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Biomedical subjects

W W Muir

Publications and source records attributed to W W Muir.

At least 109 records · Page 6Linked to original sources
PubMed1991

Hypertonic saline/dextran resuscitation of dogs with experimentally induced gastric dilatation-volvulus shock.

We investigated small-volume (5 ml/kg) 7% NaCl in 6% dextran 70 (HS/D70) as an alternative to large-volume (60 ml/kg) 0.9% NaCl for treatment of experimentally induced canine gastric dilatation-volvulus (GDV) shock. The stomach was surgically displaced and then distended with an intragastric balloon in 11 dogs anesthetized with pentobarbital. All dogs were subjected to GDV for 180 minutes before partial decompression and resuscitation. Hemodynamic values, blood gas values, and plasma volume were measured during control, shock, and resuscitation periods. Resuscitation started with 1 group (n = 6) receiving 5 ml of HS/D70/kg, iv, over 5 minutes, and the other group (n = 5) receiving 60 ml of 0.9% NaCl/kg, IV, over 60 minutes. Both groups received a surgical maintenance dosage (20 ml/kg/h) of 0.9% NaCl after initial resuscitation. Resuscitative effects of small-volume HS/D70 were similar to large-volume 0.9% NaCl during the first hour of treatment; however, cardiac output was significantly higher in the HS/D70 group for the last 2 hours of resuscitation. Changes in heart rate, left ventricular pressure change, and systemic vascular resistance appeared to be responsible for improved perfusion. Mixed venous oxygen partial pressure data supported improved perfusion in the HS/D70 group. Packed cell volume remained higher in the HS/D70 group, indicating less hemodilution and improved oxygen delivery. Resuscitation of this GDV-induced shock model was better sustained with small-volume HS/D70, compared with conventional large-volume 0.9% NaCl.

Animals↗
PubMed1991

Vagotomy alters the hemodynamic response of dogs in hemorrhagic shock.

We examined the hemodynamic response of severely hemorrhaged dogs to vagotomy to further define the role of vagal innervation in circulatory control during severe hemorrhage. When the cervical vagi were severed in severely hemorrhaged, pentobarbital-anesthetized dogs, MAP decreased immediately after vagotomy and remained lower than in vagal-intact dogs. Cardiac output (CO) and heart rate (HR) also remained lower in the vagotomized dogs. When 45 ml/kg of 0.9% NaCl was administered to vagal-intact or vagotomized, severely hemorrhaged dogs, the MAP and CO increases were attenuated by vagotomy. Blood flow increases in the renal and splanchnic, but not femoral, vascular beds were inhibited by vagotomy. Vagotomy attenuates the hemodynamic response of severely hemorrhaged dogs, limits the effectiveness of isotonic fluid therapy, and exerts a differential effect on blood flow distribution.

Animals↗
PubMed1991

Effect of sodium bicarbonate infusion on serum osmolality, electrolyte concentrations, and blood gas tensions in cats.

The effects of single IV injections of sodium bicarbonate (0.5 mEq/kg of body weight, 1 mEq/kg, 2 mEq/kg, and 4 mEq/kg) on serum osmolality, serum sodium, chloride, and potassium concentrations, and venous blood gas tensions in 6 healthy cats were monitored for 180 minutes. Serum osmolality increased and remained significantly (P less than 0.05) increased for 120 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium was increased significantly (P less than 0.05) for 30 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium decreased and remained significantly (P less than 0.05) decreased for 120 minutes in cats given 1 g of 20% mannitol/kg, and serum osmolality was significantly (P less than 0.05) decreased at 30 and 60 minutes. Serum chloride decreased significantly (P less than 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and was significantly decreased for 30 minutes in cats given 2 mEq and 4 mEq of sodium bicarbonate/kg. Serum chloride decreased and remained significantly (P less than 0.05) decreased for 30 minutes in cats given 1 g of 20% mannitol/kg. Serum sodium and serum osmolality did not change significantly (P less than 0.05) in cats given 4 ml of 0.9% sodium chloride/kg. Serum potassium decreased significantly (P less than 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and for 120 minutes in cats given 2 mEq/kg or 4 mEq/kg. There was a significantly (P less than 0.05) greater decrease in serum potassium that lasted for 30 minutes after given sodium bicarbonate at the dosage of 4 mEq/kg, compared with other dosages given.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Cardiovascular effects of xylazine and detomidine in horses.

The cardiovascular effects of xylazine and detomidine in horses were studied. Six horses were given each of the following 5 treatments, at 1-week intervals: xylazine, 1.1 mg/kg, IV; xylazine, 2.2 mg/kg, IM; detomidine, 0.01 mg/kg, IV; detomidine, 0.02 mg/kg, IV; and detomidine, 0.04 mg/kg, IM. All treatments resulted in significantly decreased heart rate, increased incidence of atrioventricular block, and decreased cardiac output and cardiac index; cardiac output and cardiac index were lowest following IV administration of 0.02 mg of detomidine/kg. Mean arterial pressure was significantly reduced for various periods with all treatments; however, IV administration of 0.02 mg of detomidine/kg caused hypertension initially. Systemic vascular resistance was increased by all treatments. Indices of ventricular contractility and relaxation, +dP/dt and -dP/dt, were significantly depressed by all treatments. Significant changes were not detected in stroke volume or ejection fraction. The PCV was significantly reduced by all treatments. Respiratory rate was significantly decreased with all treatments, but arterial carbon dioxide tension did not change. Arterial oxygen tension was significantly decreased briefly with the 3 IV treatments only.

Analgesics↗
PubMed1991

Effects of amiodarone on myocardial performance in normal canine hearts and canine hearts with infarcts.

The effects of IV administered amiodarone, a class-III antiarrhythmic agent, on myocardial contractility, early myocardial relaxation, and hemodynamic variables were evaluated in normal canine hearts and those with infarcts. In the normal canine heart, amiodarone had important, but relatively mild, depressant effects on left ventricular contractility (assessed by maximal positive first derivative of left ventricular pressure (+dP/dtmax) and maximal elastance (Emax)) and heart rate when given IV at a dose of 10 mg/kg of body weight. An effect on contractility or active relaxation (assessed by maximal negative first derivative of left ventricular pressure (-dP/dtmax) and the time constant of isovolumic pressure decrease) was not identified with smaller doses. Myocardial infarction itself caused a predictable and marked depressant effect on myocardial contractility, as indicated by decreases in +dP/dtmax, ejection fraction, Emax, and -dP/dtmax, and elevation in end diastolic pressure. Additional depressive effects on contractility and active relaxation resulted when 10 mg of amiodarone/kg was administered to dogs with myocardial infarction and these effects were sufficient to worsen acute myocardial infarction-induced heart failure. Significant changes attributable to heart rate alone could not be identified. On the basis of our findings, we suggest that amiodarone administered IV should be used with caution in dogs with compromised ventricular function.

Amiodarone↗
PubMed1991

Hemodynamic response of endotoxemic calves to treatment with small-volume hypertonic saline solution.

The hemodynamic effects of hypertonic saline solution (HSS) resuscitation on endotoxic shock were examined in pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli (055:B5) endotoxin was infused IV at dosage of 0.1 microgram/kg of body weight for 30 minutes. Endotoxin induced large decreases in cardiac index, stroke volume, maximal rate of change of left ventricular pressure (+dP/dtmax), femoral and mesenteric arterial blood flow, glomerular filtration rate, urine production, and mean aortic pressure. Severe pulmonary arterial hypertension and increased pulmonary vascular resistance were evident at the end of endotoxin infusion. Treatment with HSS (2,400 mosm of NaCl/L, 4 ml/kg) or an equivalent sodium load of isotonic saline solution (ISS: 300 mosm of NaCl/L, 32 ml/kg) was administered 90 minutes after the end of endotoxin administration. Both solutions were infused IV over a 4- to 6-minute period. Administration of HSS induced immediate and significant (P less than 0.05) increase in stroke volume and central venous pressure, as well as significant decrease in pulmonary vascular resistance. These effects were sustained for 60 minutes, after which all variables returned toward preinfusion values. The hemodynamic response to HSS administration was suggestive of rapid plasma volume expansion and redistribution of cardiac output toward splanchnic circulation. Plasma volume expansion by HSS was minimal 60 minutes after resuscitation. Administration of ISS induced significant increase in cardiac index, stroke volume, femoral arterial blood flow, and urine production. These effects were sustained for 120 minutes, at which time, calves were euthanatized. Compared with HSS, ISS induced sustained increase in mean pulmonary arterial pressure and only a small increase in mesenteric arterial blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Respiratory, renal, hematologic, and serum biochemical effects of hypertonic saline solution in endotoxemic calves.

The respiratory, renal, hematologic, and serum biochemical effects of hypertonic saline solution (HSS) treatment were examined in 12 endotoxic, pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli endotoxin (055:B5) was infused IV at a rate of 0.1 microgram/kg of body weight over 30 minutes. Endotoxin induced severe respiratory effects, with marked hypoxemia and increases in arterial-alveolar O2 gradient (P[A-a]O2), physiologic shunt fraction (Qs/Qt), and physiologic dead space to tidal volume ratio (Vd/Vt). Oxygen consumption was decreased, despite an increase in the systemic O2 extraction ratio. Peak effects were observed at the end of endotoxin infusion. The renal response to endotoxemia was characterized by a decrease in free-water reabsorption and osmotic clearance, as well as a decrease in sodium and phosphorus excretion. Endotoxemia induced leukopenia, thrombocytopenia, hyperphosphatemia, hypoglycemia, acidemia, and increased serum alkaline phosphatase concentrations. Calves were treated with HSS (2,400 mosm/L of NaCl, 4 ml/kg, n = 4) or an equivalent sodium load of isotonic saline solution (ISS; 300 mosm/L of NaCl, 32 ml/kg, n = 4 90 minutes after the end of endotoxin administration. Both solutions were infused over a 4- to 6-minute period. A control group (n = 4) was not treated. Infusion of HSS or ISS failed to induce a significant change in Pao2, P(A-a)O2, (Qs/Qt), (Vd/Vt), or oxygen consumption. Both solutions increased systemic oxygen delivery to above pre-endotoxin values. Hypertonic saline infusion induced significant (P less than 0.05) increases in serum Na and Cl concentrations and osmolality, whereas ISS induced a significant increase in serum Cl concentration and a significant decrease in serum phosphorus concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of halothane on impulse propagation in Purkinje fibers and at Purkinje-muscle junctions: relationship of Vmax to conduction velocity.

Alterations in Purkinje-to-muscle conduction may play a role in the development of cardiac arrhythmias. We compared the effects of halothane on impulse propagation in Purkinje fibers with its effects on impulse propagation across the Purkinje-muscle (P-M) junction. In canine Purkinje fibers, halothane (3%) significantly depressed conduction (P less than 0.05). Exposure to halothane altered conduction velocity (theta) in a manner predicted by cable theory; a significant correlation was noted between depression of Vmax and depression of the square of conduction velocity (theta 2) in Purkinje fibers exposed to 3% halothane (n = 11, r = 0.78, P less than 0.01). Halothane (3%) significantly slowed impulse propagation across the P-M junction (P less than 0.05). Vmax and the square of apparent P-M conduction velocity were not significantly correlated (n = 7, r = 0.34, P = 0.45). The data demonstrate that alteration of active membrane properties can account for halothane's slowing of conduction in Purkinje fibers but not for its slowing of conduction across the P-M junction. The data also suggest that a reduction in cell-to-cell coupling may contribute to depression of Purkinje-to-muscle conduction by halothane.

Action Potentials↗
PubMed1990

Treatment of atrial fibrillation in horses by intravenous administration of quinidine.

Intravenous administration of quinidine gluconate converted atrial fibrillation (AF) to sinus rhythm in 9 of 12 horses. Twelve horses that were diagnosed by ECG to have AF were administered up to 11 mg of quinidine gluconate/kg of body weight in 1.0- to 1.5-mg/kg bolus injections every 10 to 15 minutes. The total dose of quinidine administered IV ranged from 1.8 to 5.8 g. Increased ventricular rate, apprehension, and mild depression were observed during treatment. Other signs of toxicosis were not observed. One horse was successfully treated with IV administered quinidine gluconate on 3 occasions. Intravenous administration of quinidine is a safe and effective alternative for treatment of AF in some horses.

Animals↗
PubMed1990

Bilateral arytenoid cartilage paralysis after inhalation anesthesia in a horse.

An 8-year-old Quarter Horse gelding was anesthetized for surgical exploration and debridement of a chronic draining wound in the intermandibular space. Anesthesia was without complication other than persistently low PaO2. Severe airway obstruction was evident immediately after extubation, requiring tracheostomy. Endoscopic diagnosis was bilateral arytenoid paralysis, which gradually resolved over the next 7 days. Compression, trauma, or tension of the recurrent laryngeal nerves are the postulated causes of idiopathic laryngeal hemiplegia in horses. The extremely extended position of the head and neck during anesthesia, perhaps compounded by low arterial oxygen content, may have resulted in a hypoxemic insult to the recurrent laryngeal nerves and caused bilateral arytenoid paralysis in this horse.

Anesthesia, Inhalation↗
PubMed1990

Clinical and electrocardiographic characterization of cattle with atrial premature complexes.

Atrial premature complexes (APC) were identified in 16 cows over a 2-year period. Fourteen cows had concurrent gastrointestinal disease. Variation in the intensity of the first heart sound and an occasionally irregular heart rhythm were evident during thoracic auscultation. Neither cardiac murmurs nor pulse deficits were detected in any cows, and clinical signs of heart failure were lacking. Three cows had APC immediately prior to or after development of atrial fibrillation. The heart rate when APC were diagnosed ranged from 48 to 124 beats/min (mean, 77 +/- 20 beats/min), and the APC frequency ranged from less than 1 to 23/min (mean 9.4 +/- 8.0). The P-wave morphologic characteristics in 4 cows with APC was abnormal. The coupling index of the APC varied between 0.44 and 0.95, with a mean of 0.73. Aberrant ventricular activation was usually associated with a short coupling interval (coupling index less than 0.60) and was observed in 3 cows. Ten cows were determined to be hypocalcemic and 4 cows hypokalemic when APC were identified. Atrial ectopic activity could not be detected in 12 cows after resolution of the concurrent gastrointestinal disorder or electrolyte abnormality. Atrial premature complexes may be a functional cardiac disorder in cattle, unrelated to structural heart disease. The potential for APC to progress to sustained atrial arrhythmias such as atrial fibrillation should be considered.

Animals↗
PubMed1990

Haemodynamic effects of small volume hypertonic saline in experimentally induced haemorrhagic shock.

A comparison of the haemodynamic benefits of small volume hypertonic saline (2,400 mOsm/litre) versus isotonic saline (300 mOsm/litre) was conducted in 12 adult horses using a haemorrhagic shock model. The horses were anaesthetised and intravascular catheters placed for the measurement of haemodynamic data. Mean systemic arterial pressure was then reduced to 50 to 60 mmHg by controlled haemorrhage and maintained at that level for 40 mins. Cardiac output, stroke volume, mean systemic arterial pressure, plasma volume and urine production decreased significantly following blood loss. Hypertonic or isotonic saline was administered randomly by intravenous infusion and haemodynamic data recorded for a 2 h period. Treatment with hypertonic saline produced rapid elevations in cardiac output, stroke volume, mean systemic and pulmonary arterial pressures, cardiac contractility and urine output, and was accompanied by expansion of the plasma volume. The changes in cardiac output and stroke volume were maintained for the duration of the recording period, whereas increases in mean systemic arterial pressure were not as remarkable. Infusion of isotonic saline caused only transient increases in cardiac output and mean systemic and pulmonary arterial pressure, and cardiac output; urine output and plasma volume did not change. This study indicates that hypertonic saline produces haemodynamic improvements in experimentally induced haemorrhagic shock in horses.

Animals↗
PubMed1990

Haematological, serum electrolyte and blood gas effects of small volume hypertonic saline in experimentally induced haemorrhagic shock.

The effects of treatment with small volume hypertonic (2400 mOsm/litre) and isotonic (300 mOsm/litre) saline on serum electrolyte and biochemical concentrations, haemograms and blood gases were evaluated in 12 horses using a haemorrhagic shock model. Intravascular catheters were placed surgically for sample collection prior to anaesthesia. Controlled haemorrhage was initiated and continued until mean systemic pressure reached 50 to 60 mmHg. Hypertonic or isotonic saline (2 litres) was administered by intravenous infusion and data collected for 2 h. Following haemorrhage, packed cell volume (PCV), haemoglobin, blood glucose concentrations and erythrocyte numbers increased whereas plasma total protein and albumin concentrations decreased. Infusion of hypertonic saline resulted in a further decrease in total protein and albumin concentrations. Glucose concentrations and other haematological variables were unaffected. Isotonic saline administration did not affect electrolyte, total protein or albumin concentrations. Concentrations of sodium and chloride were unaffected by hypotension but increased significantly following hypertonic saline treatment, exceeding normal values during the immediate post treatment period. Serum osmolality increased concurrently. No significant changes in arterial and venous blood gas values were observed with haemorrhage or isotonic saline treatment. A transient decrease in arterial and venous blood pH and a sustained decrease in venous bicarbonate and base excess concentrations occurred following hypertonic saline administration. No significant increases in any serum biochemical concentrations occurred during hypotension or following infusion of either isotonic or hypertonic saline. These results demonstrate that small volume hypertonic saline can be administered safely to horses without producing extreme changes in electrolyte concentrations, blood gases or haematological parameters.

Animals↗
PubMed1990

An investigation of the second heart sound in the normal horse.

The second heart sound was evaluated in conscious, normal horses using intracardiac and external sound detection devices and echocardiography. The second heart sound (S2) in the normal horse is single or split by a narrow interval, not usually detected by external phonocardiographic evaluation. Splitting of S2 was classified as normal (aortic [A2] preceding pulmonic [P2] components) in 66.7 per cent and reversed (P2 preceding A2) in 33.3 per cent of the horses studied. Normal splitting appears to result from lower impedance of the pulmonary vasculature delaying the onset of P2. Reverse splitting appears to result from a delay in A2 resulting from prolongation of PEP and LVET. There does not appear to be variation in splitting of S2 due to respiration based on the cases in which this was measured.

Animals↗
PubMed1990

Renal and systemic hemodynamic responses to sustained submaximal exertion in horses.

We investigated the effects of 1 h of sustained submaximal exertion on the renal and systemic hemodynamics of six horses. The horses ran on a treadmill at a speed that produced heart rates of 55-60% of each horse's maximum heart rate. Exertion produced heart rates of 121 +/- 6.6 and 126 +/- 6.1 (SE) beats/min after 15 and 60 min, respectively. Cardiac output increased significantly (P less than 0.05) from 70.1 +/- 3.1 to 246.2 +/- 4.7 ml.min-1.kg body wt-1 after 15 min of exertion and thereafter did not change. There was no significant change from rest in p-aminohippuric acid and creatinine clearances, filtration fraction, or renal blood flow during exertion. Plasma total solid concentration and hematocrit increased by 3.8 and 8.6%, respectively, between 20 and 60 min of exertion. Pulmonary artery temperature increased significantly from 37.6 degrees C at rest to 38.6 degrees C at 60 min of exertion. This study demonstrates the ability of the horse to maintain renal hemodynamics similar to resting values and systemic hemodynamics at steady-state values despite hemoconcentration and increased body temperature during sustained submaximal exertion.

Animals↗
PubMed1990

Hemodynamic effects of carbon dioxide during intermittent positive-pressure ventilation in horses.

The hemodynamic effects of high arterial carbon dioxide pressure (PaCO2) during anesthesia in horses were studied. Eight horses were anesthetized with xylazine, guaifenesin, and thiamylal, and were maintained with halothane in oxygen (end-tidal halothane concentration = 1.15%). Baseline data were collected while the horses were breathing spontaneously; then the horses were subjected to intermittent positive-pressure ventilation, and data were collected during normocapnia (PaCO2, 35 to 45 mm of Hg), moderate hypercapnia (PaCO2, 60 to 70 mm of Hg), and severe hypercapnia (PaCO2, 75 to 85 mm of Hg). Hypercapnia was induced by adding carbon dioxide to the inspired gas mixture. Moderate and severe hypercapnia were associated with significant (P less than 0.05) increases in aortic blood pressure, left ventricular systolic pressure, cardiac output, stroke volume, maximal rate of increase and decrease in left ventricular pressure (positive and negative dP/dtmax, respectively), and median arterial blood flow, and decreased time constant for ventricular relaxation. These hemodynamic changes were accompanied by increased plasma epinephrine and norepinephrine concentrations. Administration of the beta-blocking drug, propranolol hydrochloride, markedly depressed the response to hypercapnia. This study confirmed that in horses, hypercapnia is associated with augmentation of cardiovascular function.

Animals↗