Jack K. Pruett
Georgia Regents University
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Featured researches published by Jack K. Pruett.
Critical Care Medicine | 1988
Robert P. S. Introna; Jack K. Pruett; Robert C. Crumrine; Angel R. Cuadrado
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 manufacturers 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.
Anesthesiology | 1989
John R. Blair; Jack K. Pruett; Robert P. S. Introna; Robert J. Adams; Jeffery S. Balser
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.
General Pharmacology-the Vascular System | 1993
Robert P. S. Introna; Jack K. Pruett; Edmund H. Yodlowski; Edward Grover
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.
Life Sciences | 1995
Robert P. S. Introna; M. Truett Bridges; Edmund H. Yodlowski; T. Edward Grover; Jack K. Pruett
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.
General Pharmacology-the Vascular System | 1991
Robert P. S. Introna; Jack K. Pruett; Dan C. Martin; D. Josephson; M. Manabe
Abstract 1. 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. 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 > 0.26 μM are reached. 3. 3. Sodium pentothal causes coronary constriction at clinical concentrations and this effect is additive and possibly potentiated when combined with 5-HT. 4. 4. Sufentanil inhibits coronary constriction induced by the combination of sodium pentothal and 5-HT.
Anesthesia & Analgesia | 1990
Robert P. S. Introna; Dan C. Martin; Jack K. Pruett; T. E. Philpot; J. F. Johnston
Pediatric patients having corrective surgery for congenital heart defects are often difficult to manage during the first 2P48 postoperative hours. Perioperative cardiovascular instability results from several factors including the pathophysiology resulting from the primary anatomic defect, hemodynamic effects of anesthetic drugs and ventilation techniques, inadequate myocardial preservation during cardiopulmonary bypass, damage to the myocardium as a result of the surgical repair, and pulmonary vasomotor instability secondary to extracorporeal circulation. Monitoring of cardiovascular function by pulmonary artery (PA) catheterization during the critical postoperative period can guide appropriate therapeutic interventions. It is well established that the knowledge of cardiac output is helpful in making appropriate patient-care decisions after cardiac surgery (1). Damen and Wever (2) reported that data obtained with PA catheters prompted critical therapeutic interventions in 35% of 58 children undergoing cardiac surgery. Despite the common use by anesthesiologists of the flow-directed thermodilution PA catheter in adult cardiac surgery, its utilization in pediatric congenital heart surgery is infrequent. A number of reasons may contribute to this infrequent use, including difficulty in gaining central venous access, inexperience in catheter placement, concerns as to potential complications, and questions about the accuracy of the data obtained. Few technical guidelines for insertion of PA cath-
Anesthesia & Analgesia | 1995
Robert P. S. Introna; Edmund H. Yodlowski; Jack K. Pruett; Nicola Montano; Alberto Porta; Robert S. Crumrine
Anesthesiology | 1987
Blair; Jack K. Pruett; R. S. Crumrine; Balser Jj
Anesthesiology | 1988
John R. Blair; Jack K. Pruett; Robert P. S. Introna; R. J. Adams; Robert S. Crumrine
Anesthesiology | 1993
M. Truett Bridges; Robert P. S. Introna; Jack K. Pruett