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Background: Hypoxaemia is a common concern during equine general anaesthesia. The prevalence and predictors of hypoxaemia in horses undergoing elective anaesthesia in particular are poorly documented., Objectives: To determine and compare the prevalence of hypoxaemia (defined as PaO 2  ≤ 80 mm Hg, on the lowest value recorded) in horses undergoing anaesthesia for exploratory laparotomy and elective procedures, and to identify risk factors in both subpopulations., Study Design: Retrospective cohort study., Methods: Data were collected from 774 records of 708 horses undergoing general anaesthesia between April 2017 and August 2020. Potential predictors of hypoxaemia in horses undergoing anaesthesia for exploratory laparotomy or elective procedures were investigated separately by univariable penalised maximum likelihood logistic regression, followed by multivariable analysis. The lowest recorded PaO 2 was used as a single data point for the determination of hypoxaemia and arterial oxygen partial pressure to fractional inspired oxygen ratio analysis., Results: Hypoxaemia was recorded in 23% horses undergoing exploratory laparotomy compared with 3.8% horses undergoing elective anaesthesia (P < .001). Multivariable analysis showed that weight above 550 kg, large intestinal lesions, and peak inspiratory pressure (PIP) above 30 cmH 2 O were significantly associated with hypoxaemia in horses undergoing exploratory laparotomy. Soft tissue procedures and PIP >30 cmH 2 O were significantly associated with hypoxaemia during elective anaesthesia., Main Limitations: This study only considered the minimum PaO 2 recorded during anaesthesia. Duration and treatment of hypoxaemia were not considered., Conclusions: Based on the lowest PaO 2 value during anaesthesia, in our population, horses undergoing anaesthesia for exploratory laparotomy were over six times more likely to become hypoxaemic than horses undergoing elective procedures. Bodyweight, type of procedure, and high PIP were predictors of hypoxaemia., (© 2021 EVJ Ltd.)

Background: It remains unknown how single-shot anesthesia influences physical parameters, especially respiratory function and blood oxygen level of common marmosets (Callithrix jacchus) which came to be used for laboratory research., Methods: We measured blood oxygen levels, both before and after oxygenation, in 13 common marmosets under two single-shot anesthesia conditions: ketamine/xylazine/atropine and alphaxalone., Results and Conclusions: We found that SpO 2 values decreased to about 80% in the ketamine/xylazine/atropine protocol and fell just below 90% in the alphaxalone protocol. We observed a clear decrease in PaO 2 values under the anesthetized condition compared to the awake condition. Our data indicate that single-shot anesthesia may cause hypoxemia in marmosets. Previous studies on other non-human primate have reported no SpO 2 decrease and hypoxemia; thus, our experiment suggests that marmosets may have a more fragile respiratory system and require intensive veterinary care during anesthesia., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Inadequate dissolved oxygen in the aquatic environment is a well-established cause of fish morbidity and mortality. The specific effects of hypoxia on immune function in fish, however, are not well characterized. In this study, the effects of acute hypoxia followed by reoxygenation (rapid tissue reperfusion) as a source of immunocompromise in Nile tilapia Oreochromis niloticus were investigated. Using a precision apparatus developed in our laboratory for hypoxia exposures, a series of assays of increasing specificity for immune function were performed on acutely hypoxia-stressed Nile tilapia: tier I consisted of histopathology, tier II of hematology, plasma chemistry, and determining cortisol concentration, and tier III of determining the phagocytic index and analyzing the expression of the cytokines transforming growth factor-beta (TGF-beta) and interleukin-1beta (IL-1beta). Nile tilapia were exposed to 7% oxygen saturation for 96 h, then tank water was rapidly reoxygenated. Sampling intervals were 48 and 96 h during hypoxia and 12 and 84 h during reperfusion. Histopathology showed no remarkable microscopic abnormalities in lymphoid or other tissues. Lymphopenia and neutrophilia were observed in peripheral blood. Plasma total protein, partial pressure of oxygen, and oxygen saturation were decreased in response to hypoxia. Plasma lipase decreased in response to hypoxia but returned to normal during reperfusion. Phagocytic capability and the phagocytic index decreased during hypoxia and 12 h reperfusion, whereas these values were recovered by 84 h reperfusion. The TGF-beta transcription continued to increase during the exposures, the greatest production being at 12 h reperfusion, whereas IL-1beta transcription decreased in response to hypoxia and reperfusion. We conclude that acute hypoxia triggered an overall downregulation of the immune system in the test fish. This suggests a possible factor in the pathogenesis of disease outbreaks in fish in which repeated, sublethal bouts of environmentally induced hypoxia lead to increased disease susceptibility and individual mortalities rather than massive fish kills.

Pulmonary hypertension is a well-recognised condition in dogs, and, among other mechanisms, is caused by hypoxia. In order to evaluate the effect of chronic hypobaric hypoxia on pulmonary arterial pressure in dogs, a colony of 19 clinically and biochemically healthy Greenland sled dogs living permanently at at least 2300 m above sea level (altitude dogs) and 10 clinically healthy Greenland sled dogs living at 700 to 900 m above sea level (control dogs) were examined. Investigations were made of the dogs' packed-cell volume, venous and arterial blood gases, electrocardiogram, blood pressure and echocardiograph, including the calculation of pulmonary arterial pressure by Doppler examination of tricuspid regurgitation. The altitude dogs had a marked arterial hypoxaemia with a mean (sd) oxygen partial pressure of 61.9 (7.4) mmHg and a significantly lower arterial oxygen saturation (90.7 [3.7] per cent) than the control dogs (96.7 [0.8] per cent). In eight of the altitude dogs, tricuspid regurgitation allowed calculation of the systolic pulmonary arterial pressure, which was 29.5 (10.4) mmHg. Eight of the control dogs had tricuspid insufficiency, and their derived systolic pulmonary arterial pressure was significantly lower (17.4 [3.9] mmHg).

The second day of a 3-day event is the most physically demanding of the 3 days. If this is performed under hot and humid environmental conditions, detrimental effects on cardiovascular and thermoregulatory function and, therefore, on exercise capacity, may occur due to exercise-induced dehydration. We hypothesised that the administration of fluid equivalent to 6% of the horse's bodyweight prior to a simulated second day of a 3-day event would increase plasma volume and limit increases in core temperature. Seven Standardbred geldings underwent a training protocol prior to the study. A standardised exercise test was developed for each horse so that exercise intensity at each phase would be the same percentage of the maximal heart rate for all horses. The exercise test involved 4 phases: Phase A involved 30 min exercise at 3.7 m/s (approximately 25% VO2max); Phase B 4 min exercise at 8 m/s (approximately 60% VO2max); and Phase C 50 min at 3.7 m/s, after which there was a 10 min rest. Phase D involved 14 min at 7.3 m/s (55% VO2max). In a cross-over design, horses were grouped randomly and allocated to either exercise with no fluid (control) or approximately 26 l isotonic fluid by nasogastric tube, 120 min prior to exercise. Arterial and mixed venous blood samples were collected prior to exercise, towards the end of each of the phases and during the rest period. The administration of fluid prior to exercise resulted in a pre-exercise bodyweight gain of 21.3 +/- 1.2 kg. Hyperhydration resulted in a greater degree of arterial hypoxaemia than the control group in Phases B and D, but not in Phases A and C or at rest. During Phases B and D, mean PaO2 values in the horses that received fluid were about 15 torr lower than in the control group, but there were no differences in PaCO2 values between the 2 groups. In both arterial and mixed venous blood, pH and HCO3- were significantly lower in the group that were hyperhydrated. We concluded that the most likely cause of the more severe arterial hypoxaemia in the hyperhydrated group during the intense exercise phase was some degree of pulmonary oedema, from the extravasation of the administered fluid. Hyperhydration prior to exercise may be detrimental to respiratory function and therefore care must be taken in administration of large volumes of fluid prior to exercise.

Elevated concentrations of endothelin (ET), a potent endothelium-derived vasoactive peptide, have been reported in a number of pathophysiological conditions associated with pulmonary hypertension, both in the horse and other species. We have previously shown, both in vitro and in vivo, that the pulmonary and systemic vascular response to exogenous ET is mediated predominantly via ET(A) receptors. Our hypothesis in the present study was that ET is involved in the equine hypoxic pulmonary vasoconstrictive response to acute hypoxia. In this study, we investigated the effects of a selective ET(A) receptor antagonist on hypoxic pulmonary hypertension in the mature horse. Horses were exposed to a 10 min period of hypoxia (F(I)O2 approximately 0.11) on 2 occasions, with and without pretreatment with the selective ET(A) receptor antagonist TBC11251 (10 mg/kg bwt i.v.). Hypoxia increased mean pulmonary artery pressure (PAP) from 18.3+/-0.9 (mean +/- s.e. normoxia) to 28.0+/-0.8 mmHg (hypoxia) in the session without ET(A) receptor antagonism. Carotid arterial pressure (CAP) also increased progressively throughout the period of hypoxic challenge and at the end was 153+/-5 mmHg (hypoxia) compared to during normoxia (140+/-5 mmHg). There was no significant overall effect of ET(A) receptor antagonism on the haemodynamic or ventilatory responses to acute hypoxia. However, between 5 and 10 min of hypoxia there was a trend for the mean PAP to diverge in the 2 treatments, which just failed to reach significance at 10 min of hypoxia (P = 0.053). In conclusion, this study describes the haemodynamic and ventilatory changes in response to a period of acute hypoxia in the adult horse. The results do not support a role for ET as a mediator of acute HPV in the horse, but suggest that it may be involved as a modulator or in the slower (>10 min) phase of HPV.

This study examined the ability of near infrared spectroscopy (NIRS) to noninvasively determine changes to muscle oxygenation in the resting horse. Five horses had (NIRS) performed over extremity muscle while under general anaesthesia, first with 8 min limb ischaemia, then systemic hypoxaemia for 5 min. A second group of 6 awake horses had NIRS performed over extremity muscle while being administered hypoxic gas (F(I)O2 0.10) for 5 min, and after return to steady state, limb ischaemia was induced for an additional 5 min. In the anaesthetised horses' ischaemia induced marked and significant muscle deoxygenation of haemoglobin/myoglobin (P<0.01), with corresponding arterial saturation decreasing from 98.9 to 81.9%. Hypoxaemia induced small yet significant muscle deoxygenation (P<0.01) that was 3.2% of the ischaemia deoxygenation signal, with a corresponding decrease in arterial saturation from 98.6 to 90.4%. In the awake horses muscle deoxygenation was not detectable during hypoxia despite reduction of arterial saturation from 97.8 to 86.8%, whereas ischaemia induced rapid and significant deoxygenation of muscle (P<0.05), with corresponding reduction of venous saturation from 78.4 to 75.4%. In neither group of horses was there evidence of cytochrome aa3 reduction, despite complete ischaemia for up to 8 min. NIRS changes in the resting horse muscle clearly differed between ischaemia and hypoxaemia, and can readily show muscle deoxygenation in clinically relevant hypoxaemia in the horse under anaesthesia. Further, as the deoxygenation signal induced by ischaemia was clearly detectable above a background movement artefact, NIRS application to study of muscle oxygenation in the working horse should be explored.

Three-hundred adult horses, referred from 1990 to 1993 inclusively, for pulmonary examination were assessed using standardised history taking and clinical, intrapleural pressure, arterial blood gases and pH, bronchoscopic and tracheal and broncho-alveolar lavage fluid (BALF) cytological examinations. Two-hundred and thirty-five cases were referred with overt signs of pulmonary disease and the remaining 65 cases were referred for pulmonary examination because of reduced exercise (usually racing) performance or prolonged dyspnoea after racing. No pulmonary disease was detected in 30 cases. The 270 horses with pulmonary disease included 148 cases (54.8%) of chronic obstructive pulmonary disease (COPD), 45 (16.7%) of infectious or post infectious pulmonary disease, 7 (2.6%) of Streptococcus zooepidemicus pulmonary infection, 7 (2.6%) of lungworm infection, 16 (5.9%) of primary exercise induced pulmonary haemorrhage (EIPH), 9 (3.3%) of chronic idiopathic hypoxaemia, 20 (7.4%) of miscellaneous identified pulmonary disorders and 18 (6.7%) of undifferentiated pulmonary disorders. Two cases of primary summer associated obstructive pulmonary disease (SPAOPD) were observed, but 9.5% of COPD affected horses additionally suffered from SPAOPD.

One-hundred and forty-seven of 270 (54.4%) horses suffering from pulmonary disorders were given at least one re-examination including, clinical, bronchoscopic, pulmonary function and cytological examinations after treatment and a further 83 of these horses (30.7%) had their clinical progress assessed by verbal or written reports. These examinations and progress reports showed high levels of partial or total recovery for most pulmonary disease categories, including chronic obstructive pulmonary disease, infectious, S. zooepidemicus and undifferentiated pulmonary disease and lungworm infection groups but not for the miscellaneous pulmonary disease (40% of these cases died), idiopathic chronic hypoxaemic or exercise induced pulmonary haemorrhage groups.

Examination of historical and clinical details of 270 adult horses suffering from a variety of mainly chronic pulmonary diseases showed that the chronic obstructive pulmonary disease (COPD) group (median age 9 years) were the oldest, and that the COPD, chronic idiopathic hypoxaemia and exercise induced pulmonary haemorrhage (EIPH) groups had the longest duration of disease (median durations 7, 12 and 9 months, respectively) with a median disease duration of 2 months for the remaining horses. A history of antecedent respiratory infection was present in 24.3% of all horses. Six out of 12 horses that grazed with donkeys suffered lungworm infection. Silage was fed to 11.3% of all horses, nonstraw beddings were utilised by 28.7% of horses and 8.7% of horses were maintained permanently outdoors. Environmental control had been unsuccessfully attempted in 47% of COPD cases prior to referral. Histories of poor athletic performance or of excessive post exercise dyspnoea were found to be less definitive indicators of pulmonary disease. Coughing was the most sensitive clinical indicator of pulmonary disease, being present in 71.1% of horses with pulmonary disorders. Nasal discharge was present in 50.4% of these horses and coughing or nasal discharge was present in 86.7% of horses with respiratory disorders. Unilateral nasal discharge was inexplicably present in 3.3% of horses with pulmonary disease. Other clinical findings, including the presence of increased breathing effort, abnormal thoracic or tracheal auscultatory findings were less sensitive diagnostic parameters with pulmonary diseases, and were frequently absent unless severe pulmonary disease was present.

Exercise in normal human subjects causes deterioration of matching of ventilation to blood flow in the lungs, but only in about 50% of those examined. A previous study (Wagner et al. 1989) of 5 horses showed no significant worsening of ventilation/blood flow (VA/Q) relationships during heavy exercise as determined by multiple inert gas elimination technique (MIGET). Because of the small number of horses in that study and the 50% human incidence of exercise induced VA/Q mismatch, we studied an additional 6 Thoroughbreds, comparing VA/Q relationships at the walk (1.4 m/s, 0 degrees incline) and during galloping (9.6 +/- 0.3 m/s, 7% incline). Such data were collected under 4 different conditions wherein inspired gas was 1) air, 2) 21% O2 in helium, 3) 15% O2 in N2 and 4) 15% O2 in helium. Each horse exercised 4 times (morning and afternoon of 2 days, with inspired gas conditions randomised). There was a small but significant increase in VA/Q mismatch (similar under all 4 conditions). The second moment of the VA/Q distribution (determined by the MIGET) increased significantly (P < 0.01) from 0.31 +/- 0.01 at the walk to 0.38 +/- 0.02 during gallop. This increase however is small: 0.38 is well within the range of this parameter for normal human subjects (where the 95% upper confidence limit is 0.60). This study shows that a small amount of exercise induced VA/Q mismatch can occur in the horse as in man, but the mechanism remains to be elucidated and its clinical significance remains to be established.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxaemia commonly develops during general anaesthesia and in the recovery period in horses. The Hudson demand valve has been used to increase arterial PO2, but it has been found to increase airway resistance considerably when used during spontaneous ventilation. This paper evaluates a modification of the valve designed to reduce this resistance. The effects of the valve and its modification on arterial oxygen (PaO2), and carbon dioxide (PaCO2) tensions were evaluated in four ponies anaesthetised by a total intravenous technique. The valve increased PaO2 from 8.3 +/- 1.1 to 32.7 +/- 7.6 kPa during spontaneous ventilation and to 44.2 +/- 7.4 kPa during intermittent positive pressure ventilation. With the modification, the PaCO2 was increased to 9.0 +/- 2.5 kPa during spontaneous ventilation PaO2 was unchanged by the valve (7.2 +/- 0.4 kPa to 7.1 +/- 0.7 kPa) but it was reduced to 6.4 +/- 0.9 kPa with the modification. The valve was also evaluated in 20 clinical cases during their recovery from halothane anaesthesia. It increased PaO2 from 7.4 +/- 2.1 kPa to 17 +/- 18.3 kPa during spontaneous ventilation and from 8.0 +/- 1.8 kPa to 23.4 +/- 22.2 kPa during positive pressure ventilation. With the modification, PaO2 was increased from 7.8 +/- 1.4 kPa to 10.4 +/- 3.8 kPa during spontaneous ventilation and from 7.6 +/- 1.5 kPa to 14.8 +/- 8.4 kPa during positive pressure ventilation. During spontaneous ventilation PaCO2 was increased from 5.9 +/- 0.4 kPa to 6.2 +/- 0.6 kPa with the unmodified valve and from 6.3 +/- 0.5 kPa to 6.6 +/- 0.5 kPa with the modification.(ABSTRACT TRUNCATED AT 250 WORDS)

Turkey hens were stunned by inducing anoxia with either argon (with approximately 2 per cent residual oxygen) or 30 per cent carbon dioxide in argon with 2 per cent residual oxygen, and the carcases were bled either immediately or five or 10 minutes after they had been stunned. A control group of turkeys was stunned electrically (250 mA for about four seconds) and had their necks cut immediately after stunning. The amount of blood lost was measured and expressed as a percentage of liveweight. The results showed that the necks of gas-stunned turkeys can be cut up to 10 minutes after they have been stunned without reducing the total blood loss significantly.

The pharmacokinetics of amikacin, administered iv at 7 mg/kg, every 8 h, were evaluated over the first 48 h of hospitalisation in 7 critically ill hypoxic premature foals and compared with those in 8 full-term nonhypoxic critically ill neonatal foals. The pharmacokinetic data were used to calculate dosage schedules that would maintain the plasma amikacin concentrations in individual foals within a target range of > or = 15 micrograms/ml but < 30 micrograms/ml for peak values and < or = 3 micrograms/ml for trough values. The results indicated a statistically significant increase in the amikacin serum half-life (5.39 +/- 3.46 h) and smaller elimination rate constant (0.17 +/- 0.09 h-1) in premature foals. The pharmacokinetic derangements required increasing the dose to 8.5-10.5 mg/kg bwt in 6 of 7 premature foals and an increase in the dosage interval to 12-24 h in all 7 foals. Overall, the total dosage of amikacin was decreased in the hypoxic, premature foals so that target peaks and troughs could be maintained. Our findings suggest that prematurity and hypoxia are variables related to a prolonged serum half-life of amikacin in hypoxic, premature foals. Although there was no evidence of amikacin-induced nephrotoxicity in any of these foals, daily monitoring and tailoring of the dose schedule to the individual foal are strongly advised.

The effects of hypoxia and azotaemia on the pharmacokinetics of amikacin were evaluated in 20 full-term neonatal critically ill foals which required 24-h supportive care, antibiotics and dextrose-supplemented polyionic fluids given intravenously, nasal insufflation with oxygen and nutritional supplementation. There was no association between sepsis score or survival and pharmacokinetic parameters. Concurrent hypoxia and azotaemia were associated with significantly decreased clearance and increased peak and trough serum concentrations of amikacin; however, peaks or troughs did not exceed toxic values. Derangements in serum peak, trough and clearance values, which were present on admission, persisted over the 6-day duration of this study. Daily monitoring of serum amikacin concentration revealed a tendency to underdose (particularly in foals receiving aggressive fluid therapy), which necessitated increasing the dose/kg body weight (9-12 mg/kg) and increasing the dose interval (10-12 h) in 40% (8/20) of the cases, so that blood concentrations of amikacin could be maintained within the target range of 3-15 micrograms/ml. Amikacin-induced nephrotoxicity was not indicated by conventional laboratory testing, nor was it strongly suspected after examination of post mortem lesions.

The effects of removal from water and death by anoxia on brain function and reflex movement were examined in conscious trout. Visual evoked responses (VERS) were measured in fish with a body temperature of 20 degrees C, 14 degrees C and 2 degrees C. On average the fish took 2.6 minutes at 20 degrees C, 3.0 minutes at 14 degrees C and 9.6 minutes at 2 degrees C to lose VERS, and 11.5, 27.7 and 197.6 minutes, respectively, to lose all movement. VERS were absent from fish anaesthetised with MS222. From a humanitarian standpoint these results indicate that fish killed by anoxia could be exposed to periods of distress or suffering, and that cooling them in ice prolongs this period.

The birth and fate of 818 lambs born to 571 ewes on a low-ground farm in the Scottish Borders with a history of substantial perinatal mortality were monitored with a range of physiological, biochemical and pathological measurements. In lambs which survived, the rectal temperature, birthweight and plasma concentrations of fructose, insulin, thyroxine and the third component of complement at birth, and the weight at four months of age, decreased with litter size. One hundred and thirty-seven lambs were stillborn or died within four days and seven others died later. The mothers of 77 per cent of these lambs had low condition scores, but the lamb deaths did not correlate significantly with the condition scores. From data relating to birthweight, temperature, packed cell volume and plasma composition it was deduced that placental insufficiency was involved in 24 per cent of these deaths; acute hypoxaemia at birth accounted for 35 per cent, inadequate thermogenesis for 12 per cent and starvation for 13 per cent. The remaining 16 per cent of dead lambs could not be assigned to any of these categories. Using only clinicopathological criteria, 37 per cent of the lamb deaths were attributed to antenatal influences which included immaturity, developmental anomalies, and degenerative or inflammatory changes. Thirty-three per cent of the deaths were due to post natal factors which included, in declining order of frequency, starvation, enteritis, misadventure, pneumonia, navel infections and septicaemia. No conclusions could be drawn from the pathological examinations alone in the remaining 30 per cent, although almost half of these had low rectal temperatures after birth, death being attributed to hypothermia.(ABSTRACT TRUNCATED AT 250 WORDS)

New developments in therapy for foals in respiratory distress are discussed. Therapy is based on preservation of the foal's life by maintenance of a patent airway, resuscitation with fluids and warmth, provision of humidified oxygen to raise the fractional concentration of inspired oxygen sufficient to avoid hypoxia and provision of ventilatory support when hypercapnia becomes critical. Ventilatory support described includes assisted and controlled ventilation, positive end expiratory pressure, continuous positive airway pressure and intermittent mandatory ventilation. The aims of these techniques are discussed together with their associated indications, disadvantages and complications. Secondary therapy includes coupage, airway hygiene, drug therapy and stress management. Knowledge of equine neonatology is limited in comparison with human neonatology. More information in basic physiology and pharmacology relating to equine neonatology is needed and the efficacy of various modes of therapy must be evaluated.

This paper reviews a series of clinical, post mortem and imaging studies on exercise-induced pulmonary haemorrhage (EIPH) performed on 26 Thoroughbred racehorses. Post mortem techniques included routine gross, subgross and histological examination; coloured latex perfusions of pulmonary and bronchial circulations; and microradiography and computerised tomography scans of lungs with contrast injected vasculature. The major lesions were multiple, separate and coalescing foci of moderately proliferative small airway disease accompanied by intense neovascularisation of the bronchial circulation. As a result of bronchial artery angiogenesis, the systemic circulation dominated the vascular supply of the air exchange structures in affected areas, producing an apparent left to right shunt. Extensive areas of sequestered haemosiderophages indicated previous haemorrhage from vessels apparently supplied by the bronchial arteries. Diffuse and focal parenchymal destruction and connective tissue reactions in affected areas were considered to be secondary to localised haemorrhage and macrophage-induced damage. The aetiology of EIPH was not determined, but the multifocal, small airway-centred lesions indicated that low grade bronchiolitis, possibly of viral origin, was a factor. Gravitational effects also appear to contribute to dorsal distribution of the lesions. The mild focal and subclinical lesions confined to secondary lobules are thought to evolve into the serious lung pathology observed in EIPH cases through the effects of localised hypoxia induced by maximal exercise and partial airway obstruction. Once initiated, a vicious cycle of increasing inflammatory damage and further local bleeding is set in motion.

The causes of hypothermia in 89 lambs were identified on the basis of history and clinical biochemistry. Excessive heat loss accounted for 24 per cent of the cases, and depressed heat production because of either severe hypoxia during birth, immaturity or starvation accounted for 72 per cent. Exhaustion of energy reserves and hypoglycaemia were marked characteristics of lambs which became hypothermic after 12 hours of age. Most of the lambs were either twins or triplets. The implications of the findings for both the treatment and prevention of hypothermia in newborn lambs are discussed.

Bacterial endotoxin injected intravenously into conscious ponies produced alterations in cardiopulmonary and gastrointestinal function. Specifically, tachypnoea, dyspnoea, hypoxaemia, colic, lactic acidosis and diarrhoea resulted from administration of 10 micrograms/kg Escherichia coli endotoxin. Pretreatment of the ponies with a potent prostaglandin synthetase inhibitor, flunixin meglumine, prevented these ill effects of endotoxin.

Developments in evaluation of newborn foals with respiratory distress are discussed. Major causes of respiratory distress are outlined and discussed in terms of the similar respiratory signs exhibited by foals with this clinical syndrome. History, physical examination, clinical pathology, chest radiography and blood gas analyses are discussed as important elements of the evaluation of the condition of these foals. Foals with respiratory disease are grouped into three major categories on the basis of clinical signs and arterial blood gas profiles. The evaluation of foals with respiratory distress is designed not only to reach an accurate diagnosis of the aetiology but also to define the foal's need for respiratory support.

The cause of arterial hypoxia during natural infection with bovine respiratory syncytial virus was studied in seven calves (three to nine months of age) originating from five herds with respiratory tract disease and serological evidence of infection with the virus. Blood gas values were measured during ambient air breathing and during 100 per cent oxygen breathing. The percentages of contribution to the arterial hypoxia from alveolar hypoventilation, mismatching of ventilation and perfusion, and right-to-left shunting were calculated from the measured parameters. Calculated percentages of total venous admixture varied from 14 per cent of cardiac output in relatively mild cases to 48 per cent in the worst affected animal. This venous admixture had been caused mainly by right-to-left shunting of blood, while mismatching of ventilation and perfusion became important in the more severely affected animals. Alveolar hypoventilation was only important in the worst affected animal.