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Biomedical subjects

R C Roy

Publications and source records attributed to R C Roy.

At least 19 recordsLinked to original sources
PubMed2000

Choosing general versus regional anesthesia for the elderly.

Although clinical perceptions and theoretic considerations suggest regional anesthesia should be safer than general anesthesia in elderly patients, current studies indicate no difference in outcomes. Regional anesthesia may still prove superior to general anesthesia if the right patient population or right endpoints are identified for comparison. A study of consequence of outcome, comparing the two approaches has created an expansion of the definition of anesthesia-related complications.

Aged↗
PubMed1997

Potassium channel opener-augmented cardioplegia: protection of myocyte contractility with chronic left ventricular dysfunction.

BACKGROUND: An increased number of patients with preexisting left ventricular (LV) dysfunction and congestive heart failure (CHF) are undergoing cardiac surgery with a higher risk for decreased LV contractility after hyperkalemic cardioplegic arrest. Activation of adenosine triphosphate-sensitive potassium channels by potassium channel openers (PCO) within the myocyte appears to confer a protective effect in the setting of ischemia. Accordingly, the present study was designed to determine whether PCO supplementation during hyperkalemic cardioplegic arrest would provide protective effects on myocyte contractile function, particularly in the setting of CHF. METHODS AND RESULTS: LV myocytes were isolated from control pigs (n=7) and pigs with CHF (rapid pacing, 240 beats per minute; n=7) and then assigned to the following treatment groups: normothermia (cell culture media, 2 hours, 37 degrees C); cardioplegia (24 mEq/L K+, 2 hours, 4 degrees C; then 10 minutes of reperfusion); or PCO/cardioplegia (cardioplegia supplemented with 100 micromol/L of the PCO aprikalim). Myocyte velocity of shortening was reduced in both control (66+/-2 versus 33+/-1 microm/s) and CHFmyocytes (32+/-1 versus 22+/-1 microm/s) after hyperkalemic cardioplegic arrest (P<.05). Contractility after PCO cardioplegia was similar to normothermic values in control (57+/-2 microm/s) and CHF (33+/-1 microm/s) myocytes (P<.05). Intracellular free Ca2+ increased from normothermia during hyperkalemic cardioplegia in control (81+/-4 to 145+/-7 nmol/L) and CHF (262+/-30 to 823+/-55 nmol/L) myocytes (P<.05). PCO cardioplegia attenuated the intracellular increase in free Ca2+ during the cardioplegic interval in control (110+/-6 nmol/L) and CHF (383+22 nmol/L) myocytes (P<.05). CONCLUSIONS: PCO-augmented cardioplegic arrest preserved myocyte contractility and reduced the intracellular free Ca2+ release, which therefore may be of particular benefit in the setting of preexisting LV dysfunction.

Animals↗
PubMed1997

Preservation of myocyte contractile function after hyperthermic cardioplegic arrest by activation of ATP-sensitive potassium channels.

BACKGROUND: Left ventricular (LV) dysfunction can occur after hyperkalemic cardioplegic arrest and subsequent reperfusion and rewarming. Activation of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels within the myocyte sarcolemma has been shown to be cardioprotective for myocardial reperfusion injury and ischemia and may play a contributory role in preconditioning for cardioplegic arrest. Accordingly, the present study tested the hypothesis that cardioplegic arrest and activation of KATP channels by a potassium channel opener (PCO) would attenuate alterations in ionic homeostasis and improve myocyte contractile function. METHODS AND RESULTS: Porcine LV myocytes were isolated and randomly assigned to the following treatment groups: normothermic control, incubation in cell culture media for 2 hours at 37 degrees C (n=60); hyperkalemic cardioplegia, incubation for 2 hours in hypothermic hyperkalemic cardioplegic solution (n=60); or PCO/cardioplegia, incubation in cardioplegic solution containing 100 micromol/L of the PCO aprikalim (n=60). Hyperkalemic cardioplegia and rewarming caused a significant reduction in myocyte velocity of shortening compared with normothermic control values (33+/-2 versus 66+/-2 microm/s, P<.05). Cardioplegic arrest with PCO supplementation significantly improved indices of myocyte contractile function when compared with hyperkalemic cardioplegia (58+/-4 microm/s, P<.05). Myocyte intracellular calcium increased during hyperkalemic cardioplegic arrest compared with baseline values (147+/-2 versus 85+/-2 nmol/L, P<.05). The increase in intracellular calcium was significantly reduced in myocytes exposed to the PCO-supplemented cardioplegic solution (109+/-4 nmol/L, P<.05). CONCLUSIONS: Cardioplegic arrest with simultaneous activation of KATP channels preserves myocyte contractile processes and attenuates the accumulation of intracellular calcium. These findings suggest that changes in intracellular calcium play a role in myocyte contractile dysfunction associated with cardioplegic arrest. Moreover, alternative strategies may exist for preservation of myocyte contractile function during cardioplegic arrest.

Animals↗
PubMed1997

Treatment of medically and surgically refractory angina pectoris with high thoracic epidural analgesia: initial clinical experience.

Surgical sympathectomy can relieve symptoms of angina in patients with refractory angina. However, in these high-risk patients this thoracic surgery may result in significant morbidity and mortality rates. Similar sympathetic blockade can now be produced with high thoracic epidural analgesia (HTEA). From September 1995 to August 1996, we treated 10 consecutive patients with HTEA. These eight men and two women, aged 58 +/- 5 years, with extensive three-vessel coronary disease and ejection fractions of 40% +/- 5%, had New York Heart Association (NYHA) class IV angina despite medical therapy, including nitrates, beta-blockade, calcium channel blockade, and narcotics. HTEA was performed at the T1 through T4 levels with a catheter placed either percutaneously or surgically, with radiographic confirmation of catheter placement with an epidurogram or computed tomography scan. Bupivacaine (0.25% to 0.5%), an amide local anesthetic, was given as a bolus through the epidural catheter and then maintained either as a continuous infusion or an intermittent rebolus. The epidural catheter remained in place for 7 days in four patients, 14 days in three patients, and > or =90 days in three patients. Before consideration for HTEA, each patient was deemed unsuitable for or refused coronary bypass surgery and percutaneous coronary angioplasty and had NYHA class IV symptoms of angina. Seven of 10 patients required intravenous nitroglycerin and heparin and were unable to be discharged from the intensive care unit because of anginal symptoms. Two of these seven patients also required an intraaortic balloon pump for symptom control. After HTEA, all 10 patients had improved symptoms, with five patients improving to NYHA class II symptoms and five improving to NYHA class III. All seven patients receiving intravenous nitroglycerin, heparin, or intraaortic balloon pump support had these modalities discontinued. Six of these seven patients were subsequently discharged from the hospital. One patient died from a non-HTEA related cause. There were no HTEA-related deaths. There were three catheter-related complications necessitating catheter removal during 12 months of HTEA use. Local infection developed in one patient, one had catheter occlusion caused by fibrosis, and one patient had chronic back pain exacerbation from a paraspinous muscle spasm. No patient had a myocardial infarction or a significant arrhythmia. In patients with otherwise intractable angina pectoris, HTEA is an effective modality that produces symptomatic relief of angina pectoris and allows increased activity level.

Adrenergic beta-Antagonists↗
PubMed1997

Negative and selective effects of propofol on isolated swine myocyte contractile function in pacing-induced congestive heart failure.

BACKGROUND: Although propofol (2-6 di-isopropylphenol) is commonly used to induce and maintain anesthesia and sedation for surgery, systematic hypotension and reduced cardiac output can occur in patients with or without intrinsic cardiac disease. The effect of propofol on myocyte contractility after the development of congestive heart failure (CHF) remains unknown. This study tested the hypothesis that propofol would have direct effects on myocyte contractile function in both healthy and CHF cardiac myocyte preparations. METHODS: Isolated left ventricular (LV) myocyte contractile function (shortening velocity, micron/s) was examined in myocytes from five control pigs and in five pigs with pacing-induced CHF (240 beats/min, for 3 weeks) in the presence of propofol concentrations ranging from 1-6 micrograms/ml. In addition, myocyte contractility in response to beta-adrenergic receptor stimulation (isoproterenol, 10-50 nM) in the presence of propofol (3 micrograms/ml) was examined. RESULTS: Three weeks of pacing caused LV dysfunction consistent with CHF as evidenced by increased LV end-diastolic diameter (control 3.3 +/- 0.1 cm vs. CHF 5.6 +/- 0.2 cm; P < 0.05) and reduced LV fractional shortening (control 34 +/- 3% vs. CHF 12 +/- 2%, P < 0.05). Propofol (6 micrograms/ml) caused a concentration-dependent negative effect on velocity of shortening from baseline in both control (67 +/- 2 microns/s vs. 27 +/- 3 microns/s; P < 0.05) and CHF myocytes (29 +/- 1 microns/s vs. 15 +/- 1 microns/s; P < 0.05). Importantly, CHF myocytes were more sensitive than control myocytes to the negative effects of propofol on velocity of shortening at the lower concentration (1 microgram/ml). beta-adrenergic responsiveness was reduced by propofol (3 micrograms/ml) in control myocytes only. CONCLUSIONS: Propofol has a direct and negative effect on basal myocyte contractile processes in the setting of CHF, which is more pronounced than that on healthy myocytes at reduced propofol concentrations.

Adrenergic beta-Agonists↗
PubMed1996

Direct effects of oxygenated crystalloid or blood cardioplegia on isolated myocyte contractile function.

UNLABELLED: The majority of myocardial protective techniques performed in the United States incorporate hypothermic, hyperkalemic blood or crystalloid cardioplegia. Oxygenated blood cardioplegia has not been compared with oxygenated crystalloid cardioplegia in an isolated myocyte model of hypothermic, hyperkalemic cardioplegic arrest in which direct measurements of contractile function and myocyte swelling can be made. Accordingly, isolated myocyte contractile function and myocyte profile surface area were examined after hypothermic arrest with oxygenated crystalloid or blood cardioplegia. METHODS: Isolated left ventricular pig myocytes were randomly assigned to undergo cardioplegic arrest for 2 hours at 4 degrees C. Either oxygenated crystalloid or blood cardioplegia was used. After 2 hours, myocytes were reperfused with standard cell medium at 37 degrees C and contractile function was examined. A control group of myocytes was maintained in cell medium at 37 degrees C for 2 hours. Myocyte velocity of shortening (micrometers per second) was examined at baseline and after beta-adrenergic stimulation (isoproterenol, 25 nmol/L). Velocity of shortening declined equally from baseline control values (65 +/- 2 micron n/sec) in the groups subjected to oxygenated crystalloid cardioplegia and blood cardioplegia (37 +/- 2 micron n/sec and 42 +/- 1 micron n/sec, respectively; p < 0.05). RESULTS: Although beta-adrenergic stimulation caused a significant increase in velocity of shortening in all myocyte groups, the increase was less pronounced in myocytes subjected to crystalloid cardioplegia (157 +/- 6 micron n/sec) and blood cardioplegia (159 +/- 6 micron n/sec) than in normothermic control myocytes (205 +/- microm/sec; p < 0.05). Myocyte profile surface area, an index of cell volume, was measured in all myocyte groups. Myocyte surface area increased equally after cardioplegic arrest and rewarming in both cardioplegia groups (crystalloid 4119 +/- 53 micron2; blood 3924 +/- 48 micron2); surface areas in both cardioplegia groups were significantly greater than in the normothermic control group (3158 +/- 39 micron2, p < 0.05). CONCLUSION: Equivalent effects of oxygenated crystalloid and blood cardioplegia were observed with respect to myocyte contractile function, inotropic responsiveness, and intracellular volume regulatory processes.

Animals↗
PubMed1996

Preservation of myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest with 2, 3-butanedione monoxime.

One proposed contributory mechanism for depressed ventricular performance after hypothermic, hyperkalemic cardioplegic arrest is a reduction in myocyte contractile function caused by alterations in intracellular calcium homeostasis. Because 2,3-butanedione monoxime decreases intracellular calcium transients, this study tested the hypothesis that 2,3-butanedione monoxime supplementation of the hyperkalemic cardioplegic solution could preserve isolated myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest. Myocytes were isolated from the left ventricles of six pigs. Magnitude and velocity of myocyte shortening were measured after 2 hours of incubation under normothermic conditions (37 degrees C, standard medium), hypothermic, hyperkalemic cardioplegic arrest (4 degrees C in Ringer's solution with 20 mEq potassium chloride and 20 mmol/L 2,3-butanedione monoxime). Because beta-adrenergic agonists are commonly employed after cardioplegic arrest, myocyte contractile function was examined in the presence of the beta-agonist isoproterenol (25 nmol/L). Hypothermic, hyperkalemic cardioplegic arrest and rewarming reduced the velocity (32%) and percentage of myocyte shortening (27%, p < 0.05). Supplementation with 2,3 butanedione monoxime normalized myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest. Although beta-adrenergic stimulation significantly increased myocyte contractile function under normothermic conditions and after hypothermic, hyperkalemic cardioplegic arrest, contractile function of myocytes exposed to beta-agonist after hypothermic, hyperkalemic cardioplegic arrest remained significantly reduced relative to the normothermic control group. Supplementation with 2,3-butanedione monoxime restored beta-adrenergic responsiveness of myocytes after hypothermic, hyperkalemic cardioplegic arrest. Thus, supplementation of a hyperkalemic cardioplegic solution with 2,3-butanedione monoxime had direct and beneficial effects on myocyte contractile function and beta-adrenergic responsiveness after cardioplegic arrest. A potential mechanism for the effects of 2,3-butanedione monoxime includes modulation of intracellular calcium transients or alterations in sensitivity to calcium. Supplementation with 2,3-butanedione monoxime may have clinical utility in improving myocardial contractile function after hypothermic, hyperkalemic cardioplegic arrest.

Animals↗
PubMed1996

The direct effects of propofol on myocyte contractile function after hypothermic cardioplegic arrest.

Propofol is being used more often in cardiac surgery, particularly after hypothermic, hyperkalemic cardioplegic arrest (HHCA). The purpose of this study was to examine the effects of propofol on isolated myocyte contractile function under both normothermic conditions and after simulated HHCA and rewarming. Myocytes were isolated from the left ventricle of eight pigs. Myocyte contractile function was measured under both normothermic conditions and after simulated HHCA (incubation at 4 degrees C for 2 h in crystalloid cardioplegia; K+ = 24 mEq/L) using computer-assisted videomicroscopy in the presence of 2, 4, and 6 micrograms/mL propofol (11.2, 22.4, and 33.6 microM/L, respectively). Isoproterenol (25 nM) was then added and contractile function measurements repeated. Propofol caused significant dose-dependent reductions in myocyte velocity of shortening (baseline = 67 +/- 2 microns/s; propofol = 2 micrograms/mL, 45 +/- 4 microns/s; and propofol = 6 micrograms/mL, 27 +/- 3 microns/s; P < 0.05). HHCA and rewarming caused a significant reduction in myocyte velocity of shortening (29 +/- 0.9 microns/s, P < 0.05), with further significant dose-dependent reductions in contractile function after the addition of propofol. Propofol caused a decrease in beta-adrenergic responsiveness under normothermic conditions, but not after simulated HHCA. Results from the present study demonstrated for the first time that the reduction in isolated myocyte contractile function after simulated HHCA is further decreased by propofol administration.

Adrenergic beta-Agonists↗
PubMed1995

Use of esophageal or precordial stethoscopes by anesthesia providers: are we listening to our patients?

STUDY OBJECTIVE: To ascertain current anesthesia utilization of esophageal and precordial stethoscopes in U.S. anesthesia training programs. DESIGN: Prospective, single-blind, incidence study. SETTING: Operating rooms of three tertiary care hospitals with major academic anesthesiology departments. SUBJECTS: Anesthesia faculty [MD and certified registered nurse-anesthetist (CRNA) staff] and anesthesia trainees (anesthesiology residents and student nurse-anesthetists). INTERVENTIONS: observe and record the placement (stethoscope device appropriately positioned) and utilization (stethoscope in place and connected to the ear piece of the anesthesia provider) of the esophageal or precordial stethoscope during general, regional, and monitored anesthesia care. MEASUREMENTS AND MAIN RESULTS: During 520 anesthetics, an esophageal stethoscope was inserted in 68% of subjects, a precordial stethoscope was positioned in 16%, and an anesthetic stethoscope was absent in 16% of cases. Utilization (stethoscope connected to earpiece) ranged from a low of 11% of cases to a high of 45%, depending on the institution. Overall, providers were listening via an anesthetic stethoscope in only 28% of anesthetics. CONCLUSIONS: Our data suggest infrequent utilization of esophageal and precordial stethoscopes in anesthesia training institutions. Thus, current anesthesia training may be fostering an environment where providers overlook a valuable minimally invasive, and cost-effective continuous monitor of patients' dynamic vital organ function.

Anesthesia Department, Hospital↗
PubMed1995

The direct and interactive effects of phosphodiesterase inhibition and beta-adrenergic stimulation on myocyte contractile function after hypothermic cardioplegic arrest.

The direct and interactive effects of phosphodiesterase inhibition (PDEI) and beta-adrenergic receptor (beta AR) stimulation on isolated myocyte contractile function were examined after hypothermic, hyperkalemic, cardioplegic arrest (HHCA) and under normothermic conditions. Left ventricular (LV) myocytes were isolated from porcine hearts and myocyte contractile function was measured under normothermic conditions (37 degrees C in standard media) and after HHCA (2 h at 4 degrees C in Ringer's solution with 24 mEq KCl) with subsequent rewarming. Myocytes were then randomly assigned to treatment with the beta AR agonist isoproterenol (25 nM), the phosphodiesterase inhibitor amrinone (50 microM), or a combination of these compounds and contractile function measurements repeated. Baseline myocyte contractile function was reduced by 32% after HHCA. Isoproternol alone increased myocyte contractile function more than 100% under both normothermic conditions and after HHCA, whereas amrinone alone significantly (60%) improved myocyte contractile function only after HHCA. Amrinone preincubation followed by isoproterenol improved contractile function after HHCA to a greater extent than all other treatment protocols. In contrast, combination treatment under normothermic conditions did not augment myocyte contractile function relative to isoproterenol alone. These findings suggest that amrinone has differential effects on contractile processes. Moreover, the marked improvement of contractile function after HHCA with PDEI pretreatment followed by beta AR stimulation may have implications in treatment strategies for improving myocardial function after cardiopulmonary bypass and provide insight into contractile dysfunction after HHCA.

Adrenergic beta-Agonists↗
PubMed1995

Myocyte contractile responsiveness after hypothermic, hyperkalemic cardioplegic arrest. Disparity between exogenous calcium and beta-adrenergic stimulation.

BACKGROUND: Acute left ventricular dysfunction is commonly encountered after hypothermic, hyperkalemic cardioplegic arrest (HHCA) and often requires inotropic intervention for successful separation from cardiopulmonary bypass. However, the basic mechanisms involved in depressed left ventricular function and the cellular basis for the differential effects of inotropic drugs after HHCA are unknown. Accordingly, the goal of this study was to determine the effects of calcium (Ca2+) and beta-adrenergic receptor agonists (beta AR) stimulation on isolated myocyte contractile function after HHCA. METHODS: Myocytes were isolated from the left ventricle of nine pigs and randomly assigned to one of the following treatment groups: (1) normothermic, control: incubation in oxygenated cell culture media for 2 h at 37 degrees C; and (2) cardioplegia: incubation in 4 degrees C crystalloid cardioplegia for 2 h, followed by rewarming. Steady-state myocyte contractile function was measured after pulse stimulation at baseline, in the presence of extracellular Ca2+ (3-10 mM), and in the presence of the beta AR agonist isoproterenol (2-100 nM). Myocyte profile surface area was measured for both normothermic myocytes and myocytes after HHCA. In a separate set of experiments, myocyte contractile function also was documented after 2 h of hypoxic conditions with both normothermic incubation and HHCA, in the presence and absence of beta AR stimulation. RESULTS: Baseline myocyte contractile function was significantly less in the cardioplegia group compared to control. Extracellular Ca2+ produced a dose-dependent significant increase in myocyte contractile function in the normothermic control group, whereas increased extracellular Ca2+ only minimally increased myocyte contractile function in the cardioplegia group. A dose-dependent, significant increase in myocyte contractile function was observed in both groups after beta AR stimulation by isoproterenol; however, myocyte contractile function in the cardioplegia group was decreased compared to the control group. Hypoxia under normothermic conditions significantly reduced myocyte contractile function, myocyte relaxation, and beta-adrenergic responsiveness. Hypoxia in combination with cardioplegic arrest compounded the negative effects on contractile processes but did not further impair beta-adrenergic responsiveness. Myocyte profile surface area was significantly increased after HHCA. CONCLUSIONS: The minimal improvement in myocyte contractile function after HHCA with increased extracellular Ca2+ suggests that Ca2+ depletion is not the primary mechanism for depressed myocyte contractility after HHCA. On the other hand, because beta AR administration improved myocyte contractile function after HHCA, the cellular basis for the effects of beta AR stimulation after HHCA is probably not increased myocyte Ca2+ but rather alternative mechanisms, such as changes in myofilament sensitivity to Ca2+. These results also suggest that the abnormalities in left ventricular function after HHCA result from the direct effects of hyperkalemic induced electromechanical uncoupling as well as relative hypoxic conditions.

Adrenergic beta-Agonists↗
PubMed1994

Clinical pearls in the anaesthetic management of elderly patients.

Recently published information is changing the approach of anaesthetists to pulmonary aspiration prophylaxis, drug dosing, hypertension during general anaesthesia, hypotension during spinal and epidural anaesthesia, intraoperative hypothermia, and postoperative ileus in elderly patients. Routine aspiration prophylaxis is no longer recommended. Lower drug doses are required to achieve the same endpoints in the elderly as in younger patients. Greater use of antihypertensive drugs rather than additional doses of anaesthetic agents is recommended during general anaesthesia to avoid myocardial depression or prolonged emergence. Routine preoperative volume loading prior to spinal and epidural anaesthesia is being questioned. Tolerance of mean arterial pressures of 65 mmHg during spinal and epidural anaesthesia is encouraged even in patients with hypertension. The adverse effects of inadvertent intraoperative hypothermia are discussed, including the conversion of vecuronium from an intermediate to a long-acting neuromuscular blocking agent. Spinal or epidural local anaesthetics with or without spinal or epidural opioids and ketorolac are associated with less postoperative ileus than postoperative analgesia based on opioids administered intravenously or intramuscularly. Finally, improving postoperative care will reduce perioperatively mortality to a greater extent than reducing intraoperative anaesthesia-related complications.

Aged↗
PubMed1993

Identification of patients at risk for excessive blood loss during coronary artery bypass surgery: thromboelastography versus coagulation screen.

In light of the potential morbidity associated with transfusion of blood products, a reliable preoperative screening test to identify cardiothoracic surgical patients who are at potential risk for increased intraoperative blood loss would be useful. Accordingly, we examined the efficacy of a variety of coagulation tests to predict intraoperative blood loss in 60 patients presenting for coronary artery bypass surgery (CABG). A complete coagulation screen, activated clotting time (ACT), and thromboelastograph (TEG) were performed before surgery. Intraoperative blood loss was determined by weighing sponges and measuring the quantity of blood in suction canisters. The duration of cardiopulmonary bypass was 100 +/- 4 min, and total surgery time was 5.0 +/- 0.1 h. Total crystalloid and colloid requirements were 5.5 +/- 0.2 and 1.4 +/- 0.1 L. Forty-eight percent of the patients required blood with an average requirement of 2.5 +/- 0.5 units. Total intraoperative blood loss averaged 1590 +/- 95 mL with a range from 640 to 3928 mL. Using multiple linear regression, all coagulation and TEG variables were used to model perioperative blood loss. Results showed that all components of the TEG failed to predict blood loss (r < 0.25, P > 0.78). However, three components of the routine coagulation assay, including bleeding time, prothrombin time, and platelet count could be modeled to predict perioperative blood loss (r = 0.75, P < 0.05). Although TEG has been shown to have potential in identifying postcardiopulmonary bypass coagulopathies, these results suggest that it does not appear to be useful in determining the coagulation status of CABG patients preoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗