Search PubMed⌕ Search

Biomedical subjects

E Lowenstein

Publications and source records attributed to E Lowenstein.

At least 73 records · Page 4Linked to original sources
PubMed1985

Perioperative anesthetic risk of noncardiac surgery in hypertrophic obstructive cardiomyopathy.

To determine their perioperative risk, we reviewed the records of 35 patients with hypertrophic cardiomyopathy diagnosed by cardiac ultrasound and/or catheterization who underwent general (52) or spinal (four) anesthesia--a total of 56 major surgical procedures. There were no operative or related perioperative deaths and no significant ventricular tachyarrhythmias. Intraoperative or postoperative complications included: myocardial infarction with heart failure in one patient who also had coronary artery disease and was one of three patients who had spinal anesthesia, arrhythmia requiring therapy in eight, and angina during supraventricular tachycardia in one. We conclude that the risk of general anesthesia and major noncardiac surgery is low in patients with hypertrophic obstructive cardiomyopathy. Spinal anesthesia, which decreases systemic vascular resistance and increases capacitance, may be relatively contraindicated. Concomitant coronary artery disease may increase the risk.

Adolescent↗
PubMed1985

The effect of adding mannitol or albumin to a crystalloid cardioplegic solution: a prospective, randomized clinical study.

To determine if the myocardial protection afforded by a cold crystalloid potassium cardioplegic solution could be improved by the addition of either mannitol or albumin, a prospective clinical study was undertaken in which 58 patients undergoing elective aortocoronary bypass were randomized to one of three groups. Each group featured a different cardioplegic solution. The solutions were a standard potassium crystalloid solution, a solution containing mannitol sufficient to raise the osmolality by 20 to 30 mOsm, and a solution containing 5% albumin. Preoperative, intraoperative, and postoperative evaluation included serial measurements of ejection fraction, myocardial-specific isoenzyme, and hemodynamic indexes of performance. Electrocardiographic evaluation for perioperative myocardial infarction and the need for postoperative inotropic and mechanical support were also included. No differences were found among the groups. Therefore, although the use of mannitol or albumin has been shown to be beneficial in an experimental setting, superiority of either additive could not be demonstrated clinically.

Albumins↗
PubMed1985

Postsystolic shortening of canine left ventricle supplied by a stenotic coronary artery when nitrous oxide is added in the presence of narcotics.

The effects of fentanyl and sufentanil with and without N2O on left ventricular myocardium supplied by a critically narrowed and a normal coronary artery were studied in 16 dogs. Regional ventricular function was measured by recording ventricular segment length with the use of ultrasonic length detectors in the left anterior descending (LAD) and the left circumflex (LC) coronary artery territories before and during critical stenosis of the LAD. Critical stenosis was documented by the absence of a hyperemic response following a 10-s total occlusion of the LAD. Hemodynamic variables (aortic flow and pressure, left ventricular pressure, heart rate, and coronary blood flow) were measured and the first derivative of left ventricular pressure (LVdP/dt) and coronary perfusion pressure derived. Eight dogs received fentanyl 100 micrograms X kg-1 followed by an infusion of 1 microgram X kg-1 X min-1 while ventilated with O2:N2 (1:2), and eight dogs received sufentanil 30 micrograms X kg-1 with an infusion of 0.3 micrograms X kg-1 X min-1. Replacement of N2 with N2O produced evidence of mild systolic myocardial depression but no dysfunction in either group. After application of the critical constriction, the addition of N2O rapidly produced evidence of dysfunction with significant postsystolic shortening only in the LAD territory. This was not accompanied by hypotension or a decrease in coronary flow and was not always reversible. Higher infusion rates of either narcotic (fentanyl 2 micrograms X kg-1 X min-1, 4 micrograms X kg-1 X min-1; sufentanil 0.6 micrograms X kg-1 X min-1, 1.2 micrograms X kg-1 X min-1) in the absence of N2O did not produce dysfunction but had no protective effect when N2O was added.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1983

Temperature gradients and rewarming time during hypothermic cardiopulmonary bypass with and without pulsatile flow.

Pulsatile perfusion during cardiopulmonary bypass (CPB) has been reported to have a number of beneficial effects, including attenuation of hormonal stress responses and improved organ blood flow and function. To determine the effect of pulsatile perfusion on temperature gradients and the time required for cooling and rewarming during CPB, we studied 21 patients scheduled for elective coronary artery operations. The patients were divided into two comparable groups: Group 1 (N = 11) had standard nonpulsatile perfusion, while in Group 2 (N = 10), a pulsatile pump was used. Rectal and esophageal temperatures were monitored, as were deltoid muscle temperatures and upper arm and finger skin temperatures in the same extremity. Ambient temperature, bypass flow and pressure, and bypass time were similar in both groups. Time required to cool to the lowest esophageal temperature was virtually identical for both groups (Group 1, 17 +/- 3 min; Group 2, 17.6 +/- 5 min), as was rewarming time (Group 1, 26.8 +/- 11 min; Group 2, 27.2 +/- 6 min). There were no significant differences in temperature measurements between groups except briefly during rewarming when finger skin temperature rose more rapidly in Group 1 (p less than 0.05). Temperature changes following CPB were the same for both groups, with rectal and esophageal temperatures showing an inverse relationships. These data demonstrate that pulsatile flow does not substantially alter rewarming time or temperature gradients during hypothermic CPB.

Aged↗
PubMed1983

The effect of halothane anesthesia on myocardial necrosis, hemodynamic performance, and regional myocardial blood flow in dogs following coronary artery occlusion.

The effect of halothane anesthesia on myocardial necrosis resulting from coronary artery ligation was examined in 28 anesthetized mongrel dogs. In 18 dogs, the left anterior descending coronary artery (LAD) was ligated immediately proximal to the first apical diagonal branch, and 1 h later the dogs were assigned randomly either to receive halothane, 0.5-1.0% inspired in room air for 12 h (n = 10) or to awaken without further intervention (control, n = 8). Infarct size was measured by staining the myocardium with triphenyl tetrazolium chloride 24 h after LAD ligation. Infarct size in halothane-treated dogs was 17.8 +/- 2.0% of the left ventricle, compared with 27.3 +/- 3.3% in control dogs (P less than 0.05). Myocardial salvage was present transmurally but was greatest in epicardial regions. In 10 additional dogs, hemodynamic variables (heart rate, arterial pressure, left ventricular end-diastolic pressure, peak left ventricular dP/dt, tension-time index, and rate-pressure product) were measured or calculated, and radionuclide-labeled microspheres were injected for measurement of cardiac output and regional myocardial blood flow (RMBF). Thirty minutes after LAD ligation and after initial hemodynamic measurements and microsphere injection, these dogs were assigned randomly to receive either halothane, 1.0%, inspired in room air (n = 5) or no intervention (control, n = 5). After 15 min of halothane inhalation (45 min after LAD ligation in control dogs), measurements were repeated. Halothane inhalation reduced heart rate, arterial pressure, and indexes of left ventricular contractile and pump performance. During halothane treatment, RMBF declined in normal myocardium but not in ischemic regions, while neither normal nor ischemic zone RMBF changed in control dogs. Systemic vascular resistance was unchanged in either group. Thus, halothane was associated with a 35% smaller myocardial infarct, transmural myocardial salvage, reduced heart rate, reduced left ventricular contractile and pump performance, reduced RMBF to nonischemic regions, and unchanged RMBF in the ischemic myocardium.

Anesthesia, Inhalation↗
PubMed1983

Effects of leukotrienes B4 and C4 on coronary circulation and myocardial contractility.

Arachidonic acid is metabolized to prostaglandins and thromboxane via the cyclooxygenase pathway and to leukotrienes B4, C4, D4, and E4 via the lipooxygenase pathway. A possible role played by leukotrienes in cardiogenic shock resulting from anaphylaxis prompted us to investigate the action of these compounds on coronary vessels and myocardial contractility. In this study leukotriene B4 (LTB4) and C4 (LTC4) were injected directly into the left circumflex (LCx) coronary artery of nine anesthetized Suffolk sheep. LTB4 had no effect on coronary artery blood flow or myocardial contractility, but 3 X 10(-9) mole induced profound transient circulating neutropenia, reflecting the potent chemotactic and chemokinetic properties of this compound. Injecting as little as 1.6 X 10(-11) mole of LTC4 caused a 14.5 +/- 4.3% (mean +/- SE) reduction of LCx coronary artery flow while 1.6 X 10(-10) mole caused a 26.5 +/- 3.7% decrease of LCx coronary artery flow and an 18.1 +/- 3.2% decrease in systolic shortening of the myocardial region supplied by the LCx coronary artery. Since the decrease in systolic shortening was far greater than that expected on the basis of the reduction in coronary artery flow, we postulate that LTC4 has a direct negative inotropic effect. FPL 55712, a receptor antagonist of leukotrienes C4, D4, and E4, blocked the vasoconstriction induced by LTC4 but only partially blocked the negative inotropic effects of LTC4. LTC4 is a potent vasoconstrictor and negative inotropic agent and may play an important role in anaphylactic shock.

Animals↗
PubMed1983

Temperature gradients in cardiac surgical patients--a comparison of halothane and fentanyl.

Narcotics and potent inhalation anesthetics have different effects on thermoregulation and the distribution of body heat. This study was designed to compare the effect of halothane vs fentanyl anesthesia on temperature gradients developed during and after hypothermic cardiopulmonary bypass. Twenty-two adult patients undergoing coronary artery surgery were given either fentanyl (100 micrograms/kg) or halothane (0.5-1.5%) and oxygen. Thermistor probes were inserted in rectum, esophagus, and deltoid muscle. Surface temperatures were measured on the ring finger and upper arm. All patients were cooled during cardiopulmonary bypass to 28 degrees C, and ambient temperature was maintained at 22-23 degrees C. The times to cool and rewarm were comparable in both groups. Rectal, esophageal, and skin temperatures had not reached equilibrium by 60 min after bypass, but changes in temperature were virtually identical at all sites in both groups. Regardless of differences in the effects of halothane and fentanyl on hormonal responses, blood flow, or central thermoregulation, their net effects on body temperature were the same.

Adult↗
PubMed1983

Respiratory distress syndrome with new considerations.

To help maximize the salvage rate of patients with ARDS, radiologists must become active participants in a multidisciplinary team. A clear understanding of the nature of ARDS is a prerequisite. The authors briefly consider the pathogenesis of the syndrome and then discuss at length the usefulness of plain radiography and balloon occlusion pulmonary angiography in examining the patient with ARDS.

Angiography↗
PubMed1983

Haemodynamic effects of bolus injections of atracurium in patients with coronary artery disease.

Atracurium has been reported to have minimal haemodynamic effects in healthy patients. The purpose of this study was to determine its effects in patients with coronary artery disease. Sixteen patients scheduled for elective coronary artery surgery were studied in two equal groups. Group 1 received a bolus injection of atracurium 0.3 mgkg-1 and group 2 0.4 mgkg-1. Under local anaesthesia, radial artery, pulmonary artery thermodilution and central venous catheters were placed and the appropriate vascular pressures continuously monitored, as were leads II and V5 of the electrocardiogram. Sleep was induced with lorazepam and fentanyl while the patients were breathing nitrous oxide in oxygen (50:50). Control measurements of arterial pressure (AP) (mean, systolic, diastolic), CO (thermodilution), CVP, PA, PCW and HR were obtained. Atracurium was administered as a bolus and measurements repeated at 2, 5, and 10 min. In group 1 mean and diastolic arterial pressure decreased significantly at 2 min (73 +/- 2 to 66 +/- 3 mm Hg, P less than 0.05; 58 +/- 3 to 51 +/- 2 mm Hg, P less than 0.05). The changes were not significant at 5 or 10 min. There were no significant changes in CO or SVR. One patient in this group exhibited a typical histamine response with vasodilatation and flushing. In this patient mean arterial pressure decreased from 70 to 55 mm Hg and CO increased from 4.90 to 7.24 litre min-1. Excluding this patient from group 1 eliminated the significance of the haemodynamic changes for the rest of the group (MAP = 73 +/- 2 to 68 +/- 2 mm Hg, n.s.; mean diastolic AP = 58 +/- 3 to 53 +/- 2 mm Hg, n.s.). In group 2 none of the haemodynamic parameters measured showed significant changes. These results demonstrate minimal haemodynamic effects with 0.3- or 0.4-mgkg-1 bolus injections of atracurium in 15 patients with coronary artery disease, but in one patient doses of 0.3 mgkg-1 produced a typical histamine response with marked cardiovascular changes.

Aged↗
PubMed1982

Leukotriene D4: a potent coronary artery vasoconstrictor associated with impaired ventricular contraction.

Leukotriene D4 (2 c 10(-9) mole), injected into the left circumflex coronary artery of anesthetized sheep, produced profound coronary vasoconstriction and impaired regional ventricular wall motion. This cardiac effect was neither inhibited by prior treatment of the sheep with a cyclooxygenase inhibitor nor associated with thromboxane B2 release into the coronary sinus. Intravenous FPL 55712 completely abolished the coronary vasoconstriction of leukotriene D4, but a significant reduction of regional wall shortening persisted.

Animals↗