26; L-NAME, 2.84+/-0.35 L/min per mmHg) and systemic (C, 1.55+/-0.24; L-NAME, 1.17+/-0.16 L/min per mmHg) effective vascular conductances at peak running speeds (all P<0.05). On the 50 and 80% trials, L-NAME increased O(2) extraction, which compensated for the reduced body O(2) delivery and prevented a fall in V(O(2)). However, at peak running speed in the L-NAME trial, an elevated O(2) extraction (P<0. 05) was not sufficient to prevent V(O(2)) from falling consequent to the reduced O(2) delivery. At the 50 and 80% running speeds (as for peak), L-NAME reduced pulmonary and systemic effective conductances. These data demonstrate that the NO synthase inhibitor, L-NAME, induces a profound hemodynamic impairment at submaximal and peak running speeds in the horse thereby unveiling a potentially crucial role for NO in mediating endothelial function during exercise.

Analysis of the right ventricular function in the exercising horse: use of the Fourier Transform.

The objective of this study was to develop and test a technique to allow dynamic cardiac function to be studied during exercise in the horse. Blood pressure waveforms in the exercising horse are difficult to interpret because of the large influence of stride and respiration. A method has been devised to study dynamic right ventricular variables during high-speed exercise in the horse. A Fast Fourier Transform was performed on the digitised pressure waveforms and the frequency components associated with stride and respiration were removed. An inverse Fourier Transform was then performed to generate a time-domain pressure signal. Several dynamic right ventricular variables were calculated using the derived signal. Various parameters associated with removing frequencies from the frequency-domain pressure signal were changed to determine their influence on the variables. Most of the variables were not sensitive to these parameters. When compared during separate exercise bouts, some variables differed among runs, while others were not significantly different. Using the signal separation technique described here, right ventricular function of an exercising horse can be critically analysed.

Cardio-pulmonary function in preascitic (hypoxemic) or normal broilers inhaling ambient air or 100% oxygen.

We evaluated the influence of the percentage saturation of hemoglobin with oxygen (HbO2) on the pulmonary arterial pressure in normal and preascitic (hypoxemic) broilers breathing ambient air or 100% O2. In Experiment 1, unanesthetized preascitic broilers (right:total ventricular weight ratios [RV:TV] = 0.32+/-0.02) breathing ambient air had initial values of 67% for HbO2 and 32 mm Hg for pulmonary arterial pressure. The HbO2 increased to > or =96.6% during inhalation of 100% O2; however, pulmonary arterial pressure was not reduced. In Experiment 2, anesthetized normal (RV:TV = 0.23; HbO2 = 88%) and preascitic broilers (RV:TV = 0.28; HbO2 = 76%) were compared. The groups did not differ in body weight or respiratory rate, but preascitic broilers had lower values for mean arterial pressure, total peripheral resistance, and partial pressure of O2 in arterial blood and had higher values for pulmonary arterial pressure. Inhaling 100% O2 increased HbO2 to 99.9% in both groups; however, pulmonary arterial pressure remained higher in preascitic than in normal broilers, and the pulmonary vascular resistance was not reduced during 100% O2 inhalation. Cardiac output was higher in preascitic than in normal broilers before and after, but not during, 100% O2 inhalation. Mean arterial pressure and total peripheral resistance increased in the preascitic but not in the normal group during 100% O2 inhalation. Low coefficients of determination (R2) were obtained for linear regression comparisons of HbO2 vs. pulmonary arterial pressure in both experiments. Overall, acute reversal of the systemic hypoxemia in preascitic broilers had little direct impact on pulmonary hypertension, providing no evidence of hypoxemic or hypoxic pulmonary vasoconstriction. Instead, acute reversal of the systemic hypoxemia primarily increased the total peripheral resistance and normalized the mean arterial pressure and cardiac output. A sustained reduction in cardiac output theoretically should attenuate pulmonary hypertension, but this was not observed because of the overriding influence of sustained pulmonary vascular resistance.

Effect of furosemide on pulmonary blood flow distribution in resting and exercising horses.

We determined the spatial distribution of pulmonary blood flow (PBF) with 15-micron fluorescent-labeled microspheres during rest and exercise in five Thoroughbred horses before and 4 h after furosemide administration (0.5 mg/kg iv). The primary finding of this study was that PBF redistribution occurred from rest to exercise, both with and without furosemide. However, there was less blood flow to the dorsal portion of the lung during exercise postfurosemide compared with prefurosemide. Furosemide did alter the resting perfusion distribution by increasing the flow to the ventral regions of the lung; however, that increase in flow was abated with exercise. Other findings included 1) unchanged gas exchange and cardiac output during rest and exercise after vs. before furosemide, 2) a decrease in pulmonary arterial pressure after furosemide, 3) an increase in the slope of the relationship of PBF vs. vertical height up the lung during exercise, both with and without furosemide, and 4) a decrease in blood flow to the dorsal region of the lung at rest after furosemide. Pulmonary perfusion variability within the lung may be a function of the anatomy of the pulmonary vessels that results in a predominantly fixed spatial pattern of flow distribution.

Influence of frusemide on dynamic cardiac variables during exercise.

Exercising horses have extremely high right and left atrial pressures. Limitation in ventricular function (i.e. relaxation) may play a role in these high pressures. We studied relaxation characteristics of the right ventricular myocardium and the impact of frusemide (2.0 mg/kg bwt i.v.) on these characteristics in horses exercising at 8, 10, 12 and 14 m/s. Exercise tests were performed 4 h after administration of frusemide. Right ventricular (RV) pressure was analysed using Fast Fourier Transform techniques to remove non cardiac components of the pressure signal. Mean right atrial (RA) pressure increased with exercise and was significantly attenuated at all speeds by frusemide. RV maximum and minimum rates of pressure change with respect to time (RV + dP/dtmax, RV-dP/dtmax) increased with exercise and RV relaxation time constant (RV tau) and time of RV relaxation from 65-20% of the difference between maximum and minimum ventricular pressure (delta 65-20) decreased with exercise. Frusemide produced no significant differences in +dP/dtmax, -dP/dtmax, RV tau or delta 65-20 except at 12 m/s where RV tau was longer after frusemide (23.4 ms for frusemide vs. 19.7 ms for control). Significant reductions in stroke volume were seen at 8, 10 and 14 m/s after frusemide. These results suggest that the reduction of atrial pressure by frusemide is not due to changes in ventricular relaxation rate.

Influence of feed deprivation on ventilation and gas exchange in broilers: relationship to pulmonary hypertension syndrome.

Fast-growing broiler chickens not uncommonly exhibit elevated pulmonary vascular resistance that leads to pulmonary hypertension and right ventricular failure. We tested the hypothesis that a distended gastrointestinal tract in these full-fed birds results in an abnormally low tidal volume and minute ventilation that could lead to pulmonary hypoxia, pulmonary arterial vasoconstriction, right ventricular failure, and ascites. Tidal volume, respiratory frequency, heart rate, percentage saturation of hemoglobin with oxygen (HbO2), O2 consumption, and carbon dioxide elimination were measured on fast-growing broiler chickens when full-fed and after 3, 6, and 9 h of feed deprivation. Tidal volume of full-fed birds was not abnormally low despite HbO2 values varying from above 80% to nearly 60%. Importantly, HbO2 was found to be markedly increased in the hypoxemic birds at and beyond a 3-h period without feed, despite a reduction in minute ventilation. This response was not caused by a decrease in O2 consumption. Thus, limitation of gas intake at the mouth was not the cause of the hypoxemia. The data suggest that feed deprivation results in an increase in parabronchial ventilation, possibly from improvement in aerodynamic valving, which would reduce pulmonary hypoxic vasoconstriction and right ventricular failure.

Relationship of structure and function of the avian respiratory system to disease susceptibility.

The avian respiratory system exchanges oxygen and carbon dioxide between the gas and the blood utilizing a relatively small, rigid, flow-through lung, and a system of air sacs that act as bellows to move the gas through the lung. Gas movement through the paleopulmonic parabronchi, the main gas exchanging bronchi, in the lung is in the same direction during both inspiration and expiration, i.e., from the mediodorsal secondary bronchi to the medioventral secondary bronchi. During inspiration, acceleration of the gas at the segmentum accelerans of the primary bronchus increases gas velocity so it does not enter the medioventral secondary bronchi. During expiration, airway resistance is increased in he intrapulmonary primary bronchus because of dynamic compression causing gas to enter the mediodorsal secondary bronchi. Reduction in air flow velocity may decrease the efficiency of this aerodynamic valving and thereby decrease the efficiency of gas exchange. The convective gas flow in the avian parabronchus is orientated at a 90 degree angle with respect to the parabronchial blood flow; hence, the cross-current designation of this gas exchanger. With this design, the partial pressure of oxygen in the blood leaving the parabronchus can be higher than that in the gas exiting this structure, giving the avian lung a high gas exchange efficacy. The relationship of the partial pressure of oxygen in the moist inspired gas to that in the blood leaving the lung is dependent on he rate of ventilation. A low ventilation rate may produce a ow oxygen partial pressure in part of the parabronchus, thereby inducing hypoxic vasoconstriction in the pulmonary arterioles supplying this region. Inhaled foreign particles are removed by nasal mucociliary action, by escalator in the trachea, primary bronchi, and secondary bronchi. Small particles that enter parabronchi appear to be phagocytized by the epithelial cells in eh atria and infundibulum. These particles can e transported to interstitial macrophages but the disposition of the particles from this site is unknown. The predominant site of respiratory infections in the caudal air sacs, compared to other parts of the respiratory system, can be explained by the gas flow pathway and the mechanisms present in the parabronchi for particle removal.

Quantification of exercise-induced pulmonary haemorrhage with bronchoalveolar lavage.

Exercise-induced pulmonary haemorrhage (EIPH) causes serious economic losses in the horse racing industry. Endoscopic examination indicates that 40-90% of horses exhibit EIPH following sprint exercise, but the limitations of the endoscope prevent diagnosis in many horses. Bronchoalveolar lavage (BAL) was utilised to detect red blood cells (RBCs) in the terminal airways in 6 horses. Two lavages were performed at weekly intervals prior to exercise, one within 90 min after exercise, and 5 at weekly intervals after exercise. The horses were exercised strenuously at 12.5-14.6 m/s on a treadmill (3 degree incline). Heart rates ranged from 192-207 beats/min, and mean pulmonary arterial pressures (mPAP) ranged from 80-102 mmHg. Neither epistaxis nor endoscopic evidence of EIPH was seen in any of the 6 horses following exercise. However, the number of RBCs in the lavage fluid increased significantly over control values immediately after exercise in all horses but returned to control values by one week after exercise. Haemosiderophages in the BAL fluid did not increase until one week after exercise and remained elevated for 3 weeks after exercise. Twenty per cent of the total population of alveolar macrophages contained haemosiderin. A positive relationship occurred between the number of RBCs in the lavage fluid and mPAP; the amount of haemorrhage increased as the mPAP exceeded 80 to 90 mmHg. The results with BAL used as the diagnostic tool, suggest that all strenuously exercised horses may exhibit EIPH; the amount of haemorrhage appears to be associated with the magnitude of the high pulmonary arterial pressure.

Increase in blood viscosity in the sprinting horse: can it account for the high pulmonary arterial pressure?

Blood was taken from 49 Thoroughbred horses before and after racing at the track to determine if frusemide modified the apparent viscosity of the blood and to determine the effects of changes in shear rate and packed cell volume (PCV), associated with strenuous exercise, on apparent and relative viscosities. Small increases in apparent viscosity of the blood (at a specified PCV and shear rate) occurred in horses given frusemide compared to those receiving no frusemide; however, no differences were seen in relative viscosity. Although 2 groups of horses, those receiving frusemide before racing and those not receiving this drug were studied, the results suggest no influence of frusemide on any red blood cell variable that might modify apparent blood viscosity. Apparent viscosity of the blood was slightly (but significantly) higher after racing than before racing at any given PCV and shear rate, but relative viscosity was lower in the post race than in the prerace blood sample. The most important contributing factor to the increase in apparent viscosity in blood during racing is the increase in PCV, because the blood becomes nearly shear rate independent at shear rates likely to exist in the cardiovascular system during exercise. With an increase in PCV from 40 to 65% at shear rates above 225/s, apparent viscosity approximately doubled. However, this increase alone cannot account for the elevated pulmonary vascular pressure in the running horse, and additional factors, especially those causing the high left atrial pressure, must be considered. The cause of the elevated pressure may be multifactorial in nature.

Force, speed, and oxygen consumption in thoroughbred and draft horses.

Thoroughbred (TB) and draft horses (DH) have long been selected for tasks of very different intensities and force-speed relationships. To study their adaptations, we measured O2 consumption and related variables in three TB and four DH during progressive exercise tests on a level treadmill. The horses exerted a draft force of 0, 5, 10, 15, or 20% of their body weight at speeds that increased by 2 m/s every 3 min until they could not maintain that speed. We found that TB could exert the same draft forces as DH and, at each force, TB achieved about twice the speed, twice the external power, and twice the O2 consumption as DH; thus the two breeds had the same gross efficiencies. We also found maximal O2 consumption of TB to be about twice that of DH (134 vs. 72 ml . kg-1 . min-1, respectively), suggesting adaptations to high-intensity exercise. Peak efficiency was reached at lower speeds in DH than in TB, suggesting adaptations to high-force, low-speed exercise. These differences between TB and DH in force-speed and aerobic capacities and in speed for peak efficiency likely reflect different contraction velocities in locomotor muscles.

Skeletal muscle microcirculatory structure and hemodynamics in diabetes.

Within skeletal muscle, insulin-dependent (Type 1) diabetes produces straighter, narrower capillaries. To test the hypothesis that these microvascular alterations would be associated with impaired capillary hemodynamics, intravital microscopy techniques were used to study the in vivo spinotrapezius muscle microcirculation of age-matched control (C) and streptozotocin (STZ) induced diabetic (D) rats. D rats exhibited a marked reduction in body weight (C, 266 +/- 5 g; D, 150 +/- 6 g; P < 0.001). At resting sarcomere lengths (i.e. approximately 2.7 microm), the additional capillary length arising from tortuosity and branching was less in D muscle (C, 10.5 +/- 0.8%; D, 5.3 +/- 1.0%, P < 0.01). Capillary diameter was reduced in D muscle (C, 5.4 +/- 0.1 microm; D, 4.6 +/- 0.1 microm; P < 0.001), and was positively correlated (r = 0.71) with the decreased proportion of capillaries sustaining flow (C, 85 +/- 5%; D, 53 +/- 3%; P < 0.001). Within those 'flowing' capillaries, red blood cell (RBC) velocity and flux were reduced 29 and 43%, respectively in D muscle (both P < 0.05). This reduced calculated O2 delivery by 57% per unit tissue width and 41% per unit muscle mass. Capillary 'tube' hematocrit was unchanged from control values (C, 0.22 +/- 0.02; D, 0.22 +/- 0.02). We conclude that, in the diabetic state, microvascular remodeling is associated with a reduced proportion of 'flowing' capillaries and a reduction in RBC velocity and flux in these vessels such that skeletal muscle O2 delivery is markedly reduced.

VO2 kinetics in the horse during moderate and heavy exercise.

The horse is a superb athlete, achieving a maximal O2 uptake (approximately 160 ml . min-1 . kg-1) approaching twice that of the fittest humans. Although equine O2 uptake (VO2) kinetics are reportedly fast, they have not been precisely characterized, nor has their exercise intensity dependence been elucidated. To address these issues, adult male horses underwent incremental treadmill testing to determine their lactate threshold (Tlac) and peak VO2 (VO2 peak), and kinetic features of their VO2 response to "square-wave" work forcings were resolved using exercise transitions from 3 m/s to a below-Tlac speed of 7 m/s or an above-Tlac speed of 12.3 +/- 0.7 m/s (i.e., between Tlac and VO2 peak) sustained for 6 min. VO2 and CO2 output were measured using an open-flow system: pulmonary artery temperature was monitored, and mixed venous blood was sampled for plasma lactate. VO2 kinetics at work levels below Tlac were well fit by a two-phase exponential model, with a phase 2 time constant (tau1 = 10.0 +/- 0.9 s) that followed a time delay (TD1 = 18.9 +/- 1.9 s). TD1 was similar to that found in humans performing leg cycling exercise, but the time constant was substantially faster. For speeds above Tlac, TD1 was unchanged (20.3 +/- 1.2 s); however, the phase 2 time constant was significantly slower (tau1 = 20.7 +/- 3.4 s, P < 0.05) than for exercise below Tlac. Furthermore, in four of five horses, a secondary, delayed increase in VO2 became evident 135.7 +/- 28.5 s after the exercise transition. This "slow component" accounted for approximately 12% (5.8 +/- 2.7 l/min) of the net increase in exercise VO2. We conclude that, at exercise intensities below and above Tlac, qualitative features of VO2 kinetics in the horse are similar to those in humans. However, at speeds below Tlac the fast component of the response is more rapid than that reported for humans, likely reflecting different energetics of O2 utilization within equine muscle fibers.

Effects of racing and gender on viscoelastic properties of horse blood.

Splenic contraction in racing horses increases the hematocrit (hct), thereby increasing blood viscosity. We tested as to whether racing also affects the elastic properties of blood. Mares and geldings were studied for thus purpose. After racing, there was: (i) an increased erythrocyte count independent of gender and race distance (0.32 to 1.7 km): (ii) an increased mean erythrocyte volume in both sexes; (iii) an increased heterogeneity of RBC size in both sexes; (iv) an increased plasma fibrinogen concentration and erythrocyte sedimentation rate in both sexes; and (v) an increased elastic yield stress (EYS). When corrected to a constant hct of 65%, the blood of mares, but not geldings, had increased EYS after racing. Gender differences in fibrinogen response (p = 0.72) did not account for this and the mechanism is not known. Since EYS is analogous to the point at which ketchup starts to flow from a bottle, its increase could be deleterious in vascular beds characterized by pulsatile flow, e.g. the coronary circulation.

Blood viscosity in broilers: influence on pulmonary hypertension syndrome.

Elevation in apparent blood viscosity may enhance the pulmonary hypertension that leads to pulmonary hypertension syndrome (PHS) and ascites in fast-growing broilers. We investigated the importance of packed cell volume (PCV) and shear rate in modifying apparent viscosity of the blood from broilers assigned to normal, preascites, and ascites groups. Apparent viscosity of broiler blood increased at all shear rates as PCV increased; the increase in apparent viscosity became greater as the shear rate decreased at PCV above 0.30. At the PCV of normal broilers (0.30 or below), apparent viscosity was nearly shear rate independent, at least down to 11.25 per second, the lowest shear rate studied. Apparent viscosity, at any given PCV and shear rate, was significantly lower in the blood of birds with ascites than in normal birds; however, the relative viscosity was not different between those groups, indicating that lower plasma viscosity in the birds with PHS was responsible for the finding. The results show that the principal factor responsible for increased apparent viscosity of blood in birds with PHS is the increase in PCV. The increased resistance to flow of blood as the result of higher blood viscosity may contribute to the pulmonary hypertension.

Pulmonary blood flow distribution in standing horses is not dominated by gravity.

Recent studies using microspheres in dogs, pigs and goats have demonstrated considerable heterogeneity of pulmonary perfusion within isogravitational planes. These studies demonstrate a minimal role of gravity in determining pulmonary blood flow distribution. To test whether a gravitational gradient would be more apparent in an animal with large vertical lung height, we measured perfusion heterogeneity in horses (vertical lung height = approximately 55 cm). Four unanesthetized Thoroughbred geldings (422-500 kg) were studied awake in the standing position with fluorescent microspheres injected into a central vein. Between 1,621 and 2,503 pieces (1.3 cm3 in volume) were obtained from the lungs of each horse with spatial coordinates, and blood flow was determined for each piece. The coefficient of variation of blood flow throughout the lungs ranged between 22 and 57% among the horses. Considerable heterogeneity was seen in each isogravitational plane. The relationship between blood flow and vertical height up the lung was characterized by the slope and correlation coefficient of a least squares regression analysis. The slopes within each horse ranged from -0.052 to +0.021 relative flow units/cm height up the lung, and the correlation coefficients varied from 0.12 to 0.75. A positive slope, indicating that flow increased with vertical distance up the lung (opposite to gravity), was observed in three of the four horses. In addition, blood flow was uniformly low in three of the four horses in the most cranial portions of the lungs. We conclude that in lungs of resting unanesthetized horses, animals with a large lung height, there is no consistent vertical gradient to pulmonary blood flow and there is a considerable degree of perfusion heterogeneity, indicating that gravity alone does not play the major role in determining blood flow distribution.

Minimal redistribution of pulmonary blood flow with exercise in racehorses.

We determined the spatial distribution of pulmonary blood flow at rest and during increasing levels of exercise (34, 59, and 90% of maximal oxygen consumption) in Thoroughbred racehorses (n = 4) using 15-microns fluorescent microspheres. After the horses were killed, the lungs were flushed free of blood, removed, air-dried at total lung capacity, and sliced into isogravitational planes, which were sampled in a systematic fashion for three-dimensional reconstruction. The fluorescence was measured for quantification of blood flow. Mean pulmonary blood flow heterogeneity (expressed as a coefficient of variation) did not change with increasing exercise levels [36.2 +/- 16.4 (rest) to 26.9 +/- 6.8% (gallop); P = not significant]. Greater than 70% of pulmonary blood flow variation across rest to high-exercise states is determined by a fixed spatial pattern. Thirty percent of the variation in pulmonary blood flow seen in horses over rest and exercising states is due to redistribution. The majority of flow redistribution was due to flow increasing to the dorsal region of the lung during exercise at 90% of maximal oxygen consumption (a flow gradient of 0.20 ml. min-1.cm-1 up the lung; P = 0.04).

Blood viscosity in chronically hypoxic rats: an effect independent of packed cell volume.

We compared apparent blood viscosity, measured with a cone-plate viscometer, in normoxic and chronically hypoxic rats. All comparisons were made at equal packed cell volume (PCV) and shear rate conditions. Apparent viscosity of whole blood from the hypoxic rats was significantly lower than that from normoxic littermates and was similar to that of young rats. Apparent viscosity of red cells from hypoxic rats suspended in phosphate buffered saline remained lower than that from the normoxic rats. When blood cells from the hypoxic rats were suspended in plasma from normoxic rats, apparent viscosity was lower than when blood cells from normoxic animals were suspended in plasma from hypoxic rats. The lower viscosity of the blood from hypoxic rats appears to be associated with characteristics present in newly generated red cells. The reduced apparent viscosity of blood in hypoxic rats may partially compensate for the increase in PCV, at least during the early stages of hypoxia.