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H H Erickson

Publications and source records attributed to H H Erickson.

At least 37 records · Page 2Linked to original sources
PubMed1998

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.

Animals↗
PubMed1997

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.

Animals↗
PubMed1997

Exercise-induced changes in the lung of Shetland ponies: ultrastructure and morphometry.

The ultrastructural changes in pulmonary alveoli produced by running two ponies on a high speed treadmill at 7.6 m/sec, 3-degree incline, for 2 min support the hypothesis of pulmonary capillary stress failure as an explanation for exercise-induced pulmonary hemorrhage (EIPH). Light microscopy combined with scanning and transmission electron microscopy confirmed the presence of red blood cells and proteinaceous material in the alveolar lumina and interstitial swelling in approximately one third of the pulmonary alveoli examined. Morphometric analysis revealed that the blood-gas barrier was 30-77% thicker on the thin respiratory surface of the interalveolar septa in the cranial lobe of the two exercised ponies, i.e., 0.62 and 0.46 micron, compared to that of the unexercised control pony (0.35 micron). No change in blood-gas barrier thickness was observed in the caudal lobe, although that is where EIPH lesions have been observed in race-horses. Vascular pressures were low (20 mm Hg) in the pulmonary circulation of the Shetland pony at rest but increased more than three fold to 63 mm Hg during exercise. These preliminary morphological and physiological results indicate that a short burst of near-maximal exercise in a non-athletic equine can lead to structural changes in the blood-gas barrier and leakage of blood from pulmonary capillaries despite pulmonary vascular pressures being significantly lower than previously found in the racehorse.

Animals↗
PubMed1996

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.

Animals↗
PubMed1996

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).

Animals↗
PubMed1994

Mechanisms of exercise-induced pulmonary hemorrhage in the equine athlete.

This article discusses exercise-induced pulmonary hemorrhage (EIPH), a pathophysiological syndrome which occurs worldwide in the equine athlete. It reviews the history of EIPH, the incidence in performance horses, the etiology, studies performed on the treadmill to determine the mechanisms of EIPH, and the most likely causes of stress failure of the pulmonary capillaries.

Animals↗
PubMed1992

Pulmonary artery and aortic pressure changes during high intensity treadmill exercise in the horse: effect of frusemide and phentolamine.

Intravenous frusemide (1.0 mg/kg bwt) or phentolamine (0.33 mg/kg bwt) was given to 7 horses 1 h before exercise and their effects on pulmonary artery and aortic pressure changes during strenuous exercise were examined. Short-term near-maximal treadmill exercise (10 m/sec, 3 degrees incline) produced increases in heart rate, mean pulmonary artery pressure (PAP), mean aortic pressure (AP), and packed cell volume (PCV). Frusemide did not affect heart rate, PAP or PCV during exercise. Frusemide significantly decreased mean AP by 10 to 15 mmHg during exercise. Phentolamine produced an increase in heart rate relative to control only early in exercise but not during later, more strenuous, exercise. Phentolamine had no statistically significant effect on AP, PAP, or PCV, but a significant reduction was observed between 180 and 230 sec of exercise when PAP and AP were standardised against heart rate. Frusemide did not prevent horses from haemorrhaging during exercise in this study. Treatment with phentolamine did not sufficiently reduce the PAP and AP to test our hypothesis that a reduction in PAP and AP would eliminate EIPH.

Animals↗
PubMed1992

Inhibition of equine mononuclear cell proliferation and leukotriene B4 synthesis by a specific 5-lipoxygenase inhibitor, A-63162.

The lipoxygenase metabolites of arachidonic acid have an important role in lymphocyte activation. We used a specific 5-lipoxygenase inhibitor, A-63162, to examine the role of 5-lipoxygenase (5-LO) in equine blood mononuclear cell (BMC) proliferation and leukotriene B4 (LTB4) synthesis after stimulation with mitogen (phytohemagglutinin, PHA) or calcium ionophore (A23187). The A-63162 inhibited PHA-induced equine BMC proliferation and, at the same concentration, also inhibited A23187-induced LTB4 synthesis. The presence of exogenous interleukin 2 (IL-2) or the cyclooxygenase inhibitor indomethacin, failed to reverse the immunosuppression caused by A-63162. Further, we found that A-63162, at the concentration that inhibited BMC proliferation and LTB4 synthesis, had no effect on BMC viability. The addition of the specific protein kinase C inhibitor, H-7, did not inhibit A23187-induced LTB4 synthesis. Results indicate that 5-lipoxygenase metabolites may have an important role in equine lymphocyte activation and that protein kinase C has no role in regulating LTB4 production after A23187 stimulation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Influence of cyclooxygenase inhibitors on furosemide-induced hemodynamic effects during exercise in horses.

Furosemide, which commonly is used as a prophylactic treatment for exercise-induced pulmonary hemorrhage in horses, may mediate hemodynamic changes during exercise by altering prostaglandin metabolism. To determine if furosemide's hemodynamic effects during exercise in horses could be reversed, cyclooxygenase inhibitors were administered with furosemide. Four treatments were administered 4 hours prior to treadmill exercise at 9 and 13 m/s. They included a control treatment (10 ml of 0.9% NaCl solution, IV), furosemide (1 mg/kg of body weight, IV) administered alone, and furosemide in combination with phenylbutazone (4 mg/kg, IV, q 12 h for 2 days) or with flunixin meglumine (1.1 mg/kg, IV, on the day of experiment). Five horses were randomly assigned to complete all treatments. Physiologic variables at rest prior to exercise were not influenced by treatments. Furosemide, administered alone, reduced mean right atrial pressure and mean pulmonary artery pressure during exercise. The combinations of furosemide and flunixin meglumine or furosemide and phenylbutazone, at both levels of exercise intensity, returned mean right atrial pressure and mean pulmonary artery pressure to the value of the control treatment. During rest and exercise, plasma lactate concentration, PCV, heart rate, mean carotid artery pressure, oxygen consumption, carbon dioxide elimination, and cardiac output were not altered by any of the treatments. At 5 minutes after exercise, the administration of furosemide, alone or with phenylbutazone, reduced mean right atrial pressure. Other measured variables were not significantly influenced by treatments during recovery from exercise. These results suggested that cyclooxygenase inhibition partially reverses the decrease in mean right atrial pressure or pulmonary artery pressure induced by furosemide during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Influence of furosemide on hemodynamic responses during exercise in horses.

Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only RAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.

Animals↗
PubMed1990

Pulmonary artery, aortic and oesophageal pressure changes during high intensity treadmill exercise in the horse: a possible relation to exercise-induced pulmonary haemorrhage.

This study investigated changes in packed cell volume (PCV), pulmonary artery and aortic pressures, and the interaction between oesophageal pressure and pulmonary artery and aortic pressures during strenuous exercise in the horse. It was hypothesised that oesophageal pressure changes summate with pulmonary artery and aortic pressures during exercise and contribute to exercise-induced pulmonary haemorrhage (EIPH). Acute treadmill exercise (10 m/sec, 3 degrees incline) produced increases in heart rate (HR) from 50 to 202 beats/min; mean pulmonary artery pressure (PAP) from 28 to 80 mmHg; mean aortic pressure (AP) from 108 to 157 mmHg; and PCV from 0.35 to 0.52 litres/litre. EIPH was observed in three of seven horses after treadmill exercise, but no differences in the above variables were observed between the two groups of horses. Electronic subtraction of the oesophageal pressure signal from PAP and AP signals indicated peak transmural pressures of approximately 150 mmHg pulmonary and 175 mmHg aortic pressure. The elevated PAP associated with exercise appeared related more to increased HR and less to PCV (blood viscosity) or AP (bronchial). Both pulmonary artery and aortic peak transmural vascular pressures were substantially influenced by oesophageal pressure changes; peak and mean pulmonary artery and aortic pressures were significantly higher than resting pressures, and may conceivably contribute to EIPH.

Animals↗
PubMed1990

Effects of treadmill elevation on heart rate, blood lactate concentration and packed cell volume during graded submaximal exercise in ponies.

Six ponies performed a standardised exercise test on a motorised treadmill at each of three randomly assigned treadmill elevations (1, 4, or 7 degrees). The exercise test consisted of four, 4 min increments of increasing treadmill speed from 1.0 to 3.4 m/sec. Heart rate, blood lactate concentration, and packed cell volume (PCV) were determined, during the last min of each exercise level, and at 4 and 12 mins post exercise. Regardless of treadmill elevation, no differences were observed in pre-exercise heart rate (49 +/- 2) beats/min), lactate (1.2 +/- 0.1 mM), and PCV (0.32 +/- 0.01 litres. During exercise, heart rate and PCV were highly correlated to treadmill speed and elevation. Peak exercise heart rates (determined at 3.4 m/sec) were 159 +/- 10, 182 +/- 5, and 216 +/- 6 beats/min at 1, 4, and 7 degrees, respectively, while peak PCVs were 0.37 +/- 0.01, 0.40 +/- 0.01 and 0.42 +/- 0.02 lit/litre at 1, 4, and 7 degrees, respectively. Blood lactate did not change significantly from pre-exercise levels during the exercise test at a treadmill elevation equal to 1 degree, but increased markedly at 4 and 7 degrees. Peak lactates were 1.9 +/- 0.7, 5.3 +/- 1.0, and 18.1 +/- 1.5 mM at 1, 4, and 7 degrees, respectively. There was a highly significant correlation between heart rate and lactate at all treadmill speeds and elevations. Therefore, during graded, submaximal exercise increasing treadmill elevation up to 7 degrees results in increases in heart rate, blood lactate concentration and PCV comparable to those seen with increasing treadmill speed alone.

Aging↗
PubMed1989

Changes in circulating equine erythrocytes induced by brief, high-speed exercise.

Five horses were exercised at 10m/sec at a 3 degree incline for 2 mins. Packed cell volume, erythrocyte count, haemoglobin concentration, mean corpuscular volume, plasma protein, total white cell count and lymphocytes increased significantly in blood samples taken after exercise, compared with those taken before exercise; but mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration decreased. Erythrocytes were more resistant to osmotic stress after exercise, but their shape and degree of deformity were unaffected by exercise.

Animals↗
PubMed1989

Mechanism of exercise-induced hypoxemia in horses.

Arterial hypoxemia has been reported in horses during heavy exercise, but its mechanism has not been determined. With the use of the multiple inert gas elimination technique, we studied five horses, each on two separate occasions, to determine the physiological basis of the hypoxemia that developed during horizontal treadmill exercise at speeds of 4, 10, 12, and 13-14 m/s. Mean, blood temperature-corrected, arterial PO2 fell from 89.4 Torr at rest to 80.7 and 72.1 Torr at 12 and 13-14 m/s, respectively, whereas corresponding PaCO2 values were 40.3, 40.3, and 39.2 Torr. Alveolar-arterial PO2 differences (AaDO2) thus increased from 11.4 Torr at rest to 24.9 and 30.7 Torr at 12 and 13-14 m/s. In 8 of the 10 studies there was no change in ventilation-perfusion (VA/Q) relationships with exercise (despite bronchoscopic evidence of airway bleeding in 3) and total shunt was always less than 1% of the cardiac output. Below 10 m/s, the AaDO2 was due only to VA/Q mismatch, but at higher speeds, diffusion limitation of O2 uptake was increasingly evident, accounting for 76% of the AaDO2 at 13-14 m/s. Most of the exercise-induced hypoxemia is thus the result of diffusion limitation with a smaller contribution from VA/Q inequality and essentially none from shunting.

Animals↗
PubMed1986

Effects of propranolol on cardiopulmonary function in the pony during submaximal exercise.

Cardiopulmonary responses of four ponies were monitored during standard exercise tests (SET), before and after beta-adrenergic receptor blockade with propranolol. The SET consisted of four 5 min increments of increasing speed from 1.0 to 2.8 m/sec on a treadmill at a 7 degrees incline. Data were collected at rest, throughout the SET and recovery. Administration of propranolol to ponies at rest had no effect on cardiopulmonary function. During the SET, increases in heart rate, mean pulmonary artery flow velocity (an index of cardiac output) and right ventricular dP/dt (an index of myocardial contractility) were progressively attenuated as running speed increased. Body temperature and mean pulmonary artery and right ventricular pressures were significantly elevated over normal. Propranolol treatment had no effect on the responses of mean arterial pressure, haematocrit, haemoglobin, blood lactate and arterial blood gases and pH to the SET. These results suggest that in the pony there is no sympathetic activity to the heart at rest and that during exercise there is pulmonary vasodilation mediated by beta-adrenergic receptors.

Animals↗
PubMed1984

Pain perception and alleviation in animals.

In the last 2 decades there have been substantial advances in our knowledge of the scientific basis of the mechanisms of pain. Nociceptors or pain receptors are widespread in the skin and tissues of animals; chemical mediation of nociceptor excitation may provide a key for understanding the peripheral phenomena related to pain. The expression of pain in animals involves multiple ascending and descending branches, as well as specialized pain-signaling mechanisms in the spinal cord. The importance of these different pathways varies with species and circumstances. Endogenous neural systems in the brain stem and forebrain including both opioid and nonopioid mechanisms may modulate the central transmission of nociceptive signals in animals. Noxious stimuli mediate a variety of different functions; each animal has a consistent response to noxious stimuli or a consistent pattern of escape from pain. As we better understand the mechanisms of pain, the humane treatment and alleviation of pain in experimental animals can be placed on a much firmer scientific basis.

Afferent Pathways↗
PubMed1984

Effect of exercise on oxygen consumption, heart rate, and the electrocardiogram of pigs.

Pigs were exercised for 5 min at five different treadmill speeds (1.0-1.8 m X s-1) (3 degrees incline), while oxygen consumption (MO2), carbon dioxide production (MCO2), and the electrocardiogram (ECG) were recorded continuously. Data were taken at rest, during exercise, and at 2, 5, 15, and 30 min after exercise. Values for MO2, MCO2, and heart rate (HR) showed progressive increases with increasing treadmill speed. The respiratory exchange ratio (R) increased during exercise and approached 1.0, but peak values were seen shortly after exercise. Heart rate, MO2, MCO2, and R reached steady-state values after 2 min of exercise, which were maintained for the duration of exercise. In most cases, these variables had returned to control levels 15 min after exercise. A high correlation between HR and MO2 was found in these animals. Prominent increases in T-wave amplitude of the ECG were associated with exercise and early recovery. The metabolic and cardiac changes associated with exercise in these animals were all qualitatively similar to responses seen in exercising humans. Thus, this study further supports the belief that the pig is a good model for studying the cardiopulmonary responses to exercise in humans.

Animals↗