R W McIntyre

Duke University Medical Center, Durham, NC, United States

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Publications (25)101.88 Total impact

  • D A Schwinn, R W McIntyre, J G Reves
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    ABSTRACT: Isoflurane is a potent systemic vasodilator. Because isoflurane vasodilation is clinically significant, we sought to explore whether decreases in systemic vascular resistance caused by isoflurane involve the alpha-adrenergic nervous system in humans. Specifically, we tested the hypothesis that isoflurane systemic vasodilation is mediated via inhibition of vascular alpha 1-adrenergic responsiveness. Phenylephrine pressor dose-response curves were established before anesthesia and during isoflurane/oxygen anesthesia in patients undergoing coronary artery bypass surgery; all patients included in the study (n = 11) demonstrated significant (P = 0.0001) decreases in systemic vascular resistance when isoflurane was given in concentrations adequate to produce a 20% decrease in mean arterial blood pressure. Polynomial regression of the phenylephrine dose-response curve was used to estimate the phenylephrine dose required to increase mean arterial blood pressure 15 mm Hg, designated PD15 mm Hg. Each patient served as his or her own control. Preanesthetic baseline PD15 mm Hg values (115 +/- 23 micrograms [1.4 +/- 0.3 micrograms/kg], mean +/- SEM) were not significantly different from isoflurane PD15 mm Hg values (124 +/- 20 micrograms [1.5 +/- 0.3 micrograms/kg]). End-tidal isoflurane concentration ranged from 0.6%-1.5%; isoflurane PD15 mm Hg was not correlated with end-tidal isoflurane concentration. Patient characteristics and hemodynamics did not affect PD15 mm Hg. These results suggest that isoflurane-induced systemic vasodilation is not mediated via inhibition of alpha 1-adrenergic responsiveness, disproving our hypothesis. This finding has clinical importance because it demonstrates that alpha 1-adrenergic stimulation with phenylephrine is effective in correcting hypotension in patients receiving isoflurane anesthesia.
    Anesthesia & Analgesia 12/1990; 71(5):451-9. · 3.42 Impact Factor
  • Debra A. Schwinn, R. William McIntyre, J. G. Reves
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    ABSTRACT: The effect of intravenous (IV) nitroglycerin (NTG) on perioperative myocardial ischemia as detected by single pass radionuclide angiocardiography was studied in 20 patients scheduled for elective coronary artery bypass grafting (CABG). Ten patients, selected at random, received IV NTG 1 microgram.kg-1.min-1 (NTG group) and 10 others, IV saline (control group). Anesthetic induction consisted of midazolam 0.2 mg.kg-1, vecuronium 0.1 mg.kg-1, and 50% N2O in O2. ECG leads I, II, and V5 were monitored for ST segment changes. Single pass radionuclide angiocardiography (RNA) was performed at 5 times: prior to induction, prior to tracheal intubation, and at 1, 3.5, and 6 min following intubation. The presence of new regional wall motion abnormalities (RWMA) was determined from each RNA study as compared with the preinduction measurement. Apart from one patient in the control group who developed a new "v" wave after intubation, there was no evidence of ischemia by pulmonary capillary wedge pressure. No ECG evidence of ischemia was detected in any patient. Despite this, new regional wall motion abnormalities were observed in 3 patients in the control group and 1 patient in the NTG group. Blood pressure and heart rate responses of patients with new RWMA were not significantly different from other patients. The low incidence of ischemia in this population precludes a definitive statement regarding the efficacy of IV NTG, but the lower incidence of RWMA in the NTG group suggests a protective effect.
    Anesthesia & Analgesia 07/1989; 68(6):718-23. DOI:10.1213/00000539-198906000-00004 · 3.42 Impact Factor
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    ABSTRACT: Cerebral blood flow was measured in 20 patients by xenon 133 clearance methodology during nonpulsatile hypothermic cardiopulmonary bypass to determine the effect of age on regional cerebral blood flow during these conditions. Measurements of cerebral blood flow at varying perfusion pressures were made in patients arbitrarily divided into two age groups at nearly identical nasopharyngeal temperature, hematocrit value, and carbon dioxide tension and with equal cardiopulmonary bypass flows of 1.6 L/min/m2. The range of mean arterial pressure was 30 to 110 mm Hg for group I (less than or equal to 50 years of age) and 20 to 90 mm Hg for group II (greater than or equal to 65 years of age). There was no significant difference (p = 0.32) between the mean arterial pressure in group I (54 +/- 28 mm Hg) and that in group II (43 +/- 21 mm Hg). The range of cerebral blood flow was 14.8 to 29.2 ml/100 gm/min for group I and 13.8 to 37.5 ml/100 gm/min for group II. There was no significant difference (p = 0.37) between the mean cerebral blood flow in group I (21.5 +/- 4.6 ml/100 gm/min) and group II (24.3 +/- 8.1 ml/100 gm/min). There was a poor correlation between mean arterial pressure and cerebral blood flow in both groups: group I, r = 0.16 (p = 0.67); group II, r = 0.5 (p = 0.12). In 12 patients, a second cerebral blood flow measurements was taken to determine the effect of mean arterial pressure on cerebral blood flow in the individual patient. Changes in mean arterial pressure did not correlate with changes in cerebral blood flow (p less than 0.90). We conclude that age does not alter cerebral blood flow and that cerebral blood flow autoregulation is preserved in elderly patients during nonpulsatile hypothermic cardiopulmonary bypass.
    Journal of Thoracic and Cardiovascular Surgery 05/1989; 97(4):541-7. DOI:10.1097/00132586-198912000-00044 · 3.99 Impact Factor
  • R W McIntyre, D A Schwinn
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    ABSTRACT: This report has reviewed some of the cardiovascular aspects of ANP. The emergence of the heart as an endocrine organ requires that numerous questions be asked with regard to the importance of ANP to anesthesia and surgery. It is clear that the interaction of the hormone with other vasoactive compounds, including anesthetic agents, requires further elucidation. The accumulation of more information regarding the regulation of ANP and its cardiovascular setting will define its role in hemodynamic homeostasis in the acute clinical setting. Questions of specific interest to the anesthesiologist that require elucidation are: (1) Does the presence of abnormal ANP levels, associated with specific disease states, affect perioperative cardiovascular function? (2) Do cardiac surgery and CPB affect ANP-adrenergic interaction? (3) What is the relationship among blood volume, blood pressure, cation metabolism, and the ANP-renin-angiotensin system in perioperative patients? (4) What is the role of ANP as a therapeutic modality in surgical patients?
    Journal of Cardiothoracic Anesthesia 03/1989; 3(1):91-8. DOI:10.1016/0888-6296(89)90018-5
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    ABSTRACT: Elevated catecholamines and beta-adrenergic receptor hyporesponsiveness (or desensitization) have been demonstrated in failing human myocardium, but the role of the alpha-adrenergic receptor remains unclear. The authors tested the hypothesis that alpha 1-adrenergic responsiveness decreases in patients with impaired ventricular function undergoing coronary artery revascularization. Impaired ventricular function was defined prospectively by left ventricular ejection fraction less than or equal to 40% (group I, n = 12), and normal ventricular function by ejection fraction greater than 40% (group II, n = 22). Phenylephrine (Phe) pressor dose-response curves were established prior to anesthesia, during fentanyl anesthesia, and during fentanyl anesthesia plus hypothermic cardiopulmonary bypass at the time of aortic cross-clamp (anes + CPB/AXC). Polynomial regression of the Phe dose response curve estimated the Phe dose required to increase mean arterial blood pressure 20%, designated PD20. Although pre-anesthesia PD20 and anes + CPB/AXC PD20 values were not affected by ejection fraction, significant differences in PD20 (P less than 0.05) between groups occurred during fentanyl anesthesia (group I = 2.28 +/- 1.60 micrograms.kg-1, group II 1.57 +/- 0.98 micrograms.kg-1; mean +/- SD). Anes + CPB/AXC was associated with a significant reduction in PD20 in both groups compared with pre-anesthesia (P less than 0.01). Our results suggest impairment of alpha 1-adrenergic responsiveness occurs during fentanyl anesthesia in patients with ejection fractions less than or equal to 40% (evidenced by greater PD20 values). Although this impairment may be due to altered Phe pharmacokinetics, these results also support the possible existance of alpha 1-adrenergic receptor desensitization in this group. Reduction in PD20 during anes + CPB/AXC in all patients points to more powerful effects than fentanyl anesthesia alone; such influencing effects may include hemodilution, hypothermia, elevated plasma catecholamines, exclusion of the pulmonary circulation, or altered Phe pharmacokinetics.
    Anesthesiology 09/1988; 69(2):206-17. · 6.17 Impact Factor
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    ABSTRACT: In this investigation, the hypothesis was tested that patients with valvular heart disease have higher atrial natriuretic peptide (ANP) plasma levels than patients with coronary artery disease during cardiac surgery. Six patients scheduled for valve replacement (group V) and seven scheduled for coronary artery bypass grafting (CABG) (group C) were studied. ANP plasma levels and hemodynamic measurements were obtained at several times during surgery. ANP levels were elevated in both groups compared to those measured in healthy volunteers; and ANP levels in valvular patients were found to be higher than in the CABG patients. In addition, isotonic fluid loading, rewarming during cardiopulmonary bypass, and weaning from cardiopulmonary bypass increased ANP from baseline in group C. Mean arterial pressure and ANP levels correlated in group C. Ejection fraction, pulmonary artery diastolic pressure, and right atrial pressure did not correlate with ANP levels in either group. In conclusion, patients with valvular heart disease have higher ANP levels during surgery compared to patients with coronary artery disease. This difference probably relates to different pressure and volume loads on atrial tissue.
    Journal of Cardiothoracic Anesthesia 07/1988; 2(3):274-80. DOI:10.1016/0888-6296(88)90305-5
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    ABSTRACT: Early endotracheal extubation has been shown to be a safe postoperative management option in patients having cardiac operations. However, few objective data exist on the response of ventricular performance to early termination of controlled ventilation. Seven patients undergoing routine elective coronary artery bypass grafting or adult repair of atrial septal defect were studied after intraoperative placement of left ventricular micromanometers, left ventricular minor axis dimension crystals, and left atrial and intrapleural pressure catheters. Physiologic data were recorded intraoperatively, during controlled mandatory ventilation in the intensive care unit, and during spontaneous respiration immediately after extubation. Extubation to spontaneous breathing was associated with a significant decline in intrapleural pressure and significant increases in left ventricular end-diastolic diameter, ejection diameter shortening, stroke work, and cardiac output. The augmented left ventricular diastolic filling seemed to result from the fall in intrapleural pressure and perhaps from normalization of right ventricular afterload. The preload recruitable stroke work relationship showed that myocardial contractility remained constant after extubation, and ventricular function improved primarily because of increased preload associated with shifting of the capacitance blood volume toward the chest. Thus endotracheal extubation enhances cardiac performance after uncomplicated cardiac surgical procedures, and by this mechanism early extubation may be clinically beneficial as a routine adjunct to postoperative care.
    Journal of Thoracic and Cardiovascular Surgery 06/1988; 95(5):819-27. DOI:10.1097/00132586-198902000-00034 · 3.99 Impact Factor
  • Anesthesiology 01/1988; 69(2). DOI:10.1097/00000542-198808000-00009 · 6.17 Impact Factor
  • Anesthesia & Analgesia 01/1988; 67(Supplement):197. DOI:10.1213/00000539-198802001-00197 · 3.42 Impact Factor
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    ABSTRACT: Calcium entry blocking drugs (CaEBs) produce vasodilation and, in high doses, modify alpha adrenergic receptor function. Previous laboratory data suggested that CaEBs might alter the response to alpha-adrenergic stimulation. The authors tested the hypothesis that CaEB therapy altered alpha-adrenergic responsiveness in patients chronically treated with CaEBs. Twenty-six consenting patients with coronary artery disease were given a phenylephrine challenge before anesthesia induction and during cardiopulmonary bypass while the aorta was cross-clamped. A log dose response curve was constructed for each patient, and the ED30 (dose producing 30% increase in systemic vascular resistance) was calculated. Nine patients not treated with CaEB served as controls, and 17 patients were treated with nifedipine (n = 7) or diltiazem (n = 10). Mean ED30 was increased approximately three-fold in the CaEB treated groups compared to the control group. However, there was no statistical difference in the ED30 or phenylephrine dose response slopes between CaEB treated and untreated patients. In awake patients, ED30 correlated with nifedipine levels (R = 0.953, P = 0.01). There was a significant (P less than .02) shift in the ED30 from prior to anesthesia to during aortic cross-clamp and cardiopulmonary bypass; ED30 was approximately 50% less and correlated with CaEB level (R = 0.713, P = 0.03). Hemodynamic variables were not different between groups at any interval. Our data suggest that vascular responsiveness to phenylephrine in patients treated with CaEBs is diminished, but similar to that in untreated patients. Vascular responsiveness decreases in awake patients with increasing nifedipine levels.
    Anesthesiology 11/1987; 67(4):485-91. · 6.17 Impact Factor
  • Anesthesiology 10/1987; 67(4). DOI:10.1097/00000542-198710000-00007 · 6.17 Impact Factor
  • R. William McIntyre
    Anesthesiology 04/1987; 66(3):443-4. DOI:10.1097/00000542-198703000-00047 · 6.17 Impact Factor
  • Anesthesia & Analgesia 01/1987; 66(Supplement):S111. DOI:10.1213/00000539-198702001-00111 · 3.42 Impact Factor
  • K. D Ossey, Eric Hawkins, J. G. Reves, R. W. McIntyre
    Anesthesiology 01/1987; 67. DOI:10.1097/00000542-198709001-00596 · 6.17 Impact Factor
  • Anesthesia & Analgesia 01/1987; 66(Supplement):S114. DOI:10.1213/00000539-198702001-00114 · 3.42 Impact Factor
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    ABSTRACT: Eighteen patients with normal left ventricular function scheduled for elective myocardial revascularization were anesthetized with fentanyl (52-58 micrograms/kg). At the beginning of hypothermic cardiopulmonary bypass (CPB) they were assigned to a control (C) group (n = 6) that did not receive further anesthesia, or to a group given either 1% isoflurane (n = 6) or 2% isoflurane (n = 6). Blood samples for measurement of total plasma cortisol concentrations were obtained before, during, and after CPB. Hemodynamic measurements before and after CPB were not different among groups. Patients in group C required higher infusion rates of sodium nitroprusside (P less than or equal to 0.05) and patients given 2% isoflurane received more phenylephrine (P less than or equal to 0.05) to keep mean arterial pressure at 50 +/- 10 mm Hg during CPB. Isoflurane caused a dose-related decrease in total plasma cortisol concentrations during and after CPB. We conclude that increased depth of anesthesia attenuates the cortisol (stress) response to cardiopulmonary bypass.
    Anesthesia & Analgesia 12/1986; 65(11):1117-22. DOI:10.1213/00000539-198611000-00004 · 3.42 Impact Factor
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    ABSTRACT: Substantial investigation has failed to define the mechanism of adverse cardiovascular responses to protamine.1 These responses appear to have an immunologic basis. Vasoactive compounds are probably released after exposure or reexposure to protamine or heparin-protamine complex. We document a case of acute pulmonary hypertension after protamine administration associated with massive increases in prostaglandins. This contrasts with basal low levels after cardiopulmonary bypass for coronary revascularization in normal patients, who showed no hemodynamic response to protamine.
    The American Journal of Cardiology 11/1986; 58(9):857-8. DOI:10.1016/0002-9149(86)90371-1 · 3.43 Impact Factor
  • Journal of Cardiovascular Pharmacology 01/1986; 8(6). DOI:10.1097/00005344-198611000-00063 · 2.11 Impact Factor