Biomedical subjects

W W Muir

Publications and source records attributed to W W Muir.

244 records · Page 14Linked to original sources

PubMedDate not supplied

Closed system delivery of halothane and isoflurane with a vaporizer in the anesthetic circle.

Forty-four healthy dogs undergoing elective ovariohysterectomy were anesthetized with halothane or isoflurane delivered with an in-circuit vaporizer with closed system flow rates or an out-of-circuit vaporizer with semi-closed system flow rates. When dogs were anesthetized with halothane, there were no differences in heart rate, blood pressure, body temperature, respiratory rate, or lingual venous pH, PCO2, or PO2 during induction and maintenance. Lingual venous PO2 was significantly less but still within a clinically acceptable range when isoflurane was used in an in-circuit vaporizer. Recovery times tended to be longer with in-circuit vaporizers. The amount of anesthetic used was not affected by vaporizer location. In-circuit vaporizers were suitable for delivery of halothane or isoflurane to healthy dogs.

Acepromazine↗

PubMedDate not supplied

Pulsus alternans during halothane anesthesia in a dog.

An adult dog with pyloric obstruction was anesthetized with thiamylal and halothane for surgical revision. When an ECG was attached, the QRS-complex rate was noted to differ dramatically from the peripheral pulse rate. A dorsal pedal arterial catheter was introduced, and direct arterial pressure measurements revealed a blood pressure waveform that alternated in amplitude. Blood pressure and ECG traces were recorded, and the condition was diagnosed as pulsus alternans. The inhalation anesthetic was changed to isoflurane, and the condition was resolved.

Anesthesia, Inhalation↗

PubMedDate not supplied

Effects of halothane, enflurane, and isoflurane on supraventricular and ventricular rate in dogs with complete atrioventricular block.

Complete atrioventricular (AV) block was produced in 32 chloralose-anesthetized autonomically intact dogs to determine the effects of halothane, enflurane, and isoflurane on supraventricular and ventricular rate. Halothane (n = 17), enflurane (n = 6), and isoflurane (n = 9) were administered in three separate experiments in sequential minimum alveolar concentration (MAC) multiples of 0.5, 1.0, 1.5, 2.0, 1.5, and 1.0. Supraventricular rate, ventricular rate, and mean arterial blood pressure (MAP) were measured and recorded at baseline and after a 20-minute equilibration period of each inhalation anesthetic at each MAC multiple. Increasing concentrations of enflurane and isoflurane significantly decreased supraventricular rate (P < .05). Ventricular rate was not significantly changed by sequential MAC multiples of halothane, enflurane, and isoflurane. Increasing concentrations of halothane, enflurane, and isoflurane significantly decreased MAP with enflurane producing the most significant decrease (P < .05). Ventricular arrhythmias occurred in 5 of 17 dogs anesthetized with halothane and 1 of 9 dogs anesthetized with isoflurane. Inhalation anesthesia can significantly decrease supraventricular rate and MAP, does not alter ventricular rate, and can produce ventricular arrhythmias in dogs with complete AV block.

Anesthesia, Inhalation↗

PubMedDate not supplied

Blood gas values during intermittent positive pressure ventilation and spontaneous ventilation in 160 anesthetized horses positioned in lateral or dorsal recumbency.

One hundred sixty horses were anesthetized with xylazine, guaifenesin, thiamylal, and halothane for elective soft tissue and orthopedic procedures. Horses were randomly assigned to one of four groups. Group 1 (n = 40): Horses positioned in lateral (LRG1; n = 20) or dorsal (DRG1; n = 20) recumbency breathed spontaneously throughout anesthesia. Group 2 (n = 40): Intermittent positive pressure ventilation (IPPV) was instituted throughout anesthesia in horses positioned in lateral (LRG2; n = 20) or dorsal (DRG2; n = 20) recumbency. Group 3 (n = 40): Horses positioned in lateral (LRG3; n = 20) or dorsal (DRG3; n = 20) recumbency breathed spontaneously for the first half of anesthesia and intermittent positive pressure ventilation was instituted for the second half of anesthesia. Group 4 (n = 40): Intermittent positive pressure ventilation was instituted for the first half of anesthesia in horses positioned in lateral (LRG4; n = 20) or dorsal (DRG4; n = 20) recumbency. Spontaneous ventilation (SV) occured for the second half of anesthesia. The mean time of anesthesia was not significantly different within or between groups. The mean time of SV and IPPV was not significantly different in groups 3 and 4. Variables analyzed included pH, PaCO2, PaO2, and P(A-a)O2 (calculated). Spontaneous ventilation resulted in significantly higher PaCO2 and P(A-a)O2 values and significantly lower PaO2 values in LRG1 and DRG1 horses compared with LRG2 and DRG2 horses. Intermittent positive pressure ventilation resulted in normocarbia and significantly lower P(A-a)O2 values in LRG2 and DRG2 horses. In LRG2 the PaO2 values significantly increased from 20 minutes after induction to the end of anesthesia. The PaO2 and P(A-a)O2 values were not significantly different from the beginning of anesthesia after IPPV in DRG2 or DRG3. The PaO2 values significantly decreased and the P(A-a)O2 values significantly increased after return to SV in horses in LRG4 and DRG4. The PaO2 values were lowest and the P(A-a)O2 values were highest in all horses positioned in dorsal recumbency compared with lateral recumbency and in SV horses compared with IPPV horses. The pH changes paralleled the changes in PaCO2. Blood gas values during right versus left lateral recumbency in all groups were also evaluated. The PaO2 values were significantly lower and the P(A-a)O2 values were significantly higher during SV in horses positioned in left lateral (LRLG1) compared with right lateral (LRRG1) recumbency.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia, Intravenous↗

PubMedDate not supplied

The effects of medetomidine on cardiac contractility in autonomically blocked dogs.

The effects of medetomidine on load-dependent and relatively load-independent indices of left ventricular contractility and hemodynamics were studied in 8 chloralose-anesthetized, autonomic-blocked dogs. Left ventricular contractility was assessed by the maximum rate of increase in pressure (dP/dtmax), the slope of the end-systolic pressure volume relationship (Ees), preload recruitable stroke work (PRSW), and dP/dtmax-end-diastolic volume relation (SdPV). Dogs received 5 or 10 micrograms/kg of medetomidine IV. The dP/dtmax decreased significantly 30 minutes after both doses of medetomidine. The Ees did not change. Both SdPV and PRSW increased 5 minutes after both doses of medetomidine. Mean arterial pressure, left-ventricular end-diastolic and end-systolic pressures, peripheral vascular resistance and effective arterial elastance increased 5 minutes after both doses of medetomidine. Stroke volume, cardiac output, and stroke work decreased 5 minutes after medetomidine administration. End-diastolic volume did not change. End-systolic volume increased but the difference was not significant. Our study suggests that medetomidine increases inotropy and vascular resistance in autonomic-blocked dogs and that both ventricular and vascular responses to pharmacological manipulation must be considered for a complete assessment of the inotropic effects of a drug.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Effect of platelet-activating factor antagonist L-691,880 on low-flow ischemia-reperfusion injury of the large colon in horses.

OBJECTIVE: To determine the effect of platelet-activating factor (PAF) antagonist L-691,880 on low-flow ischemia and reperfusion (I-R) of the large colon in horses. ANIMALS: 12 adult horses. EXPERIMENTAL DESIGN: Horses were anesthetized, and the large colon was exteriorized through a ventral median celiotomy and instrumented. Colonic arterial blood flow was reduced to 20% of baseline (BL) and maintained for 3 hours; flow was then restored, and the colon was reperfused for 3 hours. One of two solutions was administered intravenously 30 minutes before reperfusion: group 1, 10 mL/kg 0.9% NaCl; and group 2, 5 mg/kg PAF antagonist L-691,880 in 0.9% NaCl. Hemodynamic variables were monitored and recorded at 30-minute intervals. Systemic arterial and colonic venous blood were collected for measurement of blood gas tensions, oximetry analyses, packed cell volume, and total plasma protein concentrations. Colonic venous blood was collected for determination of lactate, 6-keto prostaglandin F1 alpha (6-kPG), prostaglandin E2 (PGE2), and thromboxane B2 (TXB2) concentrations. Full-thickness biopsy specimens were harvested from the left ventral colon for histological evaluation. RESULTS: There were no significant differences between the two groups for any hemodynamic or metabolic variables. Colonic venous pH decreased, and carbon dioxide tension and lactate concentration increased during ischemia but returned to BL values during reperfusion. Colonic venous 6-kPG concentration was significantly increased above BL value at 2 hours and remained increased through 6 hours in horses of both groups. Colonic venous PGE2 concentration was significantly greater in group 2 compared with group 1 throughout the study. Colonic venous PGE2 concentration was increased above BL value from 3 to 6 hours in horses of both groups. Colonic venous TXB2 concentration was not different between groups but was significantly increased above the BL value for the first hour of reperfusion. Low-flow I-R of the large colon caused significant mucosal necrosis, hemorrhage, edema, and neutrophil infiltration; however, there were no differences in histological variables between vehicle-control and PAF antagonist-treated horses. CONCLUSION: No protective effects of PAF antagonist L-691,880 were observed on colonic mucosa associated with low-flow I-R. Additionally, deleterious drug-induced effects on hemodynamic and metabolic variables and colonic mucosal injury were not observed.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Selected aspects of the clinical pharmacology of visceral analgesics and gut motility modifying drugs in the horse.

Comparison of the visceral analgesic effects of xylazine, morphine, butorphanol, pentazocine, meperidine, dipyrone, and flunixin in a cecal distention model of colic pain indicated that xylazine produces the most relief from abdominal discomfort. Repeated administration of xylazine may reduce visceral pain so effectively that the seriousness of abdominal disease is obscured. Xylazine decreased propulsive motility in the jejunum and pelvic flexure of healthy ponies. Morphine and butorphanol also gave relief from visceral pain in the cecal distention model. Morphine may inhibit colonic, and butophanol jejunal, motility. Whether xylazine or opiate mediated decreases in gut motility cause clinically important slowing of ingesta transit is controversial and requires further investigation. The development of behavioral changes (i.e., apprehension and pawing) in horses given opiate therapy may limit the use of these drugs. Combinations of xylazine and morphine or butorphanol produce excellent, safe, visceral analgesia and sedation without untoward behavioral effects. Although flunixin fails to demonstrate good visceral analgesic effects in the cecal distention model, this drug produces analgesia in some cases of colic by blocking prostaglandin mediated induction of pain. Improvement of propulsive gut motility in patients with ileus may follow administration of neostigmine (which is particularly effective when the large bowel is hypomotile), naloxone (which experimentally stimulates propulsive colonic motility), and metoclopramide (which stimulates stomach and proximal small intestinal motility).

Analgesics↗

PubMedDate not supplied

Hemodynamic effects of atropine, dobutamine, nitroprusside, phenylephrine, and propranolol in conscious horses.

The authors investigated the cardiovascular effects of low doses of nitroprusside, dobutamine, and phenylephrine and a beta-adrenergic blocking dose of propranolol in conscious, healthy horses with and without prior atropine administration. A parasympathetic blocking dose of atropine produced significant increases in heart rate and arterial pressures, and decreased stroke volume, ejection fraction, pulse pressure, and right-ventricular end-diastolic pressure and volume. Cardiac output was not changed by atropine administration. Nitroprusside reduced arterial pressures to a greater extent in atropinized horses but increased heart rate in both atropinized and non-atropinized horses. Dobutamine increased mean arterial pressure in both non-atropinized and atropinized horses but increased heart rate, diastolic arterial pressure, and systemic vascular resistance only in atropinized horses. Propranolol did not affect any of the hemodynamic variables that were measured. Phenylephrine, in the presence of beta-adrenergic blockade, increased mean arterial pressure and reduced cardiac output. This study showed that low doses of nitroprusside, dobutamine, and phenylephrine produce significant hemodynamic effects in conscious, healthy horses and that these effects are modified by prevailing parasympathetic tone.

Animals↗

PubMedDate not supplied

Pharmacology of furosemide in the horse: a review.

Furosemide, a diuretic, is frequently administered to horses for the prophylaxis of exercise-induced pulmonary hemorrhage and the treatment of a number of clinical conditions, including acute renal failure and congestive heart failure. Furosemide increases the rate of urinary sodium, chloride, and hydrogen ion excretion. Plasma potassium concentration decreases after furosemide administration but urinary potassium excretion in horses is minimally affected. Renal blood flow increases after furosemide administration. Systemically, furosemide increases venous compliance and decreases right atrial pressure, pulmonary artery pressure, pulmonary artery wedge pressure, and pulmonary blood volume. The systemic hemodynamic effects of furosemide are only manifest in the presence of a functional kidney, but can occur in the absence of diuresis, emphasizing the importance of the renal-dependent extra-renal effects of furosemide. The renal and systemic hemodynamic effects of furosemide are modified by prior administration of nonsteroidal anti-inflammatory drugs. Furosemide administration attenuates exercise-induced increases in right atrial, aortic, and pulmonary artery pressures in ponies. Furosemide prevents exercise and allergen-induced bronchoconstriction in humans and decreases total pulmonary resistance in ponies with recurrent obstructive airway disease. These pharmacologic effects are frequently used to rationalize its questionable efficacy in the prevention of exercise-induced pulmonary hemorrhage. Neither the effect of furosemide on athletic performance nor its efficacy in the prevention of exercise-induced pulmonary hemorrhage has been convincingly demonstrated.

Animals↗

PubMedDate not supplied

Mechanisms of gastrointestinal ischemia-reperfusion injury and potential therapeutic interventions: a review and its implications in the horse.

Restoration of blood flow after a period of intestinal ischemia is necessary to maintain cell function and viability; however, the reintroduction of oxygen can initiate a cascade of events that exacerbates tissue injury. Intestinal I-R injury is manifested as increased microvascular and mucosal permeability, and mucosal necrosis. Reperfusion injury begins with the accumulation of hypoxanthine from ATP metabolism and the conversion of XDH to XO during ischemia. Upon reperfusion, the XO catalyzes the conversion of hypoxanthine to superoxide radicals in the presence of oxygen. Superoxide radicals are further reduced to highly reactive hydroxyl radicals, which initiate lipid peroxidation. Lipoperoxidation causes functional and structural alterations in cell membrane lipids and can release numerous inflammatory mediators, which exacerbate tissue damage. Neutrophils are recruited into tissues during ischemia and on reperfusion; then they undergo degranulation and release destructive products (proteases and OFRs), which mediate further tissue injury. A limited number of experimental studies in the gastrointestinal tract of horses have shown I-R injury. Additional studies are necessary to further elucidate and sequence the precise pathophysiologic mechanisms occurring in the equine intestine during I-R. Therapy should be focused on prevention of I-R injury by pharmacologic or chemical inhibition or modification of these pathophysiologic pathways. Selected pharmacologic agents or drug combinations may offer novel, scientifically relevant and yet practical approaches to alleviating intestinal I-R injury in horses. This may improve survival of horses with naturally acquired intestinal strangulation obstruction.

Animals↗