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1. |
Humoral Mediators of Catastrophic Reactions Associated with Protamine Neutralization |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 595-596
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ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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2. |
C5a and Thromboxane Generation Associated with Pulmonary Vaso- and Broncho‐constriction during Protamine Reversal of Heparin |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 597-604
Denis,
Morel Warren,
Zapol Stephen,
Thomas Eric,
Kitain Dwight,
Robinson Jonathan,
Moss Dennis,
Chenoweth Edward,
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摘要:
The authors conducted a study in humans to determine the mediators associated with acute pulmonary vaso- and broncho-constriction occurring episodically with protamine reversal of heparin anticoagulation. Of 48 adult patients investigated prospectively after termination of cardiopulmonary bypass, two presented a sudden increase of airway pressure, acute pulmonary hypertension, and systemic hypotension 1–3 min after right atrial protamine injection. In these two subjects, plasma levels of C5a increased from 0.7 and 2.2 to 9.8 and 9.9 ng/ml, respectively, and thromboxane B2increased from 0.26 and 0.34 to 7.5 and 16.2 ng/ml 1 minute after drug injection. A third subject not identified prospectively had an identical reaction and mediator profile (C5a, 10.2 ng/ml; TxB2, 18.6 ng/ml at 1 min). The plasma levels of these mediators were unchanged in the remaining patients (C5a, 0.7 ± 1.1 [x ± S.D.] to 0.6 ± 0.9 ng/ml; TxB2, 0.16 ± 0.12 to 0.15 ± 0.07 ng/ml). Plasma histamine was not involved in this type of reaction, but increased from 0.7–10.4 ng/ml in a fourth patient who became hypotensive without acute pulmonary hypertension, bronchoconstriction, or elevation of C5a or TxB2. The authors' data indicate that the generation of high plasma levels of C5a anaphylatoxins and thromboxane is associated with pulmonary vaso- and broncho-constriction induced by protamine reversal of heparin in humans.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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3. |
Induced HypotensionAction of Sodium Nitroprusside and Nitroglycerin on the MicrocirculationA Micropuncture Investigation |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 605-613
Bernhard,
Endrich Niels,
Franke Klaus,
Peter Konrad,
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摘要:
Sodium nitroprusside (SNP)-induced hypotension is associated with tissue hypoxia in liver and skeletal muscle, suggesting a redistribution of nutritional capillary flow. To test this hypothesis, the effects of SNP and nitroglycerin (NTG) on striated muscle vessels were studied in 42 hamsters using intravital microscopy, quantitative video image analysis, a platinum multiwire electrode for local PO2measurements, and a micropuncture system for the determination of microcirculatory pressure. A transparent chamber was implanted in a dorsal skin fold. When the mean arterial pressure was reduced to 70 or 40 mmHg by SNP, the precapillaries dilated and precapillary resistance decreased, but significant changes in venular diameter were not observed. However, SNP-induced hypotension was associated with a consistent increase in intravascular pressure within the venules. As a result, the arteriolar-venular pressure gradient was reduced by more than 50%. Furthermore, the functional capillary density was less, and tissue hypoxia was present during SNP hypotension. In contrast, NTG dilated both arterioles and venules in the microvascular network. Despite a lower blood cell velocity in all segments, the functional capillary density and local PO2remained unchanged during NTG, principally because there was only a 10% reduction of the arteriolar-venular pressure gradient. These findings suggest that, in terms of tissue oxygenation, NTG may be preferable to SNP for deliberate hypotension.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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4. |
Bedside Measurement of Pulmonary Capillary Pressure in Patients with Acute Respiratory Failure |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 614-620
George,
Collee Karen,
Lynch Roger,
Hill Warren,
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摘要:
In this report, the authors present the results of 34 estimates of pulmonary capillary pressure (Pcap) in 15 adult patients receiving intensive care for acute respiratory failure (ARF). Within the pulmonary artery pressure profile during transient balloon occlusion, the authors identified two exponential pressure decay components—the slower one representing the discharge of the pulmonary capillary pressure through the pulmonary venous resistance. By extrapolating this exponential to its origin at the moment of pulmonary artery occlusion, a pressure within the pulmonary vascular bed which approximates pulmonary capillary pressure (Pcap) was identified. Pcap, and not the pulmonary artery occlusion pressure (PAOP), is the major driving pressure forcing fluid from the pulmonary microvasculature. The results indicate that a discrete value for pulmonary capillary pressure can be reproducibly measured in paralyzed ventilated patients. The data report that mean pulmonary artery pressure, pulmonary capillary pressure, and total pulmonary vascular resistance (PVR) are increased in acute respiratory failure, but there is considerable variation in the distribution of pulmonary vascular resistance between the arterial and venous beds. The data suggest that there is unequal and variable partitioning of the increased PVR during acute respiratory failure. Bedside pressure profile Pcap measurements will allow optimum reduction of Pcap during ARF by infusing vasoactive agents to modify the distribution of PVR or reducing the PAOP.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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5. |
Left Ventricular Global and Regional Function during Lumbar Epidural Anesthesia in Patients With and Without Angina Pectoris. Influence of Volume Loading |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 621-627
Jean-Francois,
Baron Pierre,
Coriat Olivier,
Mundler Michel,
Fauchet Dominique,
Bousseau Pierre,
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摘要:
The influence of lumbar epidural anesthesia without cardiac sympathectomy on global and regional left ventricular function was investigated prior to surgery in eight normal subjects (group 1) and in ten patients suffering from stable mild effort-related angina (group 2). In both groups, epidural blockade was performed with 10 ml 0.5% plain bupivacaine. To differentiate the effects due to epidural blockade from those related to volume expansion, three sets of measurements were obtained: control, epidural blockade without volume loading, and epidural blockade with volume loading (500 ml lactated Ringer's solution). Radionuclide angiography was used to determine cardiac output, left ventricular ejection fraction, end systolic and end diastolic volumes, and to analyse left ventricular wall motion. Peak systolic pressure-end systolic volume ratio was used as an index of myocardial contractility. Seventy-two hours postoperatively, a thallium 201 myocardial scintigraphy obtained after iv dipyridamole detected myocardial defects in all patients with a history of angina. These defects were fully redistributed in eight out of ten patients. Throughout the procedure, patients with a history of angina exhibited neither chest pain nor ECG evidence of myocardial ischemia. At control, left ventricular ejection fraction (LVEF) and systolic pressure-volume ratio (SPVR) were lower in group 2 than in group 1 (LVEF: 0.54 ± 0.02vs.0.64 ± 0.02,P< 0.01), (SPVR: 2.3 ± 0.2vs.3.3 ± 0.4 mmHg/ml,P< 0.05). In addition, 19 hypokinetic sectors were found in group 2. In these patients, epidural blockade before volume loading induced a slight but significant improvement in left ventricular ejection fraction (0.59 ± 0.03,P< 0.01) and in regional wall motion (five hypokinetic sectors,P< 0.01). No change in these parameters was observed in normal patients. In both groups, myocardial contractility estimated by systolic pressure volume ratio was not altered during epidural blockade. After volume loading, in group 2, left ventricular ejection fraction returned to basal value, and a reduced wall motion was seen in 11 sectors. This study indicates that, in patients with stable mild effort-related angina, decrease in left ventricular loading induced by lumbar epidural anesthesia may improve left ventricular global and regional function as long as volume loading is limited.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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6. |
Endocrinological Changes following Etomidate, Midazolam, or Methohexital for Minor Surgery |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 628-635
Thomas,
Crozier Dietmar,
Beck Michael,
Schlaeger Wolfgang,
Wuttke Dietrich,
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摘要:
Etomidate is known to inhibit adrenocorticosteroid synthesis. The extent and duration of the effects of etomidate (63 ± 6.4 mg) on spontaneous and stimulated corticosteroid levels, as well as on plasma concentrations of ACTH, β-endorphin, and catecholamines were examined and compared to those following administration of the new benzodiazepine, midazolam, or of methohexital. Twenty-nine healthy, young, male orthopedic patients were randomized into three groups receiving either etomidate/fentanyl (n = 12), midazolam/fentanyl (n = 8), or methohexital/fentanyl (n = 9). Etomidate caused cortisol levels to decrease from 12.5 ± 1.2 μg/dl preoperatively to 5.9 ± 0.8 μg/dl after operation (P< 0.001), compared to an increase from 12.0 ± 1.9 μg/dl to 18.5 ± 2.9 μg/dl in the group receiving methohexital. At 6 and 20 h postoperatively, all cortisol levels were normal. The cortisol decrease from 12.5 ± 1.7 to 7.6 ± 1.5 caused by midazolam was similar to that following etomidate, but the response to exogenous ACTH was significantly impaired in patients receiving etomidate as compared to those receiving midazolam. ACTH and β-endorphin levels increased in patients receiving etomidate, presumably as a result of the interruption of negative feedback due to cortisol synthesis inhibition. Midazolam on the other hand prevented the increase of ACTH and β-endorphin levels. Etomidate completely suppressed spontaneous aldosterone levels (from 33 ± 6.7 to 7 ± 2.1 pg/ml), as well as the response to stimulation with exogenous ACTH without affecting serum electrolytes. Etomidate had no influence on plasma catecholamines, but midazolam attenuated the stress-related epinephrine increase.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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7. |
Determinants of End Expiratory Volume in Young Children during Ketamine or Halothane Anesthesia |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 636-640
D.,
Shulman E.,
Bar-Yishay C.,
Beardsmore S.,
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摘要:
The expiratory time (Te) and the rate of lung emptying in expiration are important determinants of functional residual capacity (FRC) in infants. In order to determine whether these factors also influence FRC in children during anesthesia, 20 preschool children were studied, 10 while receiving ketamine, and 10 during halothane anesthesia. Te was measured during quiet breathing and the passive expiratory time constant (±) was determined from the passive expiratory flow volume (V/V) curve following a brief end inspiratory airway occlusion. The number of time constants available for expiration, Te/τ, was then calculated. The difference between FRC and the relaxation volume of the respiratory system (Vrs) (FRC-Vrs) was measured by extrapolating the linear segment of the V/V curve to zero flow, and measuring FRC-Vrs. During ketamine anesthesia, (τ) was markedly prolonged (1.15 s, range 0.73–2.29 s), with the result that Te/τ was, in all subjects, less than 2. Children anesthetized with halothane had shorter τ (0.38 s, range 0.24–0.65 s), and Te/τ was more than 2 in most subjects. FRC-Vrs was significantly greater in the subjects from the ketamine group (203 ml, range 115–392 ml) than in those from the halothane group (32 ml, range 1–71 ml). For the 20 subjects, there was a significant relationship between FRC-Vrs (ml) and Te/τ described by the equationFRC-Vrs = 845.0e−1.28(Te/τ)The authors conclude that, in children during ketamine anesthesia, τ is prolonged and, in these children, the relationship of Te to τ is an important determinant of FRC-Vrs. Te/τ was not related causally to FRC-Vrs in the halothane group. The elevated FRC-Vrs which results from the short Te/τ in the ketamine group may be the explanation for maintenance of adequate arterial oxygenation during spontaneous air breathing with ketamine.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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8. |
Hemodynamic Effects of Dopamine during Thoracic Epidural Analgesia in Man |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 641-646
Johan,
Lundberg Lars,
Norgren Dick,
Thomson Olof,
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摘要:
The cardiovascular effects of dopamine were studied before and during thoracic epidural analgesia (TEA) in eight patients prior to abdominal aortic surgery. Dopamine was infused at rates of 2, 4, and 8 μg·kg−1·min−1. Mean plasma dopamine concentration increased proportionally to the infusion rate. Before TEA, dopamine 8 μg·kg−1·min−1decreased systemic vascular resistance 4 ± 4 mmHg min·1−1(m ± SD) (P< 0.05), but increased mean arterial pressure 15 ± 12 mmHg (P< 0.01), cardiac output 1.9 ± 1.0 1·min−1(P< 0.01), heart rate 10 ± 9 beats·min−1(P< 0.05), and plasma norepinephrine concentration 544 ± 252 pg·ml−1(P< 0.01). After the induction of TEA, which extended above the T2 dermatome and below the L2 dermatome, saline and albumin were infused to maintain central venous and pulmonary capillary wedge pressures. TEA reduced mean arterial pressure from 96 ± 18 to 55 ± 8 mmHg (P< 0.01), cardiac output from 4.7 ± 0.9 to 3.9 ± 0.9 1·min−1(P= 0.05), systemic vascular resistance from 21 ± 6 to 14 ± 3 mmHg min·1−1(P< 0.05), and plasma norepinephrine concentration from 394 ± 141 to 207 ± 73 pg·ml−1(P< 0.01). The plasma epinephrine concentration was reduced 49% after the induction of TEA. During TEA, dopamine, 8 μg·kg−1·min−1increased mean arterial pressure by 57 ± 9 mmHg (P< 0.01), cardiac output by 2.9 ± 0.8 1·min−1(P< 0.01), heart rate by 14 ± 11 beats·min−1(P< 0.01), and plasma norepinephrine concentration by 833 ± 499 pg·ml−1(P< 0.01). Systemic vascular resistance changed in a diphasic fashion. Thus, at 2 μg·kg−1·min−1of dopamine, the value decreased further, below the level seen with TEA alone, but increased at 4 and 8 μg·kg−1·min−1. In addition, at 8 μg·kg−1·min−1, mean pulmonary artery pressure and pulmonary capillary wedge pressure were greater during than before TEA, although the values were similar without dopamine. The authors conclude that the effects of dopamine on mean arterial pressure, cardiac output, systemic vascular resistance, pulmonary capillary wedge, and mean pulmonary artery pressure were different during TEA, as compared to before the block. A moderate dose of dopamine (4 μg·kg−1·min−1) was sufficient to maintain mean arterial pressure and cardiac output at adequate levels during TEA although systemic vascular resistance remained low.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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9. |
Alteration of Blood Flow Distribution and Vascular Capacitance during Induced Hypotension in Deafferented Dogs |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 647-652
Sumio,
Hoka Daniel,
Siker Zeljko,
Bosnjak John,
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摘要:
The effects of three hypotensive agents, sodium nitroprusside (SNP), nitroglycerin (NTG), and adenosine triphosphate (ATP), on blood flow distribution and vascular capacitance were examined in dogs anesthetized with sodium pentobarbital. To eliminate the modification by the baroreflex, carotid sinus was denervated and aortic and cardiopulmonary vagal fibers were sectioned. Total systemic circulation was divided into two parallel compartments, splanchnic (SP) and extra-splanchnic (ESP) vascular beds. Alteration of vascular capacitance was assessed by a change in systemic blood volume with constant cardiac output and constant venous pressure using a total heart-lung bypass. SNP- and ATP-induced hypotension caused blood flow redistribution from the SP to ESP beds, and this redistribution is greater (P< 0.01) with ATP than that with SNP. In contrast, NTG-induced hypotension did not significantly cause redistribution. Systemic blood volume was increased during NTG- (10.4 ± 2.2 ml/kg), and SNP-induced (4.8 ± 1.1 ml/kg) hypotension. The increase by NTG was significantly greater (P< 0.05) than that by SNP. In contrast, ATP-induced hypotension did not significantly change systemic blood volume. Since redistribution can result in a passive change in vascular capacitance, the differences in capacitance among SNP, NTG, and ATP can be explained in part by differences in redistribution of blood flow. Redistribution of blood flow from SP to ESP beds can increase venous return due to increasing the slope of the venous return curve. The results suggest that redistribution should be taken into consideration in evaluating the hemodynamic changes during induced hypotension.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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10. |
Myocardial Circulatory and Metabolic Effects of Isoflurane and Sufentanil during Coronary Artery Surgery |
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Anesthesiology,
Volume 66,
Issue 5,
1987,
Page 653-658
Judy,
O'Young George,
Mastrocostopoulos Alan,
Hilgenberg Igor,
Palacios Antonis,
Kyritsis Demetrios,
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摘要:
The global and regional coronary hemodynamic and myocardial metabolic effects of isoflurane administered intraoperatively as an adjunct to sufentanil were studied in seven of nine patients who experienced increased systemic arterial pressure while undergoing elective coronary artery bypass grafting. All patients were premedicated and maintained on their preoperative medications (β-blockers, nitrates, Ca++entry blockers) up to and including the morning of surgery. Systemic and pulmonary hemodynamics and global (coronary sinus, CS) and regional (great cardiac vein, GCV) coronary blood flows were measured, and blood samples were obtained for systemic and myocardial metabolic parameters: a) after induction with 30 mcg/kg of sufentanil and 0.12 mg/kg vecuronium (FIo21.0), but prior to incision (control); b) 5 min after sternotomy; and c) during ventilation with isoflurane-oxygen. Heart rate, cardiac output, stroke volume, and GCV/CS flow ratio did not change throughout the study. Neither global nor regional myocardial lactate production was detected in any patient at any time, and the electrocardiogram (lead II, V5) remained unchanged. In response to sternotomy, seven of nine patients experienced an increase in mean systemic arterial pressure of 20% or more (27 ± 3% from control values), due to an elevation in systemic vascular resistance (30 ± 5%). Coronary sinus (CS) and great cardiac vein (GCV) flows, as well as CS and GCV lactate extractions, were unchanged 5 min after sternotomy. Both global and regional myocardial oxygen extraction increased, while coronary venous oxygen content decreased. Isoflurane was administered in a dose that restored systemic arterial pressure to baseline values (inspired concentration 0.75–1.0%). Concomitantly, global and regional myocardial oxygen extraction and venous oxygen content returned toward control values. These data suggest that, in doses which produce no significant hypotension, isoflurane is a safe and effective adjunct for control of intraoperative elevation of systemic arterial pressure and vascular resistance during high dose sufentanil anesthesia in patients undergoing elective coronary artery bypass grafting.
ISSN:0003-3022
出版商:OVID
年代:1987
数据来源: OVID
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