Biomedical subjects

W W Muir

Publications and source records attributed to W W Muir.

At least 73 records · Page 4Linked to original sources

PubMed1995

Effect of hypertonic saline solution on left ventricular afterload in normovolumic dogs.

The effects of hypertonic saline solution (HSS) and hyperosmotic dextrose (HD; 2,400 mosm/L, 4 ml/kg of body weight) on left ventricular afterload were determined in normovolumic, chloralose-anesthetized, autonomically blocked dogs (n = 8). Solutions were infused IV over 3 minutes. Left ventricular afterload was assessed by use of a dual-tipped micromanometer catheter with an electromagnetic fluid-velocity sensor located in the ascending aorta, and the impedance spectrum was calculated after Fourier analysis of signal-averaged aortic pressure and flow signals. Hypertonic saline solution and HD decreased peripheral resistance, reflection coefficient at zero frequency, and frequency of the first zero crossing of the phase angle for 3 to 5 minutes after either fluid was administered. Characteristic impedance was not altered by HSS or HD. These impedance spectrum changes indicate transient vasodilatation and afterload reduction. We conclude that the vascular effect of an ionic hyperosmotic solution (HSS) is similar to that of a nonionic hyperosmotic solution (HD), and that HSS and HD transiently decrease afterload in normovolumic dogs. The duration of the afterload reduction after HSS administration appeared to be too short to be of great clinical benefit.

Animals↗

PubMed1994

Effect of phenylbutazone on the haemodynamic, acid-base and eicosanoid responses of horses to sustained submaximal exertion.

The systemic haemodynamic and acid-base effects of the administration of phenylbutazone (4.4 mg kg-1 intravenously) to standing and running horses were investigated. Phenylbutazone, or a placebo, was administered to each of six mares either 15 minutes before, or after 30 minutes of a 60-minute submaximal exercise test which elicited heart rates approximately 55 per cent of maximal, and to the same horses at rest. The variables examined included the cardiac output, heart rate, systemic and pulmonary arterial pressures, right atrial and right ventricular pressures, and arterial and mixed venous blood gases and pH. Serum sodium, potassium and chloride concentrations, and plasma thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and prostaglandin E2 (PGE2) concentrations were measured in separate studies using similar protocols in the same horses. Running produced increases in heart rate, cardiac output, mean arterial and right ventricular pressure, and decreases in total peripheral resistance. The acid:base responses to exertion were characterised by respiratory alkalosis. Exertion did not significantly influence plasma 6-keto-PGF1 alpha or PGE2 concentrations but plasma thromboxane B2 concentrations were increased significantly by 60 minutes of exertion in the untreated horses. This exercise-induced increase in plasma thromboxane B2 concentration was inhibited by the previous administration of phenylbutazone, but phenylbutazone did not produce detectable changes in systemic haemodynamic or acid-base variables in either standing or running horses.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

Emergency analgesia and chemical restraint in the horse.

Clinical examination of the equine patient with acute abdominal pain should identify the affected body system and yield a provisional diagnosis. Determination of signalment, history, physical examination, and basic laboratory tests should assist in classification of the gastrointestinal disorder and direct the therapeutic plan. Determination of the definitive diagnosis of abdominal pain based on clinical examination is not crucial. For a successful outcome, efforts should be directed toward early recognition of the need for surgery and treatment of cardiovascular compromise in horses with severe gastrointestinal disease.

Analgesia↗

PubMed1994

Hypertonic saline is a negative inotropic agent in normovolumic dogs.

The inotropic effects of hypertonic saline (HS) and hyperosmotic dextrose (HD; 2,400 mosmol/l, 4 ml/kg) were determined in normovolumic, chloralose-anesthetized, intact (n = 14) and autonomically blocked (n = 8) dogs. Solutions were infused intravenously over 3 min. HS and HD rapidly increased preload in both intact and autonomically blocked dogs, as assessed by significant (P < 0.05) increases in plasma volume, end-diastolic volume, and end-diastolic pressure. In intact dogs, HS produced a nonsignificant decrease in end-systolic elastance (Ees) and a nonsignificant increase in the maximal rate of change of left ventricular pressure (dP/dtmax) and cardiac output, whereas HD produced a significant increase in Ees, dP/dtmax, and cardiac output. In autonomically blocked dogs, HS significantly decreased Ees and significantly increased dP/dtmax but did not alter cardiac output, whereas HD significantly increased Ees, dP/dtmax, and cardiac output. We conclude that in normovolumic animals, HS is a negative inotropic agent, HD is a positive inotropic agent, and the in vivo effect of an ionic hyperosmotic agent (HS) differs from that of a nonionic hyperosmotic agent (HD).

Animals↗

PubMed1994

Histopathologic evidence of reperfusion injury in the large colon of horses after low-flow ischemia.

Effects of low-flow ischemia and reperfusion of the large colon on mucosal architecture were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline values. Systemic hemodynamic and metabolic variables were maintained constant and in a normal physiologic range. Full-thickness biopsy specimens were obtained from the left ventral colon for histomorphologic and morphometric examination at baseline and at 30-minute intervals for 6 hours; additional biopsy specimens were collected at 185, 190, and 195 minutes (corresponding to 5-, 10-, and 15-minute periods of reperfusion in group-3 horses). There were no differences among groups at baseline or across time in group-1 horses for any of the histopathologic variables. There were significant (P < 0.05) increases in percentage of surface mucosal disruption, estimated and measured percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, and cellular debris index during 0 hour to 3 hours, compared with baseline, and from 3 hours to 6 hours, compared with 3 hours in horses of groups 2 and 3. Estimated percentage depth of mucosal loss and cellular debris index were significantly (P < 0.05) greater in group-3 horses, compared with group-2 horses during the interval from 3 to 6 hours. There were trends toward greater percentage of surface mucosal disruption and mucosal edema during the early phase of reperfusion (3 to 4 hours) and greater mucosal hemorrhage, measured percentage depth of mucosal loss, and mucosal interstitial-to-crypt ratio during the late phase (4 to 6 hours) of reperfusion in group-3 horses vs group-2 horses. Reestablishment of colonic arterial blood flow after low-flow ischemia caused greater mucosal injury than did a comparable period of continued ischemia. Thus, reperfusion injury was detected in the large colon of horses after low-flow arterial ischemia. The serial mucosal alterations that developed in the colon were comparable in horses of groups 2 and 3; however, reperfusion exacerbated colonic mucosal injury.

Analysis of Variance↗

PubMed1994

Characterization of the hemodynamic and metabolic alterations in the large colon of horses during low-flow ischemia and reperfusion.

Effects of low-flow ischemia and reperfusion of the large colon on systemic and colonic hemodynamic and metabolic variables were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Heart rate, arterial blood pressures, cardiac index, pulmonary artery pressure, right atrial pressure, and colonic blood flow were monitored. Arterial, mixed-venous, and colonic venous blood gas and oximetry analyses; PCV; and blood lactate and pyruvate and plasma total protein concentrations were measured. Data were recorded, and blood samples were collected at baseline and at 30-minute intervals for 6 hours; additionally, data were collected at 185, 190, and 195 minutes (corresponding to 5, 10, and 15 minutes of reperfusion in group-3 horses). There were no differences among groups at baseline or across time for any systemic hemodynamic or metabolic variable. Colonic blood flow did not change across time in group-1 horses. Colonic blood flow significantly (P < 0.05) decreased to 20% of baseline at induction of ischemia in horses of groups 2 and 3 and remained significantly decreased throughout the ischemic period in horses of groups 2 (6 hours) and 3 (3 hours). Colonic blood flow significantly (P < 0.05) increased above baseline by 5 minutes of reperfusion in group-3 horses. Colonic oxygen delivery and oxygen consumption, and colonic venous pH, PO2, percentage saturation of hemoglobin, and oxygen content were significantly (P < 0.05) decreased within 30 minutes after induction of ischemia in horses of groups 2 and 3; colonic venous PCO2, colonic oxygen extraction ratio, and lactate and pyruvate concentrations were significantly (P < 0.05) increased by 30 minutes of ischemia. These alterations continued throughout ischemia, but within 5 minutes of reperfusion in group-3 horses, these variables either returned to baseline (pH, PCO2, lactate, pyruvate), significantly (P < 0.05) increased above baseline (PO2, oxygen content, % saturation of hemoglobin), or significantly (P < 0.05) decreased below baseline (colonic oxygen extraction ratio). Colonic oxygen consumption remained decreased during reperfusion in group-3 horses. Colonic mucosal ischemia-reperfusion injury observed in this model of ischemia was associated with local colonic hemodynamic and metabolic alterations in the presence of systemic hemodynamic and metabolic stability.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Neutrophil accumulation in the large colon of horses during low-flow ischemia and reperfusion.

Histomorphologic/morphometric evaluation, leukocyte scintigraphy, and myeloperoxidase activity were used to determine whether neutrophils accumulate in the large colon of horses during low-flow ischemia and reperfusion. Twenty-four adult horses were assigned to 1 of 3 groups: group 1, sham-operated (n = 6); group 2, 6 hours of ischemia (n = 9); and group 3, 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia of the large colon was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Radiolabeled (99mTc) autogenous neutrophils were injected at 175 minutes, which corresponded to 5 minutes prior to reperfusion in group-3 horses. Full-thickness biopsy specimens of the left ventral colon were collected at baseline and at 30-minute intervals for 6 hours; a portion of the biopsy specimen was placed in formalin for histologic examination, and the remainder was used to measure mucosal radioactivity and myeloperoxidase activity. There were no differences in baseline mucosal neutrophil index, mucosal neutrophil numbers, submucosal venular neutrophil numbers, mucosal radioactivity, or mucosal myeloperoxidase activity among groups, or over time in group-1 horses. Neutrophils accumulated in the colonic mucosa during ischemia and further increased at reperfusion, as indicated by neutrophil index (morphology) and mucosal neutrophil numbers (morphometry); mucosal neutrophil index was significantly (P < 0.05) greater in group-3 horses during reperfusion than at the corresponding periods of ischemia in group-2 horses. Neutrophil numbers were significantly (P < 0.05) increased in submucosal venules at 10 minutes of reperfusion in group-3 horses and were significantly (P < 0.05) greater in group-3 than in group-2 horses during the interval from 3 to 6 hours. Mucosal radioactivity significantly (P < 0.05) increased at reperfusion in group-3 horses; there was a trend (P = 0.076) toward greater mucosal radioactivity in group-3, compared with group-2 horses, throughout the 3- to 6-hour interval. There were no differences in mucosal myeloperoxidase activity among or within any of the 3 groups over time. Neutrophils accumulated in the large colon of horses during low-flow ischemia and reperfusion. Neutrophil infiltration was detected by histologic examination and leukocyte scintigraphy, but not by measurement of myeloperoxidase activity. The accumulation of neutrophils during ischemia and the further neutrophil infiltration during reperfusion indicate that neutrophils may contribute to reperfusion injury of the large colon.

Animals↗

PubMed1994

Caudal analgesia induced by epidural or subarachnoid administration of detomidine hydrochloride solution in mares.

Seven adult mares were used to determine the analgesic, CNS, and cardiopulmonary effects of detomidine hydrochloride solution after epidural or subarachnoid administration, using both regimens in random sequence. At least 1 week elapsed between experiments. A 17-gauge Huber point (Tuohy) directional needle was used to place a catheter with stylet into either the epidural space at the first coccygeal interspace or the subarachnoid space at the lumbosacral intervertebral junction. Catheters were advanced so that the tips lay at the caudal sacral (S5 to S4) epidural space or at the midsacral (S3 to S2) subarachnoid space. Position of the catheter was confirmed radiographically. A 1% solution of detomidine HCl was injected into the epidural catheter at a dosage of 60 micrograms/kg of body weight, and was expanded to a 10-ml volume with sterile water to induce selective caudal epidural analgesia (CEA). A dose of 30 micrograms of detomidine HCl/kg expanded to a 3-ml volume with spinal fluid was injected into the subarachnoid catheter to induce caudal subarachnoid analgesia (CSA). Analgesia was determined by lack of sensory perception to electrical stimulation (avoidance threshold > 40 V, 0.5-ms duration) at the perineal dermatomes and no response to superficial and deep muscular pinprick stimulation at the pelvic limb and lumbar and thoracic dermatomes. Maximal CEA and CSA extended from the coccyx to spinal cord segments T15 and T14 at 10 to 25 minutes after epidural and subarachnoid drug administrations in 2 mares. Analgesia at the perineal area lasted longer after epidural than after subarachnoid administration (142.8 +/- 28.8 minutes vs 127.1 +/- 27.7 minutes). All mares remained standing. Both CEA and CSA induced marked sedation, moderate ataxia, minimal cardiopulmonary depression, increased frequency of second-degree atrioventricular heart block, and renal diuresis. All treatments resulted in significantly (P < 0.05) decreased heart rate, respiratory rate, systemic arterial blood pressure, PCV, and plasma total solids concentration. To the contrary, arterial carbon dioxide tension, plasma bicarbonate, and standard base excess concentrations were significantly (P < 0.05) increased. Arterial oxygen tension, pH, and rectal temperature did not change significantly from baseline values. Results indicate that use of detomidine for CEA and CSA in mares probably induces local spinal and CNS effects, marked sedation, moderate ataxia, mild cardiopulmonary depression, and renal diuresis.

Analgesics↗

PubMed1994

Effect of furosemide on plasma atrial natriuretic peptide and aldosterone concentrations and renin activity in running horses.

Effects of furosemide administration on exertion-induced changes in plasma renin activity and plasma concentrations of atrial natriuretic peptide and aldosterone in horses during sustained submaximal exertion were examined. Furosemide (1 mg/kg of body weight) or heparinized saline solution was administered IV to each of 6 mares not conditioned to exercise, either 4 hours or 2 minutes before 60 minutes of sustained submaximal running on a treadmill. Horses ran at a speed that induced heart rate approximately 65% of maximal after saline treatment. After 15 minutes of running, furosemide suppressed the exertion-induced increase in plasma concentrations of atrial natriuretic peptide (mean [95% confidence interval] values of 63.9 [9.9 to 421] pg/ml vs 100 [15.4 to 652] pg/ml after furosemide or saline treatment, respectively), and enhanced the response of plasma renin activity to exertion (18.6 [5.7 to 60.4] ng/ml/h vs 6.0 [1.8 to 19.4] ng/ml/h, respectively). An effect of furosemide on the exertion-induced increase in plasma aldosterone concentration was not detected.

Aldosterone↗

PubMed1993

Effects of diazepam, acepromazine, detomidine, and xylazine on thiamylal anesthesia in horses.

The cardiorespiratory effects of thiamylal (10 mg/kg of body weight, IV) and the effects of preanesthetic medication with diazepam, acepromazine, detomidine, or xylazine administered prior to a thiamylal dosage of 6 mg/kg, IV, were evaluated in 6 adult horses. The quality of recovery from thiamylal anesthesia also was evaluated. Intravenous administration of thiamylal at a dosage of 10 mg/kg increased heart rate, systemic arterial, pulmonary artery, and central venous blood pressures, as well as cardiac output and arterial partial pressure of CO2 (PaCO2). The maximal rate of right ventricular pressure increase (RVdP/dtmax), respiratory rate, and arterial partial pressure of O2 (PaO2) decreased, whereas arterial pH and systemic vascular resistance remained unchanged. Preanesthetic medication with diazepam prior to IV administration of thiamylal (6 mg/kg) did not change the pattern of this response, but diazepam did increase heart rate, cardiac output, and respiratory rate during the recovery period. Administration of acepromazine (0.1 mg/kg, IV) prior to administration of thiamylal increased heart rate and decreased systemic arterial and central venous blood pressures and systemic vascular resistance. Detomidine (10 micrograms/kg, IV), administered prior to thiamylal, decreased heart rate, cardiac output, and respiratory rate, and increased right atrial blood pressure. Administration of xylazine (0.5 and 1.0 mg/kg, IV) prior to thiamylal induced effects qualitatively similar to detomidine. Thiamylal decreased RVdP/dtmax and PaO2 in horses that received diazepam, acepromazine, detomidine, or xylazine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acepromazine↗

PubMed1993

Adverse effects of administration of propofol with various preanesthetic regimens in dogs.

The effects of propofol on anesthetic induction were evaluated in 40 dogs anesthetized with isoflurane. Propofol is a rapidly acting, nonbarbiturate drug that induces anesthesia of ultrashort duration with IV administration. Four preanesthetic regimens were used: anesthesia without preanesthetic drugs; or with preanesthetic administration of acepromazine (0.1 mg/kg of body weight, IM), diazepam (0.2 mg/kg, IV), or acepromazine (0.02 mg/kg) and butorphanol (0.4 mg/kg) IM. Heart rate, systolic arterial blood pressure (SAP), respiration, quality of induction and recovery, and adverse effects were induction and recovery, and adverse effects were recorded. Intravenous propofol administration induced a variable period of apnea in 34 of 40 dogs. Cyanosis (in 2 dogs) and signs of pain on injection (in 3 dogs) were infrequently observed during induction. One dog developed ventricular premature depolarizations after propofol administration. Venous CO2 tension increased and pH decreased immediately after propofol administration, regardless of preanesthetic regimen. The SAP significantly (P < 0.05) decreased after propofol administration in dogs treated with acepromazine (SAP, 178 mm of Hg before vs 128 mm of Hg after propofol) and with acepromazine/butorphanol (SAP, 184 mm of Hg before vs 98 mm of Hg after propofol). When used for induction, propofol induces anesthetic-related adverse effects, some of which can be minimized by preanesthetic medication. Recovery characteristics varied with preanesthetic medication, independent of propofol administration.

Anesthesia, Inhalation↗

PubMed1993

Vaporizer in circle for delivery of isoflurane to dogs.

An in-circuit vaporizer for delivery of isoflurane was evaluated. The isoflurane concentration within an isolated circle breathing circuit was determined for 1 hour in 6 in-the-circuit vaporizers with the wicks removed. A mechanical ventilator and artificial lung were connected to the circuit. Isoflurane concentration increased as vaporizer setting increased, and delivered concentration (%) at 60 minutes (mean +/- SEM) ranged from 0.46 +/- 0.10 at tap setting 1 to 3.67 +/- 0.30 at setting 5. Temperature of the isoflurane did not change. Cardiovascular and respiratory function were maintained within a clinically acceptable range in 6 dogs anesthetized with thiamylal and maintained with 1.87% end-tidal isoflurane delivered from the in-circuit vaporizer during spontaneous ventilation, controlled ventilation, and closed-circuit anesthesia. The range of vaporizer tap settings (mean +/- SEM) was lower during closed-system anesthesia (2.5 +/- 0.1 to 3.5 +/- 0.6) and during controlled ventilation (2.6 +/- 0.2 to 3.3 +/- 0.2) than during semi-closed system anesthesia (5.4 +/- 0.3 to 6.8 +/- 0.4). The in-circuit vaporizer was used to deliver isoflurane to 36 dogs anesthetized for a variety of surgical and medical procedures. Ventilation was spontaneous, assisted, and in 1 instance, controlled. Cardiovascular function, respiratory function, and recovery times were within clinically acceptable ranges. The initial vaporizer tap setting (mean +/- SEM) was 8.2 +/- 0.4, and this corresponded to an end-tidal isoflurane concentration of 3.5 +/- 0.6. The range of vaporizer settings during the maintenance phase (mean +/- SEM) was 2.8 +/- 0.5 to 4.6 +/- 1.9.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1993

Cardiovascular effects of thoracic compression in horses subjected to euthanasia.

Six horses scheduled for euthanasia were instrumented for the measurement of blood flow by thermodilution, pulmonary arterial, right atrial and arterial blood pressures and collection of arterial blood for pH and blood gas analysis. The horses were anaesthetised with intravenous (iv) thiamylal sodium (10 mg/kg) and placed in right lateral recumbency. After euthanasia with an overdose of pentobarbitone sodium (100 mg/kg, iv) and loss of the electrocardiogram and arterial pulse pressure, thoracic compression at rates of 40, 60 and 80 compressions/min was instituted. Thoracic compression was accomplished by an investigator who delivered a blow to the chest wall with his knee while dropping from a standing or crouching position. Compression rates of 40, 60 and 80/min produced blood flows of 5.65 +/- 0.5, 6.33 +/- 1.11 and 8.28 +/- 2.16 litres/min, respectively. Compression rates of 80/min produced significantly (P < 0.05) greater blood flows and mean arterial blood pressures than did slower rates. The blood flows produced by 80 thoracic compressions/min were approximately 50% of those reported for deeply anaesthetised horses and while not sufficient to sustain life might be used to prolong life in order to facilitate distribution of resuscitative drugs to vital tissues.

Animals↗

PubMed1993

Comparative effects of 7.5% NaCl in 6% Dextran 70 and 0.9% NaCl on cardiorespiratory parameters after cardiac output-controlled resuscitation from canine hemorrhagic shock.

We resuscitated severely hemorrhaged (mean arterial pressure at 40 mm Hg for 30 min) pentobarbital-anesthetized dogs to 120% of control cardiac output with 7.5% NaCl in 6% Dextran 70 (HSD) or 0.9% NaCl (IS) to compare the effects on hemodynamic and oxygen transport parameters. Hemodynamic parameters and oxygen delivery did not differ between groups. Oxygen consumption and oxygen extraction ratio tended to be higher, and mixed venous oxygen tension lower (P < 0.05) for HSD during the first hour of the postresuscitation period. Resuscitation of the HSD group required significantly less time (10.4 +/- 2.0 vs. 23.6 +/- 1.7 min; P < 0.01) and fluid volume (8.0 +/- 1.1 vs. 47.0 +/- 3.3 ml.kg-1; P < 0.01). We conclude that the resuscitation of hypovolemic dogs with HSD and IS to equivalent cardiac output results in identical improvements in hemodynamics and oxygen delivery but that HSD may provide a better oxygen supply/demand balance during the first hour postresuscitation.

Animals↗

PubMed1993

Alpha 2-adrenergic receptor agonist effects on supraventricular and ventricular automaticity in dogs with complete atrioventricular block.

Complete atrioventricular block was induced in 26 pentobarbital-anesthetized dogs to determine the effects of the alpha 2-adrenergic receptor agonists, xylazine and medetomidine, on supraventricular and ventricular automaticity. Prazosin and atipamezole, alpha-adrenoceptor antagonists, were administered to isolate alpha 1- or alpha 2-adrenoceptor effects. Six dogs served as controls and were given glycopyrrolate (0.1 mg/kg of body weight, IV) and esmolol (50 to 75 micrograms/kg/min, IV) to induce parasympathetic and beta 1-adrenergic blockade, respectively. Eight dogs were given sequentially increasing doses of xylazine (n = 5), 0.000257 mg (10(-9)M) to 25.7 mg (10(-4)M) and medetomidine (n = 3), 0.000237 mg (10(-9)M) to 2.37 mg (10(-5)M) after parasympathetic and beta 1-adrenergic blockade. Twelve dogs were given xylazine (n = 6, 1.1 mg/kg, IV) or medetomidine (n = 6, 0.05 mg/kg, IV) after parasympathetic and beta 1-adrenergic blockade. Three dogs given xylazine and 3 dogs given medetomidine were administered prazosin (0.1 mg/kg, IV) followed by atipamezole (0.3 mg/kg, IV). The order of prazosin and atipamezole was reversed in the remaining 3 dogs given either xylazine or medetomidine. Complete atrioventricular block and administration of glycopyrrolate and esmolol resulted in stable supraventricular and ventricular rates over a 4-hour period. Increasing concentration of xylazine or medetomidine did not cause significant changes in supraventricular or ventricular rate. Xylazine and medetomidine, in the presence of the alpha-adrenoceptor antagonists, prazosin (alpha 1) and atipamezole (alpha 2), did not cause significant changes in supraventricular or ventricular rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

PubMed1993

Effect of furosemide and weight carriage on energetic responses of horses to incremental exertion.

The effect of furosemide-induced weight loss on the energetic responses of horses to running was examined in a 3-way crossover study. Eight 2- to 3-year-old Standardbred mares received, in random order, 10 ml of saline solution 4 hours before running on a treadmill (control trial, C); or, during 2 trials, 1 mg of furosemide/kg of body weight, i.v., 4 hours before running. During one of the trials when the horses received furosemide, they carried weight equal to that lost over the 3.75 hours after furosemide administration while running (furosemide-loaded, FL), and during the other trial they did not carry weight equal to that lost after furosemide administration (furosemide-unloaded, FU). Horses performed an incremental exercise test on a treadmill during which rates of oxygen consumption (VO2) and carbon dioxide production (VCO2) were measured, respiratory exchange ratio was calculated, and blood samples were collected for determination of mixed venous plasma lactate concentration and arterial and mixed venous oxygen saturation. Furosemide treatment caused significantly (P < 0.001) greater weight loss than did saline administration; mean +/- SEM weight loss (exclusive of fecal loss) was 1.6, 8.8, and 10.2 kg (SEM = 2.0) for C, FL, and FU trials, respectively. The speed at which peak VO2 was achieved was 9.31, 9.56, and 9.50 (SEM = 0.16) m/s, respectively, time to fatigue was 547, 544, and 553 (SEM = 26) seconds, respectively, and the highest speed attained was 10.3, 10.2, and 10.2 (SEM = 0.2) m/s, respectively. Mean peak rate of oxygen consumption was 130.7, 129.6, and 129.6 (SEM = 1.9) ml/min/kg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

A review of laboratory animal anesthesia with chloral hydrate and chloralose.

Chloral hydrate (CH) and alpha-chloralose (CS) are often used to anesthetize laboratory animals although, to our knowledge, there have been no controlled studies of their anesthetic or analgesic effects. Induction of and recovery from anesthesia can be stressful, and anesthesia and analgesic quality have been questioned. Intraperitoneal (i.p.) administration of CH has resulted in adynamic ileus and peritonitis in rats, gastric ulcers in rats, and peritonitis in swine. Light anesthesia is induced in rats. In dogs, CH induces sedation to deep anesthesia when given intravenously. Gastric irritation in dogs can occur when CH is given orally. Chloral hydrate is considered a good sedative-hypnotic for farm animals. Intravenously administered CS anesthetizes dogs and cats for 5 to 10 hours, but the animals may require respiratory support. Chloralose appears to be a satisfactory anesthetic for dogs when stage III thiobarbiturate anesthesia is first induced. It is difficult to gauge the depth of anesthesia and analgesia with CS. In our clinical experience with swine and calves, CH given i.p. leads to adynamic ileus. We have found that CS given i.p. causes an inflammatory response in guinea pigs, rats, and calves. We observed that CS analgesia varies with the type of surgical procedure performed. Based on a literature review and our clinical experience, we suggest that CH or CS anesthesia should be preceded by administration of barbiturates, opioids, alpha-2 agonists, or phenothiazine tranquilizers. Chloral hydrate should only be used as a sedative or hypnotic for dogs; CS should not be used as a sole anesthetic agent. Neither drug should be used i.p. for survival surgery.

Anesthesia↗

PubMed1993

Effect of hypercapnia on the arrhythmogenic dose of epinephrine in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

The effect of hypercapnia on the arrhythmogenic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an endtidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [PaCO2] = 35 to 45 mm of Hg), at hypercapnia (PaCO2 = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 micrograms/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 micrograms/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean +/- SD) during hypercapnia (1.04 +/- 0.23 micrograms/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 +/- 0.38 micrograms/kg/min), whereas the ADE after return to normocapnia (1.17 +/- 0.22 micrograms/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (PaO2) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

Anesthesia↗