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Biomedical subjects

J K Pruett

Publications and source records attributed to J K Pruett.

At least 19 recordsLinked to original sources
PubMed1995

Direct effects of fentanyl on canine coronary artery rings.

The potent opioid fentanyl, is commonly used as a general anesthetic for coronary artery bypass surgery. Experiments were designed to determine the direct effects of fentanyl on unstimulated coronary artery tissue. Isolated, endothelium denuded canine epicardial rings were suspended in physiologic tissue baths. Changes in tension were measured as the concentration of fentanyl was increased. Fentanyl caused increases in ring tension at concentrations of 10(-6)M-10(-4)M, then caused a decrease in tension at 10(-3) M. Calcium channel blockade by 10(-7)M nifedipine abolished all increases in contractile responses to fentanyl and prevented the relaxation in tension produced by fentanyl. The fentanyl dose-response curve was unchanged by opioid receptor blockade with 10(-6)M naloxone and by alpha and beta adrenoceptor blockade produced by 10(-6)M prazosin and 10(-6)M propranolol. Muscarinic blockade with 10(-6)M atropine and cyclooxygenase inhibition by 10(-6)M indomethacin attenuated the constrictor response to fentanyl. The opioids alfentanil, sufentanil, morphine, and naloxone all produced a dose-response similar to fentanyl that varied only in amplitude. These findings indicate that increasing concentration of the anesthetic opioid fentanyl can cause biphasic changes in basal canine epicardial coronary artery ring tension. These responses are calcium dependent and may be characteristics of other opioid agonists and antagonists.

Adrenergic alpha-Antagonists↗
PubMed1993

Direct effects of propofol (2,6-diisopropylphenol) on canine coronary artery ring tension.

1. The direct effect of the intravenous general anesthetic propofol (2,6-diisopropylphenol) on epicardial coronary artery tone was studied in unstimulated canine coronary artery rings. 2. Rings stretched to a basal tension of 5 g and exposed to increasing concentrations of propofol generated a characteristic dose-dependent biphasic change in tension-concentrations from 10(-7) to 10(-5) M resulted in constriction (+477 +/- 118 mg) while concentrations 10(-4) and 10(-3) M resulted in relaxation (-682 +/- 75 mg). 3. The response to propofol was reversible and was not modified by the presence of endothelium, alpha 1 and beta adrenoceptor blockade or TEA sensitive potassium channel blockade. 4. The propofol induced changes in tension were altered by changes in extracellular calcium concentrations as well as by blockade of the voltage dependent calcium channel by verapamil. 5. These experiments suggest that clinical concentrations (human) of propofol may have direct vasoactive effects on epicardial coronary artery smooth muscle and that these effects may be due to actions on voltage dependent calcium channels of vascular smooth muscle.

Animals↗
PubMed1993

Test-tube equilibration of volatile anaesthetic concentrations.

We have measured concentrations of volatile anaesthetics after injection into test-tube assay solutions. In non-agitated tubes, aqueous anaesthetic concentrations decreased significantly throughout 40 min of incubation. Agitation (20-s vortex) of the tubes decreased the aqueous anaesthetic concentration by approximately 80% from concentrations in non-agitated tubes and resulted in more stable liquid anaesthetic concentrations over time. A decrease of less than 15% occurred between 10 and 50 min of incubation.

Enflurane↗
PubMed1991

Effects of sodium pentothal and sufentanil on serotonin induced constriction of canine coronary artery rings without endothelium.

1. The individual and combined effects of sufentanil and sodium pentothal on canine coronary artery vasomotor responses to 5-HT were studied in an isolated vascular ring preparation. 2. Clinical concentrations of sufentanil have little effect on basal coronary tension or constriction induced by either 5-HT or sodium pentothal individually, until very high doses greater than 0.26 microM are reached. 3. Sodium pentothal causes coronary constriction at clinical concentrations and this effect is additive and possibly potentiated when combined with 5-HT. 4. Sufentanil inhibits coronary constriction induced by the combination of sodium pentothal and 5-HT.

Anesthetics↗
PubMed1989

Cardiac electrophysiologic effects of fentanyl and sufentanil in canine cardiac Purkinje fibers.

The electrophysiologic effects of high concentrations of the opioid agonists, fentanyl and sufentanil, on isolated canine cardiac Purkinje fibers were studied. Changes in action potential parameters were examined at the following concentrations: fentanyl 94.6 nM, 0.19 microM, and 0.95 microM; sufentanil 8.6 nM, 86.4 nM, 0.17 microM, and 0.26 microM. Naloxone 5.5 microM was administered after maximal changes were induced by fentanyl in order to explore the possibility of an opioid receptor interaction. Action potential parameters measured were Vmax of phase 0, amplitude, overshoot, maximum diastolic potential, action potential duration at 50%, and 90% repolarization and membrane responsiveness. Fentanyl 0.19 microM and sufentanil-0.17 microM caused a significant lengthening of action potential duration at 50 and 90% repolarization, 6.4% and 7.3%, and 10.2% and 12.4%, respectively, P less than 0.05. Other action potential parameters were not significantly affected by the opioids. Naloxone 5.5 microM alone did not alter action potential characteristics and failed to reverse action potential prolongation produced by fentanyl. The authors suggest that fentanyl and sufentanil prolong action potential duration in canine cardiac Purkinje fibers via direct membrane actions.

Action Potentials↗
PubMed1988

Use of the Walton-Brodie strain gauge arch to measure contractile force during anaesthesia.

The Walton-Brodie strain gauge arch is an instrument that quantitatively measures CF. Like many methods, the strain gauge arch is affected by loading conditions and heart rate. Nevertheless, this methodology, when properly used, has proved very useful in describing the direct action of anaesthetic drugs. Knowledge from strain gauge arch use has stimulated research to explain the negative inotropic effect of anaesthetics and helped clinicians understand the cardiovascular effects of drugs that they may wish to use.

Anesthesia↗
PubMed1988

Use of transthoracic bioimpedance to determine cardiac output in pediatric patients.

The use of a transthoracic bioimpedance monitor to determine cardiac output was evaluated in critically ill children. The children ranged in age from 10 months to 8 yr and their height and weight ranged from the third to the 97th percentile. Each child had a thermodilution catheter in place to monitor cardiac output. The bioimpedance monitor used in this study, the NCCOM-3, required the input of a constant (L), which was obtained for each individual patient by adjusting the L setting until cardiac output measured by bioimpedance (COBI) was within 10% of cardiac output measured by thermodilution (COTD). This method of determining L was superior to using either measured thoracic length or the manufacturer's guidelines to obtain L and resulted in an excellent correlation between COTD and COBI (r = .94; p less than .05; n = 59). In children less than 125 cm in height, measured thoracic length alone was inadequate to use for L but provided a good approximation of L when multiplied by 1.25. This study suggests that the use of transthoracic bioimpedance to determine cardiac output compares favorably with thermodilution techniques and it is noninvasive.

Cardiac Output↗
PubMed1983

Effects of halothane and enflurane on right ventricular performance in hearts of dogs anesthetized with pentobarbital sodium.

The effects of enflurane and halothane on contractile force of the right ventricle were compared using the Walton-Brodie strain gage arch and pulmonary artery catheter data in dogs anesthetized with pentobarbital. Twenty mongrel dogs were studied to determine the effects of the two anesthetics on contractile force during a 30-minute exposure to four approximate multiples of MAC: 0.75, 1.0, 1.25, and 2.0, and during a 2-h exposure to 1.0 MAC of each agent. Both anesthetics caused a dose-dependent reduction in contractile force, cardiac output, and mean arterial blood pressure. Enflurane caused greater depression of all variables at all concentrations tested. After a 30-min exposure to 0.75, 1.0, 1.25, and 2.0 MAC, halothane depressed contractile force 33.9%, 37.9%, 46.1%, and 73.4%, respectively, and enflurane depressed contractile force 48.4%, 53.5%, 66.6%, and 81.3%, respectively. The depression produced by enflurane at 1.0 and 1.25 MAC was significantly greater (P less than 0.05) than the depression produced by halothane at equal MAC. The reduction of cardiac output by enflurane at 1.25 and 2.0 MAC was significantly greater than that observed with halothane (P less than 0.05). The decrease in mean blood pressure produced by enflurane was significantly greater (P less than 0.05) than the decrease produced by halothane at 1.0, 1.25, and 2.0 MAC. No significant differences between groups were found in temperature, arterial PCO2, PO2, pH, or hematocrit levels. No diminution of the differences in effect on contractility between the two agents was observed when the exposure period was lengthened to two hours at 1.0 MAC.

Anesthesia, General↗
PubMed1980

Propranolol effects on membrane repolarization time in isolated canine Purkinje fibers: threshold tissue content and the influence of exposure time.

This study has examined the relationship between the Purkinje fiber content of propranolol and effects on membrane repolarization time during prolonged exposure to low concentrations of propranolol in vitro. Canine Purkinje fibers were exposed to both dl-propranolol, 3.4 X 10(-7) M (0.1 microgram/ml) and 1.7 X 10(-6) M (0.5 micrograms/ml), and to d-propranolol, 3.4 X 10(-7) M (0.1 micrograms/ml), in Tyrode's solution for 90 to 180 min. Purkinje fibers exhibited continuous decreases in repolarization time throughout the exposure periods and fibers analyzed for propranolol content demonstrated continuous cumulation of the drug with time. A maximum 8% decrease in repolarization time was observed after 3.4 X 10(-7) M and a 30% decrease after 1.7 X 10(-6) M propranolol. A 40-fold cumulation of propranolol by the Purkinje fibers was found after both concentrations at or near equilibrium. A high degree of correlation (r = 0.98; P < .001) existed between changes in electrical activity and tissue content of propranolol. Extrapolation to zero effect showed a threshold tissue content of propranolol of approximately 1.0 microgram/g, which corresponds to a bath concentration of 25 ng/ml (8 X 10(-8) M). Changes in membrane potentials were the result of direct membrane effects of propranolol, based on the fact that d-propranolol produced membrane alterations and tissue cumulation identical to those produced by the racemic drug.

Action Potentials↗
PubMed1978

Influence of alterations in sinus rate on determination of drug-induced changes in ventricular automaticity.

The interrelationship between drug-induced changes in heart rate and drug-induced alterations in ventricular automaticity was studied in dogs with intact conduction systems and dogs with surgically-induced complete heart block. The effects of epinephrine (0.5 microgram-kg-1-min-1) and propranolol (1.0 mg-kg-1) on ventricular automaticity were shown to be partially concealed by heart rate changes produced by these agents. Partial concealment of ventricular automaticity changes was shown to result from an alteration in the degree of overdrive suppression secondary to rate changes. Changes in the degree of overdrive suppression have a masking effect on drug-induced alterations in ventricular automaticity and only when the degree of suppression was held constant could the full extent of drug effects on ventricular automaticity be determined. Following vagal stimulation or rapid pacing, the rate of recovery from overdrive suppression as measured by the number of ventricular beats in 30 s was shown to be a dependable index of ventricular automaticity. It was concluded that determinations of drug effects on ventricular automaticity should take into account changes in heart rate produced by the drug. A method for determining ventricular automaticity is described which matches overdrive suppression during the control period to that during drug action in order to cancel out the influence of changes in heart rate on ventricular automaticity.

Animals↗