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Biomedical subjects

C A DiFazio

Publications and source records attributed to C A DiFazio.

At least 55 records · Page 3Linked to original sources
PubMed1982

Cardiovascular effects of nalbuphine in patients with coronary or valvular heart disease.

Although the hemodynamic changes produced by small doses of nalbuphine given to patients with cardiac disease are minimal, the cardiovascular effects of large doses which have been used as supplements for general anesthesia have not been investigated. Cardiovascular variables were measured after incremental doses of nalbuphine, up to 2 or 3 mg/kg in fourteen patients with coronary artery disease with normal left ventricular function and in seven patients with mitral valve disease. No significant changes in cardiac index, stroke work index, mean arterial pressure, pulmonary diastolic or wedge pressure, heart rate, or central venous pressure occurred in the preoperative period. However, nalbuphine alone did not produce surgical anesthesia and the addition of diazepam, nitrous oxide, or halothane was required in all patients. The addition of halothane coupled with surgical stimulation significantly decreased cardiac and stroke indices, increased mean arterial and pulmonary wedge pressures, and increased systemic vascular resistance in patients with coronary artery disease. In patients with mitral valve disease, following surgical incision, there were small but significant decreases in cardiac index and left ventricular stoke work index, and increases in systemic vascular resistance. Despite its lack of deleterious hemodynamic effects, the place of nalbuphine in the armamentarium of the anesthesiologist must be limited to use as a premedicant, as an adjunct to balanced anesthesia, or for postoperative pain relief.

Adult↗
PubMed1982

Evaluation of the analgesic effect and urinary excretion of systemic bupivacaine in man.

Bupivacaine was infused intravenously into healthy volunteers to assess its analgesic effect. In a double-blind manner, 11 male subjects received, on separate days, saline solution or 0.1% bupivacaine, at three rates of infusion. Experimental pain was produced by the tourniquet-induced ischemia test. Times to onset of ischemic pain (threshold) and unbearable pain (tolerance) were compared. Venous blood samples were analyzed for levels of bupivacaine and its metabolite, pipecolyxylidine, by gas chromatography. No significant difference in pain threshold or tolerance was found following control and bupivacaine infusion. In the 72-hour postinfusion urine collection period, only 0.7% of the infused dose was recovered as unmetabolized bupivacaine, with 4.8% recovered as pipecolyxylidine. Systemic blood levels of bupivacaine achieved during regional anesthesia did not produce analgesia in this model.

Adult↗
PubMed1981

The effects of lidocaine on the whole body distribution of radioactively labeled microspheres in the conscious rat.

Radioactively labeled 15-micrometer microspheres were used to evaluate the effects of intravenous lidocaine on cardiac output and distribution of tissue blood flow in awake rats. After a one-hour control period, all animals (n = 22) received 85Sr-labeled microspheres for a control measurement. The animals were then divided into three groups. The control group (n = 6) received a bolus of saline and then an infusion of saline. After 40 minutes, a second microsphere (141Ce) was injected, the animals killed, and tissue blood flow determined. A second group of rats (n = 8) were similarly treated except that they received a bolus and infusion of lidocaine resulting in a plasma concentration of 1.98 +/- 0.3 microgram of lidocaine/ml. A third group of rats (n = 8) received a higher dose of lidocaine which resulted in a plasma concentration of 6.37 +/- 0.3 microgram of lidocaine/ml. In the control and low-dose lidocaine group, there were no changes in blood pressure, heart rate, cardiac output or tissue blood flow. At the higher lidocaine concentration, blood pressure remained the same but cardiac output and heart rate were decreased. Tissue blood flow to brain, heart and muscle was responsible for the increased peripheral resistance. These results suggest that high blood concentrations of lidocaine alter flow to vital organs in the rat.

Animals↗
PubMed1981

Anesthetic potency of nalbuphine and interaction with morphine in rats.

The contribution to anesthesia by nalbuphine was determined in rats by measurement of the reduction in the anesthetic requirement for cyclopropane produced by increasing doses of nalbuphine while maintaining a constant level of anesthesia (MAC). The respiratory effect of nalbuphine was evaluated by measurement of arterial PCO2 at this constant MAG level. The response produced by the addition of morphine to a constant dose of nalbuphine in further reducing the cyclopropane anesthetic requirement was also evaluated, as was the effect on arterial PCO2. The anesthetic contribution of nalbuphine was dose dependent until a plateau contribution of 0.22 MAC was achieved. Arterial PCO2 increased to a plateau level of 48 torr with nalbuphine administration from a PCO2 of 41 torr with cyclopropane alone. Further increase in PCO2 did not occur until exceedingly high nalbuphine doses were used. Morphine did not supplement the anesthetic contribution of nalbuphine, and there was no increase in PCO2 when morphine was added in nalbuphine during cyclopropane anesthesia. These results suggest that nalbuphine produces analgesia by acting at kappa opioid receptors and that nalbuphine binds but produces minimal effects on mu opioid receptors within the central nervous system.

Anesthesia, Intravenous↗
PubMed1980

Lidocaine as an analgesic for experimental pain.

The purpose of this study was to evaluate the analgesic contribution of intravenously administered lidocaine and to correlate it with blood levels of the drug. In a double-blind manner, 14 healthy male volunteers received saline solution or lidocaine, 0.2 per cent, at three increasingly greater rates of infusion on two separate days. Experimental pain was produced by means of the submaximal tourniquet-induced ischemia test of Beecher and Smith. The times to the onset of ischemic (threshold) and unbearable (tolerance) pain were recorded for three control trials to two tests for the same end points during each infusion rate. Between the two ischemic trials, while the test solution continued to be infused, venous blood samples were drawn and analyzed for lidocaine by gas chromatography. No statistically significant difference in analgesia between the control and lidocaine values for threshold or tolerance was observed at blood levels from 1 to 3 micrograms/ml. The data suggest that lidocaine at these blood levels produces sedation but not analgesia.

Analgesics↗
PubMed1977

Effects of lidocaine on the anesthetic requirements for nitrous oxide and halothane.

The effects of various plasma concentrations of lidocaine on nitrous oxide anesthesia in man and halothane requirements in the dog were studied. The response to incision of the skin was observed in 20 patients who were anesthetized with nitrous oxide, 70% inspired, and oxygen, 30%, plus various plasma levels of lidocaine. In addition, changes in the MAC of halothane in dogs were observed at various levels of lidocaine. In both circumstances lidocaine concentrations of 3 to 6 microgram/ml decreased anesthetic requirements approximately 10 to 28%. At clinically common concentrations of lidocaine, significant decreases in anesthetic requirements should be anticipated.

Adolescent↗
PubMed1975

Lidocaine and its metabolites in the newborn.

Concentrations of lidocaine and its metabolites were measured chromatographically in the blood and urine of mothers and babies after epidural administration of lidocaine to the mother for cesarean delivery. Delivery occurred a mean time of 29.83 plus or minus 8.64 minutes after a mean dose of 398.33 plus or minus 63.38 mg to the mother, at which time mean maternal venous plasma concentration was 1.70 plus or minus 0.77 mug/ml. Of the total molar quantity of lidocaine and metabolite recovered from the newborns' urine in the first 12 hours of life, 50.63 per cent appeared as unchanged lidocaine, while 49.37 per cent appeared as metabolites. In the second 12 hours of life, 23.37 per cent appeared as unchanged lidocaine, while 76.63 per cent appeared as metabolites. We conclude that the greater proportion of metabolite excretion in the second 12 hours is evidence that the new born is capable of metabolizing lidocaine.

Anesthesia, Epidural↗