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Biomedical subjects

D R Hodgson

Publications and source records attributed to D R Hodgson.

At least 145 records · Page 8Linked to original sources
PubMed1993

A survey of neurological diseases in horses.

Case records of 450 horses with signs of neurological disease are reviewed. One hundred and nineteen horses with neurological disease due to trauma were examined, of which 60 were due to spinal cord trauma, 47 to brain or cranial nerve trauma and 12 to peripheral nerve trauma. Cervical vertebral fractures/trauma were the most common injury. Basisphenoid/basioccipital bone fractures were the most common form of cranial trauma and facial nerve paralysis the most common cranial nerve injury. Eighty-nine horses with neurological disease due to malformation were examined. Cervical vertebral malformation occurred in 83 horses and congenital defects in 6 foals. Neurological disease due to inflammation or infection occurred in 30 horses. The most common disease of this type was meningitis, which occurred in 11 horses and foals. Neoplasms in the CNS caused neurological disease in 8 horses. The final category was miscellaneous neurological disease, which was diagnosed in 204 horses. Diseases in this category included neonatal (28 cases), toxic/metabolic (27 cases), idiopathic (133 cases), degenerative (3 cases) and other neurological diseases (13 cases). The most common condition was idiopathic laryngeal hemiplegia (116 cases). Where possible, diagnosis relied on a thorough neurological examination with use of ancillary tests in selected cases including rhinolaryngoscopy, radiography, myelography, ophthalmoscopy and cerebrospinal fluid analysis when indicated. In many cases necropsy and histopathological confirmation or diagnosis was necessary.

Age Factors↗
PubMed1993

Effects of sodium bicarbonate on cardiorespiratory measurements and exercise capacity in thoroughbred horses.

We examined the effects of sodium bicarbonate in 6 Thoroughbred horses during submaximal and maximal treadmill exercise. Cardiorespiratory function was assessed together with the effect on exercise capacity by determining the run time to fatigue at maximal intensities. To discriminate between sodium bicarbonate's alkalinising effects and the fluid shifts that could result from the high osmotic load, we administered an equimolar solution of sodium chloride as a control. The horses were given sodium bicarbonate (1 g/kg bwt) or an equivalent number of moles of sodium chloride by nasogastric tube. Arterial blood samples were collected before exercise and 5 h after treatment, resulting in mean standard bicarbonate values of 39.6 mmol/l in horses treated with sodium bicarbonate compared with 24.2 mmol/l in horses that received saline. The horses were exercised on a treadmill at 40, 60 and 80% of their VO2max for 4, 2 and 2 mins respectively. The horses were walked for 3 mins and accelerated rapidly to a speed approximately equivalent to 110% VO2max and run until fatigued. The horses ran for 170 +/- 20 secs (mean +/- sem) after administration of sodium bicarbonate compared with 128 +/- 13 secs after receiving sodium chloride (P < 0.02). At rest and throughout submaximal and maximal exercise, the bicarbonate-treated horses had significantly lower arterial oxygen tensions and higher arterial carbon dioxide tensions. There were no differences in cardiac output, heart rate, oxygen uptake or carbon dioxide production between the saline and bicarbonate treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Dissipation of metabolic heat in the horse during exercise.

Horses were exercised at 40, 65, and 90% of their maximum O2 uptake (VO2max) until moderately fatigued (approximately 38, 15, and 9 min, respectively) to assess heat loss through different routes. Approximately 4,232, 3,195, and 2,333 kcal of heat were generated in response to exercise at these intensities. Of this, approximately 7, 16, and 20% remained as stored heat 30 min postexercise. Respiratory heat loss, estimated from the temperature difference between blood in the pulmonary and carotid arteries and the cardiac output, was estimated to be 30, 19, and 23% of the heat produced during exercise at the three intensities. The kinetics of the increases in muscle and blood temperature were similar, with the greatest change in temperature occurring in muscle (+3.8, 5.2, and 6.1 degrees C after exercise at 40, 65, and 90% of VO2max, respectively). The temperature of blood in the superficial thoracic vein was approximately 2 degrees C below that of arterial blood at rest. This difference had increased to approximately 3 degrees C during the last minute of exercise. The rate of sweating at sites on the back and neck increased with exercise intensity to a common peak of approximately 40 ml.m-2.min-1. If complete evaporation had occurred, water loss in response to exercise (estimated to be 12, 10, and 7.7 liters for the different intensities of exercise) greatly surpassed that required for dissipation of the metabolic heat load.

Animals↗
PubMed1993

Equine plasma and blood volumes decrease with dehydration but subsequently increase with exercise.

The effects of dehydration and 40 min of exercise at approximately 40% of maximal O2 consumption on plasma volume (PV) and blood volume (BV) were studied in six horses. Horses were exercised while euhydrated (C); 4 h after administration of furosemide (1.0 mg/kg i.v.; FDH), which induced isotonic dehydration; and after 30 h without water (DDH), which caused hypertonic dehydration. Dehydration resulted in decreases of 6.3 and 9.9% for PV and BV, respectively, with FDH and 10.7 and 8.5%, respectively, with DDH. During exercise in C, PV and BV increased by 12.7 and 20.0%, respectively; during exercise with FDH, they increased by 11.7 and 26.1%, respectively; and during exercise with DDH, PV decreased by 1.3% from predehydration values, while BV increased by 18.7%. Hematocrit and total plasma protein concentration rose to higher values throughout exercise in FDH and DDH than in C; plasma [Na+] was higher in DDH than in FDH and C, [Cl-] was higher in DDH and lower in FDH than in C, and [K+] was lower in FDH and DDH than in C through exercise and recovery. From these results, we conclude that increases in PV and BV are normal features of low-intensity exercise in the horse. The increases in BV not only augment O2 carriage but also help maintain circulating volume. These increases can be modified by preexercise dehydration, the nature of which affects the extent of modification.

Animals↗
PubMed1993

Effects of dehydration on thermoregulatory responses of horses during low-intensity exercise.

Effects of dehydration on thermoregulatory and metabolic responses were studied in six horses during 40 min of exercise eliciting approximately 40% of maximal O2 consumption and for 30 min after exercise. Horses were exercised while euhydrated (C), 4 h after administration of furosemide (FDH; 1.0 mg/kg i.v.) to induce isotonic dehydration, and after 30 h without water (DDH) to induce hypertonic dehydration. Cardiac output was significantly lower in FDH (144.1 +/- 8.0 l/min) and in DDH (156.6 +/- 6.9 l/min) than in C (173.1 +/- 6.2 l/min) after 30 min of exercise. When DDH, FDH, and C values were compared, dehydration resulted in higher temperatures in the middle gluteal muscle (41.9 +/- 0.3, 41.1 +/- 0.2, and 40.6 +/- 0.2 degrees C, respectively) and pulmonary artery (40.8 +/- 0.3, 40.1 +/- 0.2, and 39.7 +/- 0.2 degrees C, respectively). Temperatures in the superficial thoracic vein and subcutaneous sites on the neck and back and peak sweating rates on the neck and back were not significantly different in DDH and C. In view of higher core temperatures during exercise after dehydration and decrease in cardiac output without concomitant increases in peripheral temperatures or reduced sweating rates, we conclude that the impairment of thermoregulation was primarily due to decreased transfer of heat from core to periphery.

Animals↗
PubMed1993

The effect of roughage source on exercise performance and metabolism in thoroughbred horses.

The effects of roughage source on metabolism and exercise capacity were investigated using 6, previously conditioned, mature thoroughbred horses in a cross-over experiment. The horses were assigned to either non-alfalfa or alfalfa roughage diets which were isocaloric. The diets were fed for 2 weeks, after which the horses were exercise tested and then fed the alternate diet. Horses were exercised on a high-speed treadmill using a rapid incremental test. Arterial blood samples were collected for blood gas analysis and acid base measurements and venous blood samples for lactate and red blood cell potassium analysis. Mixed expired gas samples were collected for measurement of oxygen uptake, carbon dioxide production and respiratory exchange ratio. Heart rate was measured by telemetry ECG and respiratory frequency by observation. When the 2 diets were compared there were no significant differences in treadmill exercise capacity nor in any of the metabolic or cardiorespiratory measurements made before, during or after the exercise period. We concluded that roughage source has no effect on cardiorespiratory and metabolic function during or after exercise, and does not affect endurance performance during a treadmill exercise test.

Animal Nutritional Physiological Phenomena↗
PubMed1992

Ultrastructural changes in skeletal muscle after fatiguing exercise.

Thoroughbred horses were exercised to fatigue at 40, 85, and 100% of their maximal oxygen consumption (VO2max) on a treadmill and completed a 1,600-m gallop on a track to identify the effect of exercise of various durations and intensities on the ultrastructure of mitochondria and sarcoplasmic reticulum (SR) from the middle gluteal muscle. The percentage of the total area occupied by mitochondria and SR increased in electron micrographs of muscle samples collected at the termination of exercise and at 30 and 60 min of recovery compared with those collected before exercise. Mitochondrial area increased 3- to 4-fold and SR area approximately 1.6-fold after exercise at the intensities greater than 40% of the VO2max. Smaller increases occurred in response to exercise at 40% of the VO2max. Areas were not different from rest in samples collected after 60 min of recovery. The reversal of ultrastructural alterations paralleled the trend toward normalization of muscle temperature, muscle pH, and the concentrations of selected muscle metabolites.

Animals↗
PubMed1992

Effects of transport on constituents of bronchoalveolar lavage fluid from horses.

To determine whether road transport affected pulmonary phagocyte activity, 7 healthy Thoroughbred horses were shipped 1,160 kilometers over 36 hours. Fluid collected by bronchoalveolar lavage (BAL) 12 hours, and 7 and 14 days after transport was analyzed. Results were compared to those from the same horses pre-transport, and 7 non-transported control horses that had BAL performed at the same times as the transported horses. Of cells recovered with BAL the percentage of viable pulmonary alveolar macrophages (PAMs) declined from 90.0 +/- 0.9% pre-transport to 80.0 +/- 3.7% by 2 weeks post transport. Although the ability of PAMs to inhibit the growth of Staphylococcus epidermidis had decreased by 2 weeks post-transport (19.2 +/- 3.7% vs. 8.8 +/- 2.3% inhibition) this could not be attributed to transport as a similar effect occurred in the control group. In contrast, the ability of PAMs to phagocytose sheep erythrocytes labelled with rabbit anti-erythrocyte antibodies increased from 74.0 +/- 8.1% to 92.3 +/- 1.5% by 12 hours post-transport. As all variables were unchanged or only mildly altered following transport, we conclude that this form of transport did not alter the PAM functions we assessed.

Albumins↗
PubMed1990

Respiratory and metabolic responses in the horse during moderate and heavy exercise.

Thoroughbred horses were exercised to fatigue on a treadmill at 62% and 100% of their VO2max. Hypoxemia occurred at the onset of exercise under both exercise conditions. This hypoxemia persisted to fatigue during the heavy exercise but progressively diminished as the exercise continued and had disappeared by the end of exercise at the lighter load. As a result of the hypoxemia the oxygen content of arterial blood during exercise at VO2max was 17% below its carrying capacity. However, under both experimental conditions the CaO2 still exceeded that of rest owing to an elevation in hemoglobin concentration. The temperature of blood at the point of fatigue was similar, 41.0 +/- 0.2 degrees C and 41.1 +/- 0.2 degrees C, for exercise at 62% and 100% VO2max, respectively. Muscle samples collected at rest and at the termination of exercise did not demonstrate major differences between the exercise conditions except for a higher [lactate] and lower pH following the heavy exercise. From these results it can be suggested that the combined effects of an elevated body temperature, changes in muscle pH, and oxygen delivery may all be factors contributing to limit exercise capacity in the horse.

Adenosine Triphosphate↗
PubMed1990

The effect of high-intensity exercise on the respiratory capacity of skeletal muscle.

The effect of high-intensity exercise on the respiratory capacity of skeletal muscle was studied in horses which ran five 600-m bouts on a track with 2 min of rest between exercise bouts, or once to fatigue on a treadmill at an intensity that elicited the maximal oxygen uptake. Venous blood and biopsy samples of the middle gluteal muscle were collected at rest, after each exercise bout, and 30 and 60 min post-exercise. Blood samples were analyzed for lactate concentration and pH and muscle samples for metabolites, pH, and respiratory capacity. Venous blood and muscle pH declined to 6.91 +/- 0.02 and 6.57 +/- 0.02, respectively, after the fifth track run and to 6.98 +/- 0.02 and 6.71 +/- 0.07, respectively, after treadmill running. Muscle metabolite changes were consistent with the metabolic response to high-intensity exercise. Muscle respiratory capacity declined greater than 20% (P less than 0.05) after a single exercise bout and was 45% of the control value after the fifth track run. Tissue respiration was depressed 60 min post-exercise but was normal 24 h later. These observations suggest that high-intensity exercise impairs the respiratory capacity of the working muscle. Although this occurred in parallel with reductions in pH, other factors could be responsible for this response.

Animals↗
PubMed1990

Kinetics of VO2 and VCO2 in the horse and comparison of five methods for determination of maximum oxygen uptake.

To determine whether maximum oxygen uptake (VO2max) in the horse in influenced by type of exercise test, five different protocols were evaluated in eight untrained Thoroughbreds exercised on a treadmill. With all protocols, horses were given a 5 min warm-up on a 10 per cent treadmill slope. Three protocols were at a 10 per cent slope and included: 1) increasing the running speed by 1 to 2 m/sec every 60 secs from 4 m/sec to a maximum of 12 m/sec; 2) running at 12 m/sec until fatigue; and 3) running for 3 to 4 mins at speeds ranging from 6 to 12 m/sec with rest pauses between exercise bouts. The fourth protocol employed a 24 per cent slope where animals exercised for 5 mins at 2 m/sec followed by 3 mins at 5 m/sec, and 2 mins at 6 m/sec. The fifth test involved running at 11 m/sec while the slope of the surface was increased every 2 mins until the horses could not maintain the pace. A plateau in VO2 occurred in all protocols except when exercise was performed on a 24 per cent slope. Slow speed exercise at a steep grade (24 per cent) produced the highest VO2 (P < 0.05) even though there was no plateau in the VO2. A steady state for VO2 and VCO2 existed 90 secs after the onset of exercise with all protocols which involved 2 mins or more at each speed. The VO2 and VCO2 values at all speeds of the rapid incremental exercise test were not different to those found at steady state in the third exercise protocol.

Animals↗
PubMed1990

Effects of acetazolamide on metabolic and respiratory responses to exercise at maximal O2 uptake.

Changes in blood gases, ions, lactate, pH, hemoglobin, blood temperature, total body metabolism, and muscle metabolites were measured before and during exercise (except muscle), at fatigue, and during recovery in normal and acetazolamide-treated horses to test the hypothesis that an acetazolamide-induced acidosis would compromise the metabolism of the horse exercising at maximal O2 uptake. Acetazolamide-treated horses had a 13-mmol/l base deficit at rest, higher arterial Po2 at rest and during exercise, higher arterial and mixed venous Pco2 during exercise, and a 48-s reduction in run time. Arterial pH was lower during exercise but not in recovery after acetazolamide. Blood temperature responses were unaffected by acetazolamide administration. O2 uptake was similar during exercise and recovery after acetazolamide treatment, whereas CO2 production was lower during exercise. Muscle [glycogen] and pH were lower at rest, whereas heart rate, muscle pH and [lactate], and plasma [lactate] and [K+] were lower and plasma [Cl-] higher following exercise after acetazolamide treatment. These data demonstrate that acetazolamide treatment aggravates the CO2 retention and acidosis occurring in the horse during heavy exercise. This could negatively affect muscle metabolism and exercise capacity.

Acetazolamide↗
PubMed1989

Exercise-induced hypercapnia in the horse.

The effects of exercise intensity and duration on blood gases in thoroughbred horses were studied to characterize the apparent exercise-induced failure in pulmonary gas exchange that occurs in these animals. In response to 2 min of exercise, arterial CO2 tension (PaCO2) decreased in mild and moderate exercise, returned to normocapnic levels in moderate to heavy exercise, and rose 5-10 Torr above resting values during very heavy exercise when CO2 production (VCO2) exceeded 20 times the resting value, and mixed venous CO2 tension approximated 140 Torr. Exercise-induced hypoxemia occurred at the onset of heavy exercise and was associated with the absence of a hyperventilatory response and an alveolar-arterial PO2 difference that increased four to six times above rest with very heavy exercise. PaCO2 was related to VCO2 but not fb, as changes in breathing frequency (fb) of 8-20 breaths/min at comparable VCO2 did not affect PaCO2. Prolonging very heavy exercise from 2 to 4 min caused a severe metabolic acidosis (arterial pH less than 7.15) and hypoxemia was maintained; however, CO2 was no longer retained, as PaCO2 gradually fell to below resting levels, due to an increased tidal volume at constant fb. We conclude that a truly compensatory hyperventilation to very heavy exercise in the horse is not achieved because of the excessive volumes and flow rates required by their extraordinarily high VCO2 and VO2. On the other hand, the frank CO2 retention during short-term high-intensity exercise occurs even though the horse is not apparently mechanically obligated to tolerate it.

Analysis of Variance↗