Cardiorespiratory, endocrine and metabolic changes in ponies undergoing intravenous or inhalation anaesthesia

Six Welsh gelding ponies (weight 246 ± 6 kg) were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) followed by 0.02 mg/kg of detomidine i.v. Anaesthesia was induced with 2 mg/kg of ketamine i.v. Ponies were intubated and lay in left lateral recumbency. On one occasion anaesthesia was maintained for 2 h using 1.2% halothane in oxygen. The same group of ponies were anaesthetized 1 month later using the same induction regime and anaesthesia was maintained with a combination of detomidine, ketamine and guaiphenesin, while the ponies breathed oxygen-enriched air. Electrocardiogram, heart rate, mean arterial blood pressure, cardiac output, respiratory rate, blood gases, temperature, haematocrit, glucose, lactate and cortisol were measured and cardiac index and systemic vascular resistance were calculated in both groups. Beta-endorphin, met-enkephalin, dynorphin, arginine vasopressin (AVP), adrenocorticotrophic hormone (ACTH) and catecholamines were measured in the halothane anaesthesia group only and 11-deoxycortisol during total intravenous anaesthesia (TIVA) only. Cardiorespiratory depression was more marked during halothane anaesthesia. Hyperglycaemia developed in both groups. Lactate and AVP increased during halothane anaesthesia. Cortisol increased during halothane and decreased during TIVA. There were no changes in the other hormones during anaesthesia. Recovery was smooth in both groups. TIVA produced better cardiorespiratory performance and suppressed the endocrine stress response observed during halothane anaesthesia.     

Endocrine response to lactate infusion during pentobarbitone anaesthesia

Lactic acid was infused iv in 6 Welsh ponies during pentobarbitone anaesthesia to investigate whether lactate triggers the pituitary-adrenal response to anaesthesia. Ponies were premedicated with acepromazine and anaesthesia was induced with pentobarbitone iv and maintained with pentobarbitone/oxygen for 2 h. Immediately after induction, 3% L(+) lactic acid infusion was started and adjusted to maintain plasma lactate concentration between 2 and 2.5 mmol/l. Cardiorespiratory function, temperature. PCV, plasma glucose, lactate, βendorphin, ACTH, cortisol and catecholamine concentrations were measured before, during and after anaesthesia. Hypothermia, reduced PCV, slight hypotension (minimum value 84 ± 6 mmHg 20 min after induction of anaesthesia), hyperoxia and marked bradypnoea developed during anaesthesia. No acidaemia occurred. Plasma glucose concentration increased at the end of anaesthesia. There were no changes in plasma ACTH, cortisol and catecholamine concentrations, but plasma & endorphin increased after induction until the end of anaesthesia. There was a correlation between plasma lactate and β-endorphin concentrations (P<0.001, r=0.63), which may suggest that lactate stimulates βendorphin release. Beta-endorphin was apparently secreted independently from ACTH and appears to be a sensitive marker of a stress response.     

Midazolam and ketamine induction before halothane anaesthesia in ponies: cardiorespiratory, endocrine and metabolic changes

Six Welsh gelding ponies were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) prior to induction of anaesthesia with midazolam at 0.2 mg/kg and ketamine at 2 mg/kg i.v.. Anaesthesia was maintained for 2 h using 1.2 % halothane concentration in oxygen. Heart rate, electrocardiograph (ECG), arterial blood pressure, respiratory rate, blood gases, temperature, haematocrit, plasma arginine vasopressin (AVP), dynorphin, ß-endorphin, adrenocorticotropic hormone (ACTH), cortisol, dopamine, noradrenaline, adrenaline, glucose and lactate concentrations were measured before and after premedication, immediately after induction, every 20 min during anaesthesia, and at 20 and 120 min after disconnection. Induction was rapid, excitement-free and good muscle relaxation was observed. There were no changes in heart and respiratory rates. Decrease in temperature, hyperoxia and respiratory acidosis developed during anaes-thesia and slight hypotension was observed (minimum value 76 ± 10 mm Hg at 40 mins). No changes were observed in dynorphin, ß-endorphin, ACTH, catecholamines and glucose. Plasma cortisol concentration increased from 220 ± 17 basal to 354 ± 22 nmol/L at 120 min during anaesthesia; plasma AVP concentration increased from 3 ± 1 basal to 346 ± 64 pmol/L at 100 min during anaesthesia and plasma lactate concentration increased from 1.22 ± 0.08 basal to 1.76 ± 0.13 mmol/L at 80 min during anaesthesia. Recovery was rapid and uneventful with ponies taking 46 ± 6 min to stand. When midazolam/ketamine was compared with thiopentone or detomidine/ketamine for induction before halothane anaesthesia using an otherwise similar protocol in the same ponies, it caused slightly more respiratory depression, but less hypotension. Additionally, midazolam reduced the hormonal stress response commonly observed during halothane anaesthesia and appears to have a good potential for use in horses.     

Physiological stimuli of thirst and drinking patterns in ponies

The stimuli that elicit thirst were studied in four ponies. Nineteen hours of water deprivation produced an increase in plasma protein from 67 +/- 0.1 g/litre to 72 +/- 2 g/litre, a mean (+/- se) increase in plasma sodium from 139 +/- 3 to 145 +/- 2 mmol/litre and an increase in plasma osmolality from 297 +/- 1 to 306 +/- 2 mosmol/litre. Undeprived ponies drank 1.5 +/- 0.9 kg/30 mins; 19 h deprived ponies drank 10.2 +/- 2.5 kg/30 mins and corrected the deficits in plasma protein, plasma sodium and plasma osmolality as well as compensating for the water they would have drunk during the deprivation period. In order to determine if an increase in plasma osmolality would stimulate thirst, 250 ml of 15 per cent sodium chloride was infused intravenously. The ponies drank when osmolality increased 3 per cent and when plasma sodium rose from 136 +/- 3 mmol/litre to 143 +/- 3 mmol/litre. Ponies infused with 15 per cent sodium chloride drank 2.9 +/- 0.7 kg; those infused with 0.9 per cent sodium chloride drank 0.7 +/- 0.5 kg. In order to determine if a decrease in plasma volume would stimulate thirst, ponies were injected with 1 or 2 mg/kg bodyweight (bwt) frusemide. Plasma protein rose from 68 +/- 2 g/litre pre-injection to 75 +/- 2 g/litre 1 h after 1 mg/kg bwt frusemide and to 81 +/- 1 g/litre 1 h after 2 mg/kg bwt frusemide.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiopulmonary effects of romifidine and detomidine used as premedicants for ketamine/halothane anaesthesia in ponies

The cardiopulmonary effects of romifidine at 80 microg/kg (R80) or 120 pg/kg (R120), and detomidine at 20 pg/kg (D20) when used as premedicants for ketamine/halothane anaesthesia were investigated in six ponies. Using a blinded crossover design, acepromazine (0-04 mg/kg) was administered followed by the alpha-2 agonist. Anaesthesia was induced with ketamine at 2.2 mg/kg and maintained with halothane (expired concentration 1.0 per cent) in oxygen for three hours. During anaesthesia, arterial blood pressure, cardiac index, PaO2 and PmvO2 decreased, and systemic vascular resistance and PaCO2 increased. The cardiac indices for R80, R120 and D20 were, respectively, 39, 39 and 32 ml/kg/minute at 30 minutes and 29, 29 and 26 ml/kg/minute at 180 minutes. The alpha-2 agonists had similar cardiovascular effects, but PaO2 was significantly lower with R120. The quality of anaesthesia was similar in all three groups.     

Effects of etomidate on adrenocortical function in canine surgical patients

Adrenocortical function in canine surgical patients given etomidate at 1 of 2 dosages (1.5 mg/kg of body weight or 3 mg/kg, IV) was evaluated and compared with that of dogs given thiopental (12 mg/kg, IV). The adrenocortical function was evaluated by use of adrenocorticotropic hormone (ACTH) stimulation tests and determination of plasma cortisol concentrations at 0 minute (base line) and 60 minutes after ACTH administration. At 24 hours before administration of either drug (ie, induction of anesthesia), each dog had an increase in plasma cortisol concentration when given ACTH. The ACTH stimulation tests were repeated 2 hours after induction of anesthesia. Dogs given thiopental had base-line plasma cortisol concentrations greater than preinduction base-line values, but did not increase plasma cortisol in response to ACTH stimulation. Postinduction ACTH stimulation tests in dogs given etomidate at either dose indicated base-line and 60-minute plasma cortisol concentrations that were not different from preinduction base-line values. Therefore, adrenocortical function was suppressed 2 and 3 hours after the administration of etomidate in canine surgical patients.     

Adrenocortical and metabolic responses to dobutamine infusion during halothane anaesthesia in ponies

The study investigated whether hypotension in halothane-anaesthetised ponies is the stimulus inducing an endocrine stress response by assessing the effect of maintenance of normotension with a dobutamine infusion. Groups of six ponies were studied. After premedication with acepromazine (0.04 mg/kg) anaesthesia was induced with thiopentone (10 mg/kg) and maintained for 120 min with halothane (group AN). Dobutamine was infused to effect (1.1–4.4 μg/kg/min) to maintain arterial pressure at pre anaesthetic levels. The conscious group (CON) were prepared as for AN and then received only dobutamine infusion 1.0 μg/kg/min for 120 min. Arterial blood pressure, pH, oxygen and carbon dioxide tension, pulse rate, haematocrit, and plasma cortisol, glucose and lactate concentrations were measured before, at 20 min intervals during anaesthesia, and 20 and 120 min after anaesthesia ceased. Blood pressure remained close to control in both groups. The AN group became hypercapnic and acidotic, pulse rate and haematocrit increased, cortisol increased more than twofold and plasma glucose and lactate did not change. All values remained at control in the CON group except for small increases in haematocrit and decreases in pulse rate. Maintenance of normotension during halothane anaesthesia did not blunt the adrenocortical response to anaesthesia nor did the same dose of dobutamine alone increase plasma cortisol. Hypotension appears not to be the sole stimulus to equine adrenocortical activity during halothane anaesthesia.     

Total intravenous anaesthesia in the horse with propofol

The use of propofol, solubilised in a non-ionic emulsifying agent, for the induction and maintenance of anaesthesia in experimental ponies was assessed. Pilot studies revealed that premedication with xylazine (0.5 mg/kg bodyweight [bwt]) intravenously (iv) followed by propofol (2.0 mg/kg bwt) iv provided a satisfactory smooth induction. Two infusion rates (0.15 mg/kg bwt/min and 0.2 mg/kg bwt/min) were compared for maintenance of anaesthesia. An infusion rate of 0.2 mg/kg/min produced adequate anaesthesia in these ponies. Cardiovascular changes included a decrease in arterial pressure and cardiac output during maintenance. Respiratory depression was manifested by a decrease in rate and an increase in arterial carbon dioxide tension. Recovery after 1 h anaesthesia was rapid and smooth. In conclusion, induction and maintenance of anaesthesia with propofol in premedicated ponies proved a satisfactory technique.     

Doxapram infusion during halothane anaesthesia in ponies

Doxapram, 0.05 mg/kg bodyweight/min, was infused during the second hour of 2 h halothane anaesthesia in six ponies. Two of the ponies were anaesthetised on a second occasion as controls and given 5 per cent dextrose in place of the doxapram. Respiratory depression typical of halothane anaesthesia in ponies developed in the first hour of anaesthesia and continued during the second hour in the control animals. During doxapram infusion arterial carbon dioxide tension decreased and pH increased. Arterial blood pressure increased but there was no change in pulse rate, the electrocardiogram or arterial oxygen tension. Anaesthesia lightened during doxapram infusion necessitating an increase in the vapouriser setting in order to prevent arousal. Recovery from anaesthesia appeared unaffected by the doxapram infusion.     

Effects of naloxone on endotoxin-induced changes in ponies

The value of naloxone (1 mg/kg of body weight/hr for 4 hrs), a beta-endorphin antagonist, was assessed in the management of endotoxin-induced shock in ponies. Three groups of 5 ponies each were used: controls, ponies given Escherichia coli endotoxin put untreated, and ponies given endotoxin and then treated with naloxone. Endotoxin-induced changes in hemodynamics, blood chemical values, regional blood flow, plasma enzymes, and energy supplies were measured at selected times during the first 6 hours after endotoxin was given. There was no evidence that beta-endorphins released during shock were responsible for the hemodynamic changes, blood flow changes, plasma enzyme changes, or energy deficits, because naloxone, at this dosage level, did not prevent these endotoxin-induced changes.     

Endocrine and metabolic responses to plasma volume expansion during halothane anaesthesia in ponies

The study was designed to contribute to identification of the stimulus to adrenocortical activity during halothane anaesthesia in equidae . Two groups of six ponies were premedicated with acepromazine before induction of anaesthesia with thiopentone and maintenance for 120 min with halothane in oxygen. In group H Haemaccel® modified gelatine plasma replacer was infused (48 ± 13 mL/kg) to maintain mean arterial blood pressure (MABP) close to preanaesthetic values. In group DH, blood pressure was maintained close to preanaesthetic levels with a lower dose of Haemaccel® (10 mL/kg) combined with an infusion of dobutamine. Measurements were made before anaesthesia, at 20 min intervals during anaesthesia and 20 and 120 min after anaesthesia. MABP and blood gases, pulse and respiratory rates were measured, and blood was withdrawn for assay of cortisol, adrenocorticotrophic hormone (ACTH), glucose and lactate. Ponies in both groups became hyperoxic, hypercapnic and developed a respiratory acidosis; pulse rate increased in both groups but this was more marked in group H. Haematocrit decreased by 50% in H and by 20% in DH. Cortisol and ACTH did not change significantly during anaesthesia in either group and the area under the time curve ( AUC _(0–140)) was lower in the DH group. Plasma glucose and lactate remained stable. After the H treatment all ponies had a watery nasal discharge and one pony died from endotoxaemia. This investigation demonstrated that the adrenocortical response to halothane anaesthesia in ponies can be ameliorated by manipulation of ABP using plasma expansion with or without inotrope infusion; however, low dose Haemaccel® with dobutamine was safer and more practical. It is suggested that, although hypotension is not the sole stimulus to adrenocortical activity during halothane anaesthesia, it may contribute, probably through an effect on tissue perfusion.     

Effects of single intravenous doses of dexamethasone on baseline plasma cortisol concentrations and responses to synthetic ACTH in healthy dogs

The duration of adrenocortical suppression resulting from a single IV dose of dexamethasone or dexamethasone sodium phosphate was determined in dogs. At 0800 hours, 5 groups of dogs (n = 4/group) were treated with 0.01 or 0.1 mg of either agent/kg of body weight or saline solution (controls). Plasma cortisol concentrations were significantly (P less than 0.01) depressed in dogs given either dose of dexamethasone or dexamethasone sodium phosphate by posttreatment hour (PTH) 2 and concentrations remained suppressed for at least 16 hours. However, by PTH 24, plasma cortisol concentrations in all dogs, except those given 0.1 mg of dexamethasone/kg, returned to control values. Adrenocortical suppression was evident in dogs given 0.1 mg of dexamethasone/kg for up to 32 hours. The effect of dexamethasone pretreatment on the adrenocortical response to ACTH was studied in the same dogs 2 weeks later. Two groups of dogs (n = 10/group) were tested with 1 microgram of synthetic ACTH/kg given at 1000 hours or 1400 hours. One week later, half of the dogs in each group were given 0.01 mg of dexamethasone/kg at 0600 hours, whereas the remaining dogs were given 0.1 mg of dexamethasone/kg. The ACTH response test was then repeated so that the interval between dexamethasone treatment and ACTH injection was 4 hours (ACTH given at 1000 hours) or 8 hours (ACTH given at 1400 hours). Base-line plasma cortisol concentrations were reduced in all dogs given dexamethasone 4 or 8 hours previously.(ABSTRACT TRUNCATED AT 250 WORDS)     

Feline plasma cortisol (hydrocortisone) measured by radioimmunoassay.

Plasma cortisol (hydrocortisone) was measured by radioimmunoassay in 6 normal cats. Blood was collected from the cats by venipuncture at intervals of 3 hours for 3 days. Resting plasma cortisol concentrations averaged 17.0 +/- 2.8 (SD) ng/ml and ranged from nondetectable (less than 3 ng/ml) to 82.8 ng/ml. Of 144 plasma samples, 95% contained less than 40 ng of cortisol/ml. Circadian rhythm of cortisol secretion was not detected, suggesting that adrenal function tests may be started in feline patients at any time of day. Intramuscular injection of 2.2 U of ACTH gel/kg of body weight caused detectable increase in plasma cortisol concentrations at 1 and 2 hours after injection. Maximal response to ACTH in the 6 cats ranged from 41.6 to 178.4 ng/ml. Oral administration of 0.1 mg of dexamethasone/kg suppressed plasma cortisol to nondetectable concentrations for 32 hours in 5 of the 6 cats.     

Plasma cortisol response to ketoconazole administration in dogs with hyperadrenocorticism

The effect of orally administered ketoconazole on plasma cortisol concentration in dogs with hyperadrenocorticism was evaluated. Every 30 minutes from 0800 hours through 1600 hours and again at 1800 hours, 2000 hours, and 0800 hours the following morning, 15 clinically normal dogs and 49 dogs with hyperadrenocorticism had plasma samples obtained and analyzed for cortisol concentration. The mean (+/- SD) plasma cortisol concentration for the initial 8-hour testing period was highest in 18 dogs with adrenocortical tumor (5.3 +/- 1.6 micrograms/dl), lowest in 15 control dogs (1.3 +/- 0.5 micrograms/dl), and intermediate in 31 dogs with pituitary-dependent hyperadrenocorticism (PDH; 3.4 +/- 1.2 micrograms/dl). Results in each of the 2 groups of dogs with hyperadrenocorticism were significantly (P less than 0.05) different from results in control dogs, but not from each other. The same cortisol secretory experiment was performed, using 8 dogs with hyperadrenocorticism (5 with PDH; 3 with adrenocortical tumor) before and after administration at 0800 hours of 15 mg of ketoconazole/kg of body weight. Significant (P less than 0.05) decrease in the 8-hour mean plasma cortisol concentration (0.9 +/- 0.2 microgram/dl) was observed, with return to baseline plasma cortisol concentration 24 hours later. Twenty dogs with hyperadrenocorticism (11 with PDH, 9 with adrenocortical tumor) were treated with ketoconazole at a dosage of 15 mg/kg given every 12 hours for a half month to 12 months. The disease in 2 dogs with PDH failed to respond to treatment, but 18 dogs had complete resolution of clinical signs of hyperadrenocorticism and significant (P less than 0.05) reduction in plasma cortisol responsiveness to exogenous adrenocorticotropin (ACTH).(ABSTRACT TRUNCATED AT 250 WORDS)     

Stress responses during total intravenous anaesthesia in ponies with detomidine - guaiphenesin - ketamine

Six ponies were anaesthetised for two hours with intermittent injections of a combination of guaiphenesin (72 mg/kg/hr), ketamine (1.4 mg/kg/hr) and detomidine (0.015 mg/kg/hr) after premedication with detomidine 0.01 mg/kg and induction of anaesthesia with guaiphenesin 50 mg/kg and ketamine 2 mg/kg. Induction of anaesthesia was smooth, the ponies were easily intubated and after intubation breathed 100% oxygen spontaneously. During anaesthesia mean pulse rate ranged between 31–44 beats per minute and mean respiratory rate between 12–23 breaths per minute. Mean arterial blood pressure remained between 110–130 mm Hg, mean arterial carbon dioxide tension between 6.1–6.9 kPa and pH between 737–7.42. Arterial oxygen tension was over 23 kPa throughout anaesthesia. Plasma glucose increased to more than 25 mmol per litre during anaesthesia; there was no change in lactate or ACTH concentration and plasma cortisol concentration decreased. Recovery was rapid and smooth. A guaiphenesin, ketamine and detomidine combination appeared to offer potential as a total intravenous technique for maintenance of anaesthesia in horses.     

Effects of glucose infusion on the endocrine, metabolic and cardiorespiratory responses to halothane anaesthesia of ponies.

Glucose was infused intravenously into six ponies during halothane anaesthesia, to evaluate its effect on their endocrine response to anaesthesia. The ponies were premedicated with acepromazine, and anaesthesia was induced with thiopentone and maintained with halothane in oxygen for two hours. Glucose was infused to maintain the plasma glucose concentration above 20 mmol/litre. Anaesthesia was associated with hypothermia, a decrease in haematocrit, hypotension, hyperoxaemia, respiratory acidosis and an increase in the plasma concentrations of lactate and arginine vasopressin. The concentration of beta-endorphin in plasma increased transiently after 20 minutes but there were no changes in concentrations of adrenocorticotrophic hormone, dynorphin, cortisol or catecholamines. These data suggest that the glucose infusion attenuated the normal adrenal response of ponies to halothane anaesthesia.     

Effects of phenylbutazone and anabolic steroids on adrenal and thyroid gland function tests in healthy horses

Adrenal and/or thyroid gland function tests were evaluated in horses at various times during short-term therapy with phenylbutazone, stanozolol, and boldenone undecylenate. There were no significant treatment or time effects on mean basal plasma cortisol concentrations in horses during treatment with the following: phenylbutazone, given twice daily (4 to 5 mg/kg, IV) for 5 days; stanozolol, given twice weekly (0.55 mg/kg, IM) for 12 days; boldenone undecylenate, given twice weekly (1.1 mg/kg, IM) for 12 days; or nothing. There was no significant effect of phenylbutazone treatment on the changes in plasma cortisol concentration during the combined dexamethasone-suppression adrenocorticotropic hormone (ACTH)-stimulation test. Plasma cortisol concentration was significantly decreased from base line at 3 hours after dexamethasone administration and was significantly increased from base line at 2 hours after ACTH in all horses (P less than 0.05). Likewise, the stimulation of basal plasma cortisol concentrations at 2 hours after administration of ACTH (P less than 0.05) was not affected by treatment with stanozolol or boldenone undecylenate. There were no significant treatment effects on mean basal plasma concentrations of thyroxine (T4) or triiodothyronine (T3) among horses during the following treatments: stanozolol, given twice weekly (0.55 mg/kg, IM) for 12 days; boldenone undecylenate, given twice weekly (1.1 mg/kg, IM) for 12 days; or nothing. There was a significant time effect on overall mean basal plasma T4 and T3 concentrations (P less than 0.05): plasma T4 was lower on day 8 than on days 1, 10, and 12; plasma T3 was higher on day 8 than on days 4 and 12.(ABSTRACT TRUNCATED AT 250 WORDS)     

Attenuation by an opioid agonist of the oestradiol-induced LH surge in anoestrous ewes and its reversal by naloxone

The effects of a potent opioid peptide agonist [D-ala2-Phe4, Met(0)ol5-enkephalin (FK 33-824) on the magnitude of the oestradiol-induced LH surge and on basal plasma LH concentrations were examined in intact and chronically-ovariectomized ewes during the late-anoestrous period. In intact ewes, treatment with FK 33-824 (0.5 mg i.v. every 3 hr) for a 24 hr period commencing at the time of oestradiol-17 beta administration (25 micrograms i.m. bolus) was associated with non-significant 65% reduction in the peak plasma LH level observed and a significant (P less than 0.05) 58% reduction in the total amount of LH released during the surge (calculated from the area under the curve). Concurrent treatment with the opioid antagonist naloxone (10 mg i.v. every 3 hr) partially reversed this suppressive effect on the magnitude of the LH-surge. In ovariectomized ewes no significant effects on the oestradiol-induced LH surge of either FK 38-824 alone or FK 33-824 in combination with naloxone were observed. Administration of FK 33-824 at a 6-fold higher dose rate (0.5 mg every 30 min) failed to modify basal plasma LH concentration in intact ewes. In ovariectomized ewes, however, a significant (P less than 0.05) 25% fall in basal plasma LH was observed, an effect which was completely reversed by combined treatment with naloxone (10 mg every 30 min). These results support the conclusion that endogenous opioid peptides may contribute to the neuroendocrine mechanism through which oestradiol promotes a preovulatory-like surge in the anoestrous ewe.     

Plasma levels of cortisol, progesterone, oestradiol-17 beta and prostaglandin F2 alpha metabolite after ACTH (Synacthen Depot) administration in ovariectomized gilts

In order to elucidate the effect of stress on reproductive hormones, the present study was designed to investigate the effect of adrenocorticotropic hormone (ACTH) on the plasma levels of cortisol, progesterone, oestradiol-17 beta and prostaglandin F2 alpha metabolite in ovariectomized gilts. Ovariectomy and cannulation of the jugular vein were performed within 1 week of oestrous detection, under general anaesthesia. Approximately 1 week after surgery, two gilts were each administered ACTH (Synacthen Depot) intravenously, at a dose of 0.01 mg/kg body weight, and one gilt was given saline solution (5 ml). The reverse was performed on the following day. The administration of ACTH was followed by a concomitant elevation of cortisol, progesterone and prostaglandin F2 alpha metabolite but not of oestradiol-17 beta. Peak cortisol, progesterone and prostaglandin F2 alpha metabolite levels were reached at 80 +/- 10.0, 80 +/- 10.0 and 46.6 +/- 13.3 min after ACTH administration and the durations of the peaks were 181.8 +/- 19.8, 308.1 +/- 49.7 and 181.8 +/- 7.9 min, respectively. The total area under the curve for cortisol, progesterone and prostaglandin F2 alpha metabolite was significantly higher in the ACTH than in the control group. The present results indicate that during stress, cortisol, progesterone and prostaglandin F2 alpha levels are elevated while the level of oestradiol-17 beta is less affected. It can be concluded that the administration of ACTH to ovariectomized gilts, results in the elevation of cortisol, progesterone and prostaglandin F2 alpha metabolite but not of oestradiol-17 beta.     

Effects of endotoxin on lung water, hemodynamics, and gas exchange in anesthetized ponies

Effects of endotoxemia on lung water, hemodynamics, and gas exchange were determined in ponies breathing a mixture of halothane and 100% O2. Escherichia coli endotoxin was infused IV at 20 micrograms/kg of body weight for 1 hour followed by 10 micrograms/kg/hr the subsequent 4 hours. By 0.25 hour, endotoxin increased mean pulmonary artery pressure and pulmonary vascular resistance; this was followed by a return to base-line values by 0.5 and 1 hour, respectively. A 2nd increase in pulmonary vascular resistance occurred by 5 hours of endotoxemia. During the last 2 hours of endotoxin infusion, cardiac index was significantly (P less than 0.05) decreased. Hematocrit was increased from 1 to 5 hours of endotoxemia, whereas, the plasma protein concentration was increased from 2 to 4 hours, indicating a loss of plasma volume. The PaO2 and PaCO2 were unchanged. After 5 hours of endotoxemia, lung extravascular thermal volume, postmortem bronchoalveolar lavage albumin content, and extravascular lung water/extravascular dry weight ratio of bloodless lungs were not increased, indicating no increase in alveolar-capillary permeability or pulmonary edema.