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Biomedical subjects

J C Thurmon

Publications and source records attributed to J C Thurmon.

At least 19 recordsLinked to original sources
PubMed1992

Yohimbine/flumazenil antagonism of hemodynamic alterations induced by a combination of midazolam, xylazine, and butorphanol in dogs.

Reversal of hemodynamic alterations induced by midazolam maleate (1.0 mg/kg of body weight), xylazine hydrochloride (0.44 mg/kg), and butorphanol tartrate (0.1 mg/kg) with yohimbine (0.1 mg/kg) and flumazenil (0.25 mg/kg) was evaluated in 5 dogs. The dogs were anesthetized with isoflurane for instrumentation. With return to consciousness, baseline values were recorded, and the midazolam/xylazine/butorphanol mixture with glycopyrrolate was administered IV. Hemodynamic data were recorded for 60 minutes, and then a reversal mixture of yohimbine and flumazenil was administered IV. All variables were measured 1 minute from beginning of the reversal injection. Mean arterial pressure, pulmonary arterial pressure, systemic vascular resistance, and right ventricular stroke work index increased significantly (P < 0.05) above baseline at 60 minutes. Cardiac index and central venous pressure significantly decreased below baseline at 60 minutes. After reversal, mean arterial pressure and central venous pressure significantly decreased from baseline, whereas cardiac index, pulmonary arterial pressure, and right ventricular stroke work index increased significantly above baseline. Heart rate, cardiac index, and right ventricular stroke work index increased significantly above the 60-minute value after reversal. Mean arterial pressure and systemic vascular resistance decreased significantly (P < 0.05) below the 60-minute value after reversal. The hemodynamic alterations accompanying midazolam/xylazine/butorphanol sedation-anesthesia may be rapidly reversed with a combination of yohimbine and flumazenil.

Anesthesia↗
PubMed1992

DNA adduct dosimetry and DNA repair in rats and pigs given repeated doses of procarbazine under conditions of carcinogenicity and human cancer chemotherapy respectively.

Procarbazine (PCZ), an antineoplastic agent that produces methylated bases in DNA after metabolic activation, has been implicated in the development of secondary cancers in patients treated for a primary neoplasm. The repair of the important promutagenic lesion, O6-methylguanine (O6-meG) by O6-alkylguanine-DNA alkyl transferase (AGT) is believed to be crucial for the stability of O6-meG and for the tumorigenic outcome after exposure to methylating carcinogens. Using two different animal models, we investigated methyl DNA adduct dosimetry and DNA repair in (i) female rats given repeated doses of PCZ for 20 weeks under conditions of carcinogenicity, and (ii) female pigs administered repeated doses of PCZ for 4 weeks according to a regimen comparable to that given to human subjects undergoing cancer chemotherapy. After each successive week, four rats and three pigs were killed and tissues including blood, liver, mammary gland, spleen, thymus and lymph node were taken. The levels of O6-meG, 7-methylguanine (7-meG) in DNA and of AGT were determined in these tissues. In the rat, O6-meG in the liver DNA, and to a lesser degree in the spleen was efficiently removed throughout the 20 week dosing period, as indicated by the O6-meG/7-meG ratio being much less than 0.11. In the target organs, accumulation of O6-meG began in the mammary gland after 9 weeks, and in the lymph node and thymus after 3 weeks of dosing. Interestingly, the accumulation of O6-meG in the mammary gland correlates well with a concomitant decrease in AGT level as from week 10 and may be related to the induction of mammary gland tumors, first detected in two animals at week 10. In pigs, after a total dose of 750-4000 mg of PCZ, the range of 7-meG detected in leukocyte DNA was 21-66 mumol/mol G, which compares well with recent findings in cancer patients treated with PCZ. Similar levels of 7-meG were detected in the pig liver, thymus and lymph node. O6-MeG was only detectable in leukocyte DNA at week 4 with our present method. Compared with control pig tissues, a depressed AGT level was found in the leukocyte, lymph node and brain of the treated animals.

Animals↗
PubMed1992

A comparison of medetomidine-propofol and medetomidine-midazolam-propofol anesthesia in rabbits.

We evaluated and compared the effects of medetomidine-propofol and medetomidine-midazolam-propofol anesthesia in rabbits. Fourteen New Zealand White rabbits were randomly assigned to receive either medetomidine (0.25 mg/kg, i.m.)-atropine (0.5 mg/kg, i.m.)-propofol (4 mg/kg, i.v.) (n = 7) or medetomidine (0.25 mg/kg, i.m.)-atropine (0.5 mg/kg, i.m.)-midazolam (0.5 mg/kg, i.m.)-propofol (2 mg/kg, i.v.) (n = 7). Five minutes after medetomidine-atropine or medetomidine-atropine-midazolam i.m. injection, propofol was administered i.v. Both medetomidine and medetomidine-midazolam rapidly (within 5 minutes) immobilized all rabbits and greatly eased the i.v. administration of propofol. Endotracheal intubation was accomplished easily after propofol injection in both groups. There was no significant difference between medetomidine-propofol and medetomidine-midazolam-propofol-treated rabbits in heart rate, respiratory rate, mean arterial pressure, or end-tidal CO2. The addition of midazolam to the medetomidine-propofol regimen significantly (P < 0.05) prolonged the duration of ear-pinch analgesia (25.0 +/- 7.1 vs. 36.7 +/- 8.9 minutes), the time from extubation to sternal recumbency (0.0 vs. 26.7 +/- 8.1 minutes), and the time from extubation to standing (0.0 vs. 39.5 +/- 11.3 minutes) without inducing significant changes in arterial blood pressure and end-tidal alveolar CO2. We consider both medetomidine-propofol and medetomidine-midazolam-propofol combinations to be safe and effective regimens for induction and short-term anesthesia in rabbits.

Anesthesia, General↗
PubMed1992

Ketamine, Telazol, xylazine and detomidine. A comparative anesthetic drug combinations study in ponies.

This study was designed to assess the effects of 5 anesthetic drug combinations in ponies: (1) ketamine 2.75 mg/kg, xylazine 1.0 mg/kg (KX), (2) Telazol 1.65 mg/kg, xylazine 1.0 mg/kg (TX), (3) Telazol 2 mg/kg, detomidine 20 micrograms/kg (TD-20), (4) Telazol 2 mg/kg, detomidine 40 micrograms/kg (TD-40), (5) Telazol 3 mg/kg, detomidine 60 micrograms/kg (TD-60). All drugs were given iv with xylazine or detomidine preceding ketamine or Telazol by 5 min. Heart rate was decreased significantly from 5 min to arousal after TD-20 but only at 60 and 90 min after TD-40 and TD-60 respectively. Respiratory rate was decreased significantly for all ponies. Induction time did not differ between treatments. Duration of analgesia was 10 min for KX, 22.2 min for TX, 27.5 min for TD-20, 32.5 min for TD-40, and 70 min for TD-60. Arousal time was significantly longer with detomidine and Telazol. Smoothness of recovery was judged best in ponies receiving KX and TD-40. All ponies stood unassisted 30 min after signs of arousal.

Anesthetics↗
PubMed1991

Hemodynamic response of calves to tiletamine-zolazepam-xylazine anesthesia.

Six healthy Holstein calves were anesthesized with isoflurane in O2 and instrumented for hemodynamic studies. A saphenous artery was catheterized for measurement of blood pressure and withdrawal of blood for determination of the partial pressure of carbon dioxide (PaCO2), oxygen (PaO2), and arterial pH (pHa). Respiration was controlled throughout the study. The ECG and EEG were monitored continuously. A thermodilution catheter was passed via the right jugular vein into the pulmonary artery for determination of cardiac output and measurement of central venous pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure. Baseline values (time 0) were recorded following recovery from isoflurane. Tiletamine-zolazepam (4 mg/kg)-xylazine (0.1 mg/kg) were administered IV immediately after recording baseline values. Values were again recorded at 5, 10, 20, 30, 40, 50, and 60 minutes after injection. Changes in left ventricular stroke work index, PaCO2, and pHa were insignificant. Arterial blood pressure and systemic vascular resistance increased above baseline at 5 minutes and then gradually decreased below baseline at 40 minutes, demonstrating a biphasic response. Values for pulmonary capillary wedge pressure, pulmonary arterial pressure, central venous pressure, and PaO2 were increased above baseline from 5 to 60 minutes. Stroke volume, stroke index, and right ventricular stroke work index were increased from 20 or 30 minutes to 60 minutes. Pulmonary vascular resistance increased at 10 minutes, returned to baseline at 20 minutes, and was increased again at 60 minutes. Heart rate, cardiac output, cardiac index, and rate pressure product were decreased at 5 minutes, and with the exception of cardiac output, remained so for 60 minutes. Cardiac output returned to the baseline value at 30 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1991

Effect of midazolam preanesthetic administration on thiamylal induction requirement in dogs.

The thiamylal sparing effect of midazolam was studied in 30 healthy Beagle and mixed-breed dogs. Using a replicated Latin square design, all dogs were given placebo (saline solution) and 0.025, 0.05, 0.1, and 0.2 mg of midazolam/kg of body weight prior to IV administration of thiamylal sodium. The 0.1 and 0.2 mg/kg dosages significantly decreased the amount of thiamylal required to obtund swallowing reflex and easily achieve endotracheal intubation. Midazolam at 0.1 and 0.2 mg/kg reduced thiamylal requirement by 16.4% and 18.9%, respectively, whereas the 0.05 mg/kg dosage decreased thiamylal requirement by only 6.8%. The 0.2 mg/kg dosage did not further decrease thiamylal requirement beyond that achieved with the 0.1 mg/kg dosage of midazolam. This study demonstrates that the preanesthetic IV administration of midazolam reduces the thiamylal dose necessary to accomplish intubation. The optimal preanesthetic dosage (lowest dosage with significant effect) was 0.1 mg/kg.

Animals↗
PubMed1990

General clinical considerations for anesthesia of the horse.

The peculiarities of the equine species present a number of unique situations that must be addressed when horses are anesthetized. Perhaps the most troublesome situation is related to the horse's size. Though the horse's large lungs are responsible in part for its sustainable athletic ability, they are detrimental to effective ventilation when the horse is anesthetized and placed in a recumbent position. Of major concern is depression of ventilation and cardiovascular function. Hypercapnia and hypoxemia usually result from hypoventilation, and with time all anesthetized horses suffer from some degree of cardiovascular depression. Decreased blood flow coupled with the horse's weight pressing downward on the undermost tissues frequently disturbs microcirculation and causes injury to muscle tissue. Of major importance is the product of anesthetic depth and anesthetic time. Only through careful observation and initiation of supportive measures can injuries related to anesthesia or surgery be kept to a minimum. Because of the horse's nature, safe anesthesia cannot always be assured, even when state-of-the-art anesthetic techniques are practiced.

Anesthesia↗
PubMed1990

Intravenous anesthesia.

Anticholinergics, tranquilizers, and sedative-hypnotics are the usual agents used for preanesthetic sedation of the horse. Of these drugs, the anticholinergics are of little importance in the horse. Acepromazine is the most useful and widely used tranquilizer, whereas xylazine is a safe and popular sedative. A newer sedative recently made available to the veterinarian for clinical use in horses is detomidine. Thiobarbiturates are seldom used alone any longer but are still useful when combined with guaifenesin for induction and maintenance of anesthesia. Other, more contemporary drug combinations that have largely replaced thiobarbiturates and chloral hydrate include xylazine with ketamine, xylazine with Telazol, detomidine with Telazol, and guaifenesin with ketamine and xylazine.

Anesthesia, Intravenous↗
PubMed1990

Management of anesthesia in the foal.

Several unique pharmacologic and physiologic factors must be considered when attempting to anesthetize premature or neonatal foals. Juvenile foals are similar to adults in their physiology and metabolism. Anesthetic drug and protocol selection should reflect the differences between these two age groups. Neonates are best anesthetized using an inhalation technique, whereas older foals can be safely anesthetized with either parenteral or inhalation anesthetic agents. Careful monitoring is absolutely essential when anesthetizing foals. The clinician should plan to routinely administer fluids and measure electrolyte levels. A basic plan and knowledge of the methods and agents used to treat hypovolemia, severe cardiopulmonary collapse, and life-threatening arrhythmias can result in survival of many critically ill foals.

Anesthesia↗
PubMed1990

Pharmacokinetics of etomidate in cats.

Pharmacokinetic variables of etomidate were determined after IV administration of etomidate (3.0 mg/kg of body weight). Blood samples were collected for 6 hours. Disposition of this carboxylated imidazole best conformed to a 2- (n = 2) and a 3- compartment (n = 4) open pharmacokinetic model. The pharmacokinetic values were calculated for the overall best-fitted model, characterized as a mixed 2- and 3-compartmental model. The first and most rapid distribution half-life was 0.05 hour and a second distribution half-life was 0.35 hour. Elimination half-life was 2.89 hours, apparent volume of distribution was 11.87 +/- 4.64 L/kg, apparent volume of distribution at steady state was 4.88 +/- 2.25 L/kg, apparent volume of the central compartment was 1.17 +/- 0.70 L/kg, and total clearance was 2.47 +/- 0.78 L/kg/h.

Animals↗
PubMed1990

Influence of Rhodococcus equi on the respiratory burst of resident alveolar macrophages from adult horses.

Opsonized Rhodococcus equi activated the respiratory burst of resident alveolar macrophages (AM) from adult horses in a logarithmic-linear, mass-related manner. The effect of R equi was not significantly different from that of equal masses of opsonized zymosan A. Therefore, R equi does not appear to attenuate the respiratory burst of equine AM. The stimulatory effect of R equi was not reflected by increased production of superoxide anion (O2-), but increased activity of the hexose monophosphate shunt was observed. These results suggest a similarity between the respiratory burst of AM from horses and that of AM from rabbits. We concluded that resident AM from adult horses do not produce O2- concurrently with an increase in activity of the hexose monophosphate shunt when stimulated with either opsonized zymosan A or opsonized R equi. This suggests that O2- is not an important component of the antibacterial defenses of equine AM. Whether equine AM are incapable of producing O2- or require different stimuli to produce it was not determined.

Animals↗
PubMed1989

Laryngotracheal lesions following routine orotracheal intubation in the horse.

Sequelae of routine orotracheal intubation under clinical conditions were characterised in 38 healthy horses presented at three veterinary medical teaching hospitals. Four of these were necropsied and their tissues studied histologically. To minimise variation, 30 mm id cuffed silicone endotracheal tubes or Cole cuffless tubes were used in all patients. Fibreoptic endoscopic examination of upper respiratory and tracheal areas was accomplished pre-intubation, immediately post extubation and after 24 h. Endoscopy revealed that intubation was associated with laryngeal and/or tracheal lesions in all horses. Observations included abundant tracheal mucus, epithelial ecchymoses, basement membrane haemorrhage and mucus covered diphtheritic membrane plaques. Histological examination of lesions from the upper respiratory system of the four necropsied horses confirmed that the damage was comparable to that associated with tracheal intubation and reported in other species.

Animals↗
PubMed1988

Pharmacokinetics of N-nitrosodimethylamine in swine.

The pharmacokinetics of N-nitrosodimethylamine (NDMA) have been studied in swine. They were studied following i.v. administration of 0.1, 0.5 and 1.0 mg/kg, and following oral doses of 1.0 and 5.0 mg/kg of NDMA. Following a bolus i.v. dose, the concentration of NDMA in blood declined biphasically with a mean distribution half-life of 7 min and a mean elimination half-life of 28 min. The areas under the blood concentration versus time curves (AUC) were roughly proportional to dose indicating that the pharmacokinetics in this dose range were first order. The mean systemic clearance from blood was 65.8 ml/min/kg, the steady-state volume of distribution was 1.4 l/kg, and the mean residence time was 20 min. Following the oral doses, the AUC and peak concentration in blood were not proportional to the dose. It is likely that the pharmacokinetics at the lower dose were first order, but at the higher dose the pharmacokinetics were no longer first order because metabolism was saturated. The bioavailability of the 1.0 mg/kg dose was 67%. Since the clearance was probably due to metabolism and the clearance from blood exceeded hepatic blood flow, the high bioavailability suggests that extrahepatic metabolism plays an important role in the systemic clearance of NDMA in swine.

Animals↗
PubMed1988

Alterations in epinephrine-induced arrhythmogenesis after xylazine and subsequent yohimbine administration in isoflurane-anesthetized dogs.

Effects of xylazine (1.1 mg/kg of body weight, IV bolus, plus 1.1 mg/kg/h infusion) and subsequent yohimbine (0.125 mg/kg, IV bolus) administration on the arrhythmogenic dose of epinephrine (ADE) in isoflurane (1.8% end-tidal)-anesthetized dogs were evaluated. The ADE was defined as the total dose of epinephrine that induced greater than or equal to 4 premature ventricular contractions within 15 seconds during a 3-minute infusion period or within 1 minute after the end of infusion. Total ADE values during isoflurane anesthesia, after xylazine administration, and after yohimbine injection were 36.6 +/- 8.45 micrograms/kg, 24.1 +/- 6.10 micrograms/kg, and 45.7 +/- 6.19 micrograms/kg, respectively. Intravenous xylazine administration significantly (P less than 0.05) increased blood pressure and decreased heart rate, whereas yohimbine administration induced a significant (P less than 0.05) decrease in blood pressure. induced a significant (P less than 0.05) decrease in blood pressure. After yohimbine administration, the ADE significantly (P less than 0.05) increased above that after isoflurane plus xylazine administration. After yohimbine administration, blood pressure measured immediately before epinephrine-induced arrhythmia was significantly (P less than 0.05) less than the value recorded during isoflurane plus xylazine anesthesia. Heart rate was unchanged among treatments immediately before epinephrine-induced arrhythmia. Seemingly, yohimbine possessed a protective action against catecholamine-induced arrhythmias in dogs anesthetized with isoflurane and xylazine.

Anesthesia, Inhalation↗
PubMed1988

Pharmacokinetics of thiamylal in cats.

Pharmacokinetics of thiamylal were determined after 13.2 mg of thiamylal/kg of body weight was administered IV to 6 healthy cats. Blood samples were obtained for 12 hours. Disposition of thiamylal best conformed to 2 multicompartmental models, a 2-compartment (n = 1) and a 3-compartment (n = 5) open pharmacokinetic model. The pharmacokinetic values were calculated for the overall best-fitted model, a mixed 2- and 3-compartmental model. The first or rapid distribution half-life was 1.91 minutes and a second, or slower, distribution half-life was 26.51 minutes. The elimination half-life was 14.34 hours. The apparent volume of distribution was 3.61 +/- 1.8463 L/kg, whereas the apparent volume of the central compartment was 0.46 +/- 0.2034 L/kg, and the total clearance was 0.135 +/- 0.0616 L/kg/h.

Animals↗