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Biomedical subjects

W J Tranquilli

Publications and source records attributed to W J Tranquilli.

At least 73 records · Page 4Linked to original sources
PubMed1985

Anesthetic potency of nitrous oxide in young swine (Sus scrofa).

Determination of nitrous oxide (N2O) potency was accomplished by extrapolation using the concepts of minimum alveolar concentration (MAC) and additivity among inhalation anesthetics. Halothane and isoflurane anesthetic requirement (alveolar concentration) necessary to achieve MAC in 9 pigs decreased with each successive increase in the percentage of inspired N2O (25%, 50%, 75%). Halothane and isoflurane MAC was determined to be 0.94 +/- 0.03 and 1.75 +/- 0.01 volumes percent, respectively. Halothane and isoflurane requirements decreased to 0.74 +/- 0.02, 0.66 +/- 0.02, and 0.58 +/- 0.02; and to 1.56 +/- 0.02, 1.38 +/- 0.02, and 1.08 +/- 0.03 volumes percent with 25%, 50%, and 75% N2O, respectively. The line of best fit derived from regression analysis of the combined data (isoflurane and halothane MAC values) had a correlation coefficient of 0.987 and an X intercept equivalent to 195% N2O. The potency of N2O in pigs was similar to that of other domesticated mammals and reduced halothane and isoflurane anesthetic requirements by approximately 50% of the reduction observed in human beings.

Anesthesia, Inhalation↗
PubMed1985

Influence of nifedipine on xylazine-induced acute pressor response in halothane-anesthetized dogs.

Effects and interaction of nifedipine (Ca channel blocker) and xylazine (mixed alpha agonist) during halothane anesthesia were examined in 6 dogs. After achievement of steady-state halothane (1.35%) anesthesia, blood pressure (BP) and heart rate (HR) were recorded in these dogs during 3-minute saline or nifedipine (20 micrograms/kg) infusion periods. Seven minutes after the end of saline or nifedipine infusion, xylazine (1.1 mg/kg of body weight) was infused over a 2-minute period. After saline pretreatment, xylazine administration increased diastolic BP (33.67 +/- 3.91 mm of Hg) and decreased HR. Nifedipine infusion induced a transient reduction in BP, accompanied by a more persistent increase in HR. Compared with saline pretreatment, nifedipine pretreatment significantly decreased the acute increase in diastolic BP (33.67 +/- 3.91 vs 14.00 +/- 2.94 mm of Hg) which occurred during xylazine injection. After saline and nifedipine infusions, xylazine administration decreased HR 30 +/- 15.02 and 36.5 +/- 10.36 beats/min, respectively. A pronounced sinus arrhythmia and/or 2nd-degree atrioventricular block developed in all dogs during xylazine injection after saline infusion. Arrhythmias were not observed in the dogs after nifedipine infusion. Nifedipine's Ca blocking action depressed xylazine-induced acute vasoconstriction and concomitant increase in diastolic BP. Because alpha 2-, but not alpha 1-adrenoceptor-mediated vasoconstriction is Ca-dependent, these results indicate that a portion of the acute pressor response induced by IV xylazine in halothane-anesthetized dogs may be alpha 2-mediated. Seemingly, nifedipine-induced hypotension and damping of xylazine-induced increases in BP attenuated xylazine's actions on cardiac rate and rhythm.

Anesthesia, General↗
PubMed1985

Cardiopulmonary effects of an intravenous infusion of guaifenesin, ketamine, and xylazine in dogs.

A 5% solution of dextrose in water containing 50 mg of guaifenesin, 0.25 mg of xylazine, and 1 mg of ketamine/ml was infused IV at the rate of 2.2 ml X kg-1 X hour-1 in dogs. Heart rate, systemic vascular resistance, mean arterial blood pressure, rate-pressure product, and arterial oxygen tension were not altered significantly from baseline values during 2 hours of anesthesia. Cardiac index was significantly (P less than 0.05) decreased from base-line values. Hypoventilation resulted in increased arterial carbon dioxide tension and decreased arterial pH. After the dogs were given glycopyrrolate, cardiac index returned to base line, and heart rate, mean arterial pressure, and rate-pressure product were significantly greater (P less than 0.05) than base-line values.

Anesthesia, General↗
PubMed1984

Halothane-sparing effect of xylazine in dogs and subsequent reversal with tolazoline.

Halothane MAC (the minimum alveolar concentration of halothane to produce anaesthesia in 50% of the animals tested) was determined to be 0.92 +/- 0.16 volumes % in eight English Pointer dogs. Alterations in halothane MAC induced by an intravenous bolus of xylazine (1.1 mg/kg) and then tolazoline (5 mg/kg) was determined in each dog following control (halothane MAC) measurement. Following xylazine administration, MAC significantly decreased to 0.57 +/- 0.023%. Immediately following determination of the xylazine-halothane MAC value in each dog, tolazoline was administered and the halothane requirement (MAC) was again assessed. Halothane MAC significantly increased to 1.24 +/- 0.036%. Tolazoline administration induced immediate arousal in the xylazine-halothane anaesthetized dogs requiring a rapid increase in halothane concentration to maintain anaesthesia. Thus, the administration of tolazoline, an alpha adrenergic antagonist, following xylazine administration significantly increased the anaesthetic requirement (MAC) of halothane. Xylazine, an alpha 2 adrenergic agonist, decreased halothane anaesthetic requirement (MAC) in the eight dogs studied. These results are consistent with the hypotheses that stimulation of central alpha 2 receptors is the mechanism by which xylazine produces sedation and that inhibition of CNS excitatory neurotransmitter release decreases halothane anaesthetic requirement.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1984

Hyperglycemia and hypoinsulinemia during xylazine-ketamine anesthesia in Thoroughbred horses.

Plasma glucose and serum insulin concentrations in Thoroughbreds administered xylazine hydrochloride (1.1 mg/kg; IV) and ketamine hydrochloride (2.2 mg/kg; IV) at dosages sufficient to induce short periods of recumbency and anesthesia were measured. Samples of blood were collected from 6 adult horses before, during, and after the anesthetic period. Plasma glucose (mg/dl) was significantly increased above control (-30 minute concentration) from 15 to 150 minutes after xylazine administration with the peak value occurring at 30 minutes. Serum insulin (microU/ml) was significantly decreased from control from 5 to 90 minutes after xylazine administration, with the nadir occurring at 15 minutes. The alterations in plasma glucose and serum insulin concentrations in xylazine-ketamine-anesthetized horses were similar to the changes in xylazine-sedated horses.

Anesthesia↗
PubMed1983

Organ blood flow and distribution of cardiac output in hypocapnic ketamine-anesthetized swine.

Organ blood flow and distribution of cardiac output (CO) were determined in 9 awake (control) and ketamine-anesthesized swine (4 mg/kg bolus followed by continuous infusion of 0.3 mg/kg/min, IV), using 15 micron diameter radionuclide-labeled microspheres. Absolute values of blood flow (per 100 g basis) were determined for various organs and peripheral tissues. Internal organs of the swine, which constituted 8.25 +/- 0.79% of the total body mass, received 55.83 +/- 5.13% of the CO. The fraction of CO received by brain, heart, kidneys, liver (via hepatic artery), and gastrointestinal tract was 1.10%, 2.67%, 19.84%, 11.81%, and 16.84%, respectively. During ketamine anesthesia, the fraction of CO perfusing the kidneys and liver (hepatic artery) increased from control and values for brain, heart, and splanchnic organs remained unchanged. Blood flow (per unit weight) of brain, cardiac, and splanchnic organs decreased; kidney and skeletal muscle blood flow was unaltered; and hepatic arterial blood flow increased from the awake (control) values. The hyperdynamic state often associated with ketamine anesthesia was not evident in these pigs during intermittent positive-pressure ventilation resulting in hypocapnia.

Anesthesia, Inhalation↗
PubMed1982

Systemic and regional blood flow distribution in unanesthetized swine and swine anesthetized with halothane + nitrous oxide, halothane, or enflurane.

In order to study the distribution of cardiac output during various anesthetic regimens, we measured regional organ blood flow using 15 micrometers diameter radionuclide-labeled microspheres injected into the left atrium. Studies were carried out in nine pigs during resting unanesthetized state (control), during halothane (inspired concentration = 1.25 per cent) + nitrous oxide (50 per cent) anesthesia, during halothane (inspired concentration = 2.25 per cent) anesthesia, and during enflurane (inspired concentration = 4.0 per cent) anesthesia. The order of the last two treatments [halothane (2.25 per cent) and enflurane (4.0 per cent)] was randomized among the nine pigs. All anesthetic steps employed intermittent positive-pressure ventilation to maintain PaCO2 close to control values. Animals were allowed to recover towards the control state before changing to the next anesthetic regimen. Forty-five minutes were allowed for equilibration with each anesthetic regimen before hemodynamic measurements were made. In unanesthetized resting swine blood flow received by brain, cardiac ventricles, kidneys, liver (via hepatic artery), gastrointestinal tract, and skeletal muscle was 63.70 +/- 5.56, 128.56 +/- 14.92, 280.89 +/- 19.72, 21.95 +/- 3.25, 148.55 +/- 15.29 and 13.76 +/- 4.12 ml . min-1 . 100 g-1, respectively (mean +/- SEM). Corresponding values for the percentage of cardiac output received by the brain, cardiac ventricles, kidneys, liver (via hepatic artery), and gastrointestinal tract were 1.13 +/- .08, 3.04 +/- 0.13, 12.95 +/- 1.54, 4.27 +/- 0.76, and 18.71 +/- 0.91 per cent, respectively. Cardiac output and mean arterial blood pressure decreased significantly from control values with each of the three anesthetized steps. The decrease in cardiac output was greatest with the halothane anesthesia and least with halothane + N2O. Blood flow per unit weight of the cardiac, renal, and splanchnic tissues decreased significantly with each anesthetic regimen whereas brain blood flow and hepatic arterial blood flow were unaltered from control values. Thus, the per cent cardiac output received by the brain had increased with halothane (119 per cent) and enflurane (102 per cent) anesthesia while it was unaltered from the heart, renal, and splanchnic organs. Percentage of total cardiac output received by liver via the hepatic artery increased by 162 per cent during halothane anesthesia and 133 per cent during enflurane anesthesia, when compared to control values. During halothane + nitrous oxide anesthesia, the per cent of cardiac output going to the brain was not increased significantly. It is concluded that cardiac output as well as individual organ/tissue blood flow was better maintained during halothane + nitrous oxide anesthesia in comparison to halothane or enflurane anesthesia.

Animals↗
PubMed1982

Regional myocardial blood flow and coronary vascular reserve in unanesthetized young calves exposed to a simulated altitude of 3500 m for 8--10 weeks.

We determined regional myocardial blood flow (15-micrometer tracer microspheres) and hemodynamics in nine normal calves, seven calves with right ventricular (RV) hypertrophy induced by pulmonary artery banding (PAB) at sea level, and five calves exposed to simulated high altitude (HA) of 3,500 m (PB = 500 mm Hg) for 8--10 weeks. Progression of RV hypertrophy was very rapid in HA calves. RV weight:body weight ratio of 2.74 +/- 0.20 g/kg at 8--10 weeks of sojourn at HA significantly exceeded that in PAB calves (1.98 +/- 0.11 g/kg) 20 weeks post-banding. All calves were studied unanesthetized at sea level before (control) and during maximal coronary vasodilation (iv adenosine; 4 microM/kg per min). Normal and HA calves were also studied during acute hypoxemia (PaO2: 42 +/- 1 mm Hg) induced by administration of 12--13% O2 + N2 in the inhaled gas. RV myocardial blood flow was significantly increased only in PAB calves, whereas in HA calves it was similar to that in normal calves. Left ventricular (LV) mass and blood flow were identical in three groups of calves. Polycythemia did not occur in HA calves. Minimal coronary vascular resistance per unit weight of the hypertrophied RV was identical to that in the normal RV myocardium. This suggested that, despite very fast progression of RV hypertrophy in HA calves, functional cross-sectional area of the RV coronary vascular bed kept pace with the increase in cardiac mass. Minimal coronary vascular resistance per unit weight of the left ventricular myocardium was also identical in three groups of calves. This suggested that chronic hypoxemia by itself did not cause an increase in the functional cross-sectional area of the LV coronary vascular bed. Acute hypoxemia resulted in a significant increase in myocardial blood flow in all calves, but in HA calves, RV endo:epi perfusion ratio decreased below 1.00. Transmural RV myocardial blood flow and RV systolic pressure in HA calves during acute hypoxemia significantly exceeded that in normal calves.

Altitude Sickness↗
PubMed1982

Organ blood flow and distribution of cardiac output in nonanesthetized swine.

Organ blood flow and distribution of cardiac output (CO) were determined in awake resting swine, using radionuclide-labeled 15-micrometer diameter microspheres. Absolute values of blood flow (per 100-g basis) were determined for various organs and peripheral tissues. Internal organs of the swine, which constituted 8.25 +/- 0.79% of the total body mass, received 45.46 +/- 2.64% of the resting CO. The fraction of CO received by brain, heart, kidneys, liver (via hepatic artery), and gastrointestinal tract was 1.13%, 3.04%, 12.95%, 4.27%, and 18.71%, respectively.

Animals↗
PubMed1981

A technique for catheterisation of the coronary sinus in adult ponies (Equus caballus).

Long-term catheterisation of the coronary sinus using a specially designed catheter was accomplished in 6 ponies via a right lateral thoracotomy. The catheter comprised a 10 to 12 cm long stiff segment (Teflon) joined to a 100 cm length of pliable medical grade (vinyl) tubing. Catheters were kept functional up to 10 weeks postoperatively. Location of the catheter tip was verified by determining the oxygen tension of anaerobically withdrawn blood samples. Normal values of oxygen tension of the coronary sinus blood in ponies were similar to those reported for the dog, whereas oxygen content was significantly lower.

Animals↗
PubMed1981

Chronic catheterization of coronary sinus in large domestic animals.

A technique was developed for long-term catheterization of the coronary sinus in calves and ponies. A catheter with a 10 to 12 cm-long stiff segment was implanted via right lateral thoracotomy. Catheters were kept patent up to 10 weeks after the surgical procedure. At that time, location of the catheter tip was confirmed both by determining oxygen tension of the anaerobically sampled blood and by radiography. Base-line values of oxygen venous blood of non-anesthetized calves and ponies are reported.

Animals↗
PubMed1981

Surgical technique and considerations for implantation of electromagnetic blood flow transducer and occluder onto the coronary arteries.

A technique was developed for the implantation of an electromagnetic flow probe and vascular occluder onto the right and left coronary arteries in the calf and pony. Surgical manipulation was well tolerated in the animals. The subcutaneous housing on the peripheral ends of these devices of the lateral thoracic wall served as a maintenance-free technique for chronic exteriorization of these devices. Implantation onto the coronary arteries required a surgical technique which accomplished the prerequisites for proper flow probe function. A reactive hyperemic response was elicited in each animal by implanting an inflatable vascular occluder distal to the flow probe. The correct function of these devices postoperatively established the feasibility of this surgical technique for implanting these devices on the coronary arteries for chronic studies of coronary circulation.

Animals↗
PubMedDate not supplied

The hemodynamic response of calves to tiletamine-zolazepam anesthesia.

Six isoflurane-anesthetized calves were instrumented for hemodynamic studies and allowed to recover from anesthesia. When the mean arterial blood pressure rose to 100 mmHg or when vigorous movement occurred, a 1:1 tiletamine-zolazepam mixture (4 mg/kg) was administered intravenously (IV). Values for cardiac output, cardiac index, stroke index, central venous pressure, and right ventricular stroke work index did not change significantly. Systolic, mean, and diastolic arterial blood pressures and systemic vascular resistance were significantly decreased below baseline at 5 minutes; they were significantly increased above baseline at 20 minutes and remained so throughout the 60 minute study. Changes in left ventricular stroke work index and rate pressure product were similar to those of arterial blood pressure and systemic vascular resistance, although they were not significant. Heart rate and pulmonary capillary wedge pressure decreased significantly but gradually returned to baseline at 40 minutes and then increased significantly above baseline by the end of the study. Minor venous-arterial shunting or perhaps mismatching of ventilation and perfusion appeared to have developed in the later stages of the study. This was reflected in a minor increase in the arterial partial pressure of carbon dioxide (PaCO2) and a decrease in the arterial partial pressure of oxygen (PaO2) and arterial pH. At the dose administered, the hemodynamic changes induced by tiletamine-zolazepam were minimal and were compatible with safe anesthesia in calves.

Anesthesia↗
PubMedDate not supplied

Evaluation of three midazolam-xylazine mixtures. Preliminary trials in dogs.

The depressant effects of midazolam and xylazine on the central nervous system (CNS) were evaluated in 12 dogs. Xylazine was administered to six dogs (1.1 mg/kg intravenously [IV]) followed in 5 minutes by midazolam (1.0 mg/kg intramuscularly [IM]). In a second group of six dogs, xylazine (2.2 mg/kg IM) was followed in 5 minutes by midazolam (1.0 mg/kg IV). Both drug regimens induced rapid and profound sedation or anesthesia. Duration of action varied with the doses and routes of administration. Dogs given the high dose of xylazine IM had an arousal time of 95.4 +/- 8.9 minutes and a walking time of 155.4 +/- 8.8 minutes. These values exceeded the IV xylazine values threefold. Partial reversal of CNS depression was accomplished with either a benzodiazepine antagonist (flumazenil) or an alpha-2 antagonist (yohimbine). In a separate trial, a mixture of xylazine (0.55 mg/kg), midazolam (1.0 mg/kg), and butorphanol (0.1 mg/kg) with and without glycopyrrolate was evaluated in eight dogs. As with the xylazine-midazolam combinations, the CNS depressant effect of this mixture was clinically indistinguishable from anesthesia achieved with other rapid-acting injectable agents. Clinical signs of CNS depression were readily and completely antagonized by the simultaneous injection of flumazenil and yohimbine.

Anesthesia↗