硝普钠控制性降压对心率变异性的影响

目的　观察硝普钠控制性降压对心率变异性的影响。方法　ASAⅠ级鼻内窥镜手术病人 5 2例。降压前、降压稳定即刻、此后 10、30分钟、复压前、复压稳定即刻和此后 5分钟 ,记录LF/HF、LF、HF及TP。结果　降压稳定即刻的LF/HF较降压前增加 ,降压稳定后 10、30分钟LF/HF较降压稳定即刻降低 (P <0 0 5 )。复压稳定即刻LF/HF大于复压前 ,复压稳定后 5分钟LF/HF小于复压稳定即刻 ,HF大于复压稳定即刻 (P <0 0 5 )。结论　硝普钠控制性降压初期交感迷走神经张力的均衡性改变 ,交感神经张力的增高较迷走神经张力的增高幅度大。血压稳定后交感 迷走神经张力达到新的平衡。复压稳定后 5分钟迷走神经的张力进一步增高     

Systemic haemodynamic and metabolic effects of deliberate hypotension with isoflurane anaesthesia or sodium nitroprusside during total hip arthroplasty

Isoflurane (ISO) was examined as an alternative hypotensive agent to nitroprusside (SNP) in 16 patients (mean age: 60 years) anaesthetized for total hip arthroplasty. MAP was decreased to 50 per cent of the awake level by infusion of SNP in Group I (n = 8) and with ISO in Group II (n = 8). Fentanyl (10-16 micrograms X kg-1) was administered to both groups. Haemodynamic measurements were repeated in the lateral position before, during and after hypotension. Polygeline and fresh frozen plasma were infused throughout the study period in volumes sufficient to maintain pulmonary capillary wedge pressure in the 7-9 mmHg range. The MAP decrease was the same in both groups, as were perioperative blood replacement (mean 500 ml), and postoperative haematocrits. Total perioperative fluid replacement was higher (p less than 0.01) in Group I (mean 2500 ml) than in Group II (mean 1300 ml). Venous tone was more affected by SNP than by ISO. ISO decreased the systemic vascular resistance index and oxygen consumption (VO2) without any change in CI or in Qs/Qt, in contrast to SNP which increased CI, VO2 and Qs/Qt.     

Cerebral oxygen tension in rats during deliberate hypotension with sodium nitroprusside, 2-chloroadenosine, or deep isoflurane anesthesia

Thirty-four male Sprague-Dawley rats were divided into four groups: control animals and those receiving sodium nitroprusside (SNP), 2-chloroadenosine, or a high, inspired concentration of isoflurane to produce deliberate hypotension to a mean arterial blood pressure of 50 mmHg. Ventilation was controlled (FIo2 = 0.3); control animals and those treated with sodium nitroprusside or 2-chloroadenosine breathed isoflurane 1.4 vol%, whereas isoflurane, 3.9 vol%, was required to produce hypotension by deep anesthesia alone. Multiple tissue oxygen tension values (PtO2) were measured at intervals of 10 micron over a distance of 2 mm by advancing an oxygen microelectrode through the parietal cerebral cortex of all animals. The frequency of low tissue PO2 values (less than 10 mmHg) was increased with all forms of deliberate hypotension, but the magnitude of this change (a shift to the left in the frequency histogram) was significantly different among techniques. The shift toward lower PtO2 values during hypotension was least in animals receiving deep isoflurane anesthesia, intermediate in those receiving SNP, and greatest in those treated with 2-chloroadenosine. In rats, areas of the brain appear to be at risk for significant tissue hypoxia during hypotension produced by 2-chloroadenosine.     

硝普钠-艾司洛尔用于神经外科控制性降压的临床研究

目的　研究硝普钠或硝普钠 艾司洛尔用于轻或中度颅内高压患者控制性降压对脑氧代谢和颅内压的影响。方法　 1 8例颅内压轻度增高的颅内肿瘤患者 ,在持续丙泊酚静脉麻醉 (目标血浓度 5 μg/ml)下行开颅手术。采用硝普钠或硝普钠 艾司洛尔控制性降压至动脉压 6 4～ 6 8/ 4 0～4 5mmHg,持续 1h。监测降压前后及降压期间颈内静脉血氧饱和度及动脉氧分压、颅内压、心率、血压变化。结果　在丙泊酚全身麻醉下硝普钠降压不引起颅内压增高 ,脑氧代谢良好。合并使用艾司洛尔 5 0 μg·kg 1 ·min 1 ,有助于维持较低的颅内压 ,并可减慢心率 ,防止硝普钠停药后反跳性高血压 ,硝普钠用量亦减少约 4 5 %。结论　硝普钠降压用于丙泊酚静脉麻醉的神经外科病人 ,脑氧代谢良好 ,联合使用硝普钠、艾司洛尔优于单纯使用硝普钠     

Plasma renin activity and prostaglandin E2 in hypotension induced by sodium nitroprusside

Sodium nitroprusside (SNP) is a potent, effective and readily reversible vasodilating agent frequently used in anaesthesia for deliberate hypotension. Moderate hypotension induced by SNP activated catecholamine and vasopressin secretions, and the renin-angiotensin system, resulting in partial antagonism of the hypotensive response to SNP. Furthermore, this increase in renin release was involved in the hypertensive rebound after SNP withdrawal. This activation of vasoconstrictor systems led to pharmacological associations aimed at reducing the risk of cyanide poisoning. The physiological interrelationship between prostaglandins and renin secretion has now been well established but, as far as we know, no paper existed concerning prostaglandins during SNP-induced hypotension. In such hypotension (Pa: -30%), monitored by invasive and non invasive haemodynamic techniques (pulsed Doppler), the variations in plasma renin activity (PRA) and in venous and arterial plasma PGE2 concentrations (V PGE2 and A PGE2), determined by radioimmunoassay, were studied in anaesthetized dogs. Invasive haemodynamic data were similar to previous reports. Common carotid diameter increased (p less than 0.05), with a constant common carotid blood flow. PRA (p less than 0.05), V PGE2 (p less than 0.05) and A PGE2 (p less than 0.05) increased. PRA and V PGE2 were highly correlated before and after SNP. SNP resulted in hypotension with reflex sympathetic activation and dilatation of large arteries. Carotid blood flow autoregulation was maintained. Whilst pulmonary removal of PGE2 remained unchanged, an increase in A PGE2 may have been involved in the vasodilator mechanisms.     

前列腺素E1与硝普钠控制性降压对犬血流动力学影响的对比研究

对比研究了普鲁卡因复合麻醉下前列腺素Ｅ１（ＰＧＥ１）与硝普钠（ＳＮＰ）控制性降压时犬血流动力学变化。结果表明，ＳＮＰ降压组有显著的反射性心动过速和反跳性高血压，ＰＧＥ；降压组两者均无。ＰＧＥ１降压时心指数、肺动脉压等其它血流动力学参数亦比ＳＮＰ稳定，提示在保证心肌氧供求平衡及防止血管意外方面ＰＧＥ１降压优于ＳＮＰ。     

Baroreceptor reflex response to acute blood loss during induced hypotension--a comparison of sodium nitroprusside, prostaglandin E1 and trimethaphan

This experiment was designed to evaluate the reflexive heart rate (HR) response to acute blood loss during sodium nitroprusside (SNP), prostaglandin E1 (PGE1) and trimethaphan (TM) induced-hypotension in isoflurane anesthetized dogs. Reflexive increase in HR to acute blood loss was significantly greater during PGE1 induced-hypotension than during that with SNP. TM inhibited the reflexive HR response to acute blood loss. These results suggest that PGE1 induced-hypotension provides a safer margin than that with SNP and TM when rapid bleeding occurs during anesthesia and surgery.     

Effects of deliberate hypotension induced by labetalol with isoflurane on neuropsychological function

The effect of deliberate hypotension on brain function measured by neuropsychological tests was studied in 41 adult patients. Twenty-four patients were anaesthetized for middle-ear surgery with deliberate hypotension induced by labetalol with isoflurane (hypotensive group). Seventeen patients without hypotension served as a control group. The mean arterial pressure was 77 ± 2 mmHg (10.3 ± 0.3 kPa) before hypotension and 50 ± 0 mmHg (6.7 ± 0.0 kPa) during hypotension in the hypotensive group, and 86 ± 2 mmHg (11.5 ± 0.3 kPa) during anaesthesia in the control group. The following psychological tests were performed: four subtests of the Wechsler Adult Intelligence Scale (similarities, digit span, vocabulary and digit symbol), Trail-Making tests A and B, Zung tests (self-rating anxiety scale and self-rating depression scale) and two-part memory test battery with immediate and delayed recall. The tests were performed preoperatively and 2 days postoperatively. There were no statistically significant differences between the groups in any of the tests in the changes from preoperative value to postoperative value. The results indicate that hypotension induced by labetalol with isoflurane has no significant harmful effects on mental functions compared to normotensive anaesthesia.     

Myocardial hemodynamics during induced hypotension: a comparison between sodium nitroprusside and adenosine triphosphate

Adenosine triphosphate (ATP) has been reported to be a hypotensive agent similar in effect to sodium nitroprusside (SNP). The purpose of this study was to examine and compare the effects of both SNP and ATP on general coronary hemodynamics, myocardial O2 consumption, and circulating catecholamines. Twelve dogs were anesthetized with 1.0% halothane and given either SNP or ATP by controlled infusion to reduce their systemic blood pressure by 50% for a 2-h period followed by a (blood pressure) recovery period. The ATP-induced hypotension was rapid, easily controlled, not accompanied by tachyphylaxis over the 120 min studied, and resulted in an increase in coronary sinus blood flow (CSBF), which plateaued at 260% above control. The increase in CSBF was almost immediate and remained at this elevated level for the duration of the induced hypotension. During the ATP-induced hypotension, there was no change in heart rate or circulating catecholamines. A 60% reduction in myocardial O2 uptake was observed, presumably from the cardiac unloading. In contrast, SNP-induced hypotension required a marked increase in dose over time, did not significantly increase CSBF, did increase heart rate, and resulted in large increases in circulating plasma catecholamines. Neither agent affected cardiac output. ATP-induced hypotension resulted in no change in cardiac lactic acid uptake, while SNP caused lactic acid production, indicating possible cardiac ischemia or cyanide toxicity.     

Effect of clonidine on sympathoadrenal response during sodium nitroprusside hypotension

Supplementation of the antihypertensive action of the peripheral vasodilator sodium nitroprusside (SNP) with clonidine, a centrally-acting agent, was studied in ten dogs anesthetized with isoflurane to evaluate the efficacy of clonidine for reducing the amount of SNP required during induced hypotension. The dose of SNP required to lower mean arterial blood pressure (MAP) by 40% was determined prior to the administration of intravenous clonidine (control), and after incremental doses of 1, 4, and 15 micrograms/kg. After each dose of clonidine, hypotension was induced with SNP and maintained for 30 min, followed by a 30-min recovery period. Plasma levels of norepinephrine (NE) and epinephrine (EPI) were determined before hypotension, at 5 min and 30 min during hypotension, and at 5 min and 30 min during recovery. During the control period (no clonidine), SNP-induced hypotension resulted in increases in plasma catecholamine levels, with larger increases in EPI (from 70 +/- 26 to 851 +/- 140 pg/ml, at 30 min) than NE (from 171 +/- 26 to 334 +/- 58 pg/ml, at 30 min). There was no significant difference between the control MAP and the MAP after each incremental dose of clonidine. In these anesthetized dogs with low sympathetic tone there was no significant decrease in EPI levels after administration of up to 20 micrograms/kg of clonidine. Increasing doses of clonidine correlated inversely with depression in catecholamine output during induced hypotension and the dose of SNP required to produce this hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of hydralazine and prostaglandin E1 on regional myocardial function in the ischemic canine heart

The effects of hydralazine and prostaglandin E1 on regional myocardial function were studied in dogs. Sixteen dogs were randomly assigned to one of two drug treatment groups of eight dogs each. The first group (G1) was treated with 0.4 mg/kg hydralazine administered as a bolus. The second group (G2) received prostaglandin E1 given as an infusion for a total dose of 0.8 micrograms/kg. Regional myocardial function was assessed through the measurement of myocardial segment shortening during systole. We call this index percent systolic shortening (%SS). An ischemic heart preparation was created by partial occlusion of coronary blood flow. The degree of induced ischemia was determined by following the reduction in %SS. Hydralazine reduced %SS of the ischemic myocardium while increasing the cardiac index, stroke volume index, and coronary blood flow. Prostaglandin E1 increased %SS, cardiac index, and stroke volume index in the ischemic heart preparation. Hydralazine, therefore, induced dissociation between global ventricular function and regional myocardial function whereas prostaglandin E1 did not. The present findings emphasize that evaluation of vasoactive drugs should consider their effects on regional myocardial function as well as on global hemodynamics.     

Pharmacokinetics of epidurally administered bupivacaine during prostaglandin E1- or trimetaphan-induced hypotension]

The effects of prostaglandin E1 (PGE1) and trimetaphan (TMP) on the plasma concentrations and derived pharmacokinetic parameters of bupivacaine were studied in 14 women after its epidural administration. Patients, whose ages ranging from 35 to 60 years for mastectomy, received 50 mg of bupivacaine without epinephrine injected into the cervical epidural space during PGE1- or TMP-induced hypotension (80-90 mmHg of the systolic arterial pressure) under general anesthesia with nitrous oxide, oxygen and isoflurane 0.3-0.5%. No significant differences in pharmacokinetic parameters for the absorption and distribution of bupivacaine were found between the two groups. However, the mean elimination half-life of bupivacaine was significantly longer in patients with TMP [5.0 +/- 1.7 (SD) hr] compared with those with PGE1 (3.1 +/- 1.4 hr). The total clearance of bupivacaine was greater in patients with PGE1 (345 +/- 150 ml.min-1) compared with those with TMP (248 +/- 66 ml.min-1). The results of this pharmacokinetic study indicate that the plasma bupivacaine concentration decreases more rapidly during PGE1-induced hypotension than during TMP-induced hypotension.     

The interaction of sodium nitroprusside, hypotension, and isoflurane in determining cerebral vasculature effects

Eighteen mongrel dogs were anesthetized with isoflurane and prepared for determining cerebral blood flow (CBF, sagittal sinus outflow), cerebral metabolic rate (CMRO2), and ICP. Dogs were divided into three groups of six each. Group 1 dogs were maintained on 1 MAC isoflurane and, following control measurements (step 1), sodium nitroprusside (SNP) was infused to decrease mean arterial pressure (MAP) to 60 mmHg (step 2). After 20 min SNP was discontinued and a second control period of 20 min followed (step 3). Thereafter, SNP was repeated for 20 min as in step 2, but MAP was maintained by inflating a balloon in the descending aorta (step 4). SNP was again discontinued followed by a final 20 min control period (step 5). During SNP with hypotension (step 2) there was a significant 21% decrease in CBF and no change in ICP. During SNP with normotension (step 4) both CBF and ICP increased (16 and 39%, respectively). In group 2 dogs isoflurane was discontinued and a spinal anesthetic was administered. Thereafter, these dogs were studied as in group 1. The only significant change in these dogs was a 35% increase in ICP during SNP with normotension. Group 3 dogs were studied identically to group 2, but hypotension was induced with trimethaphan (TMP). There were no significant changes in these dogs. The authors conclude that SNP, in the absence of isoflurane, dilates capacitance vessels because ICP increased without a concomitant increase in CBF at normotension. In the presence of isoflurane, SNP dilates both capacitance and resistance vessels because ICP and CBF increased concomitantly at normotension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Labetalol attenuates the negative effects of deliberate hypotension induced by isoflurane

The effect of labetalol on deliberate hypotension was studied in 24 adult patients undergoing middle-ear surgery. Hypotension was induced in Group I (12 patients) with isoflurane 3.0 vol% in inspiratory gas, and in Group II (12 patients) with labetalol 0.5 mg.kg-1 i.v., in addition to isoflurane. The induction time of hypotension was 4.9 +/- 1.0 (s.e.mean) min in Group I, and 1.8 +/- 0.2 min in Group II (P less than 0.01). The mean isoflurane concentration in inspiratory gas for the maintenance of hypotension was 1.4 +/- 0.2 vol% in Group I, and 0.7 +/- 0.1 vol% in Group II (P less than 0.01). There were no differences in urine flow rates (UF) between the groups during any phase, though UF decreased in Group I from the prehypotensive value 0.58 +/- 0.12 ml.min-1 to 0.07 +/- 0.02 ml.min-1 during hypotension (P less than 0.01) and increased to 1.28 +/- 0.17 ml.min-1 after anaesthesia (P less than 0.05). UF in Group II were 0.56 +/- 0.17, 0.25 +/- 0.10 and 0.56 +/- 0.06 ml.min-1, respectively. Creatinine clearances per 1.73 m2 body surface area (CCreat) in Group I were 78 +/- 14 ml.min-1, and in Group II 78 +/- 11 ml.min-1 before hypotension. During hypotension, CCreat were lower in Group I (8 +/- 1 ml.min-1) than in Group II (33 +/- 8 ml.min-1) (P less than 0.01). After anaesthesia, there was no difference in CCreat between the groups (Group I: 110 +/- 17 ml.min-1 and Group II: 120 +/- 17 ml.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of controlled hypotension induced by prostaglandin E1 on the cerebral blood flow

The effect of controlled hypotension induced by prostaglandin E1 (PGE1) on the cerebral blood flow (CBF) was studied in 14 patients undergoing neurosurgery. CBF was measured by thermal diffusion using a flow probe with a Peltier stack. PGE1 was injected i.v. continuously, at a dose of 0.05, 0.1 and 0.2 micrograms.kg-1.min-1. CBF tended to increase dose-dependently but not significantly by PGE1 administration. Cerebral vascular resistance was reduced significantly by every dose of PGE1 administered. Therefore, the results indicate that the cerebral vascular beds are dilated directly by PGE1. In conclusion, this study suggests that PGE1 can be used safely to control hypotension without reducing CBF during neurosurgery.     

Haemodynamic changes during induced hypotension — comparison of trimethaphan with prostaglandin E1 assessed using transoesophageal echocardiography

Haemodynamic changes during induced hypotension depend upon the hypotensive agent used. We investigated if, using transoesophageal echocardiography (TEE), we could identify the haemodynamic differences between trimethaphan and prostaglandin E₁. Twenty-nine patients undergoing total hip replacement were selected for study. Hypotension was induced to a mean arterial pressure of 8.0– 9.3 kPa with either trimethaphan (5–20 μg · kg^?1 min^?1) or prostaglandin E₁ (0.5–2.0 μg · kg^?1 min^?1). The left atrial dimension, cardiac output, fractional shortening, pulmonary venous flow and mitral valve flow were evaluated using TEE. During induced hypotension, left atrial dimension decreased in both trimethaphan and prostaglandin E₁ groups (P < 0.05). In the trimethaphan-treated patients systolic velocity in pulmonary venous flow decreased from 41.9 ± 4.8 cm · sec^?1 before induced hypotension to 27.8 ± 4.2 cm · sec^?1 by 30 min after stable hypotension had been established (P < 0.01). The late/early ratio of peak velocity in mitral blood flow decreased in prostaglandin E₁ treated patients. Cardiac output increased from 4.2 ± 0.5 L · min^?1 to 5.3 ± 0.4 L · min^?1 during 30 min hypotension with prostaglandin E₁ administration (P < 0.05), but cardiac output decreased from 5.0 ± 0.5 to 3.5 ± 0.4 L · min^?1 with trimethaphan (P < 0.01). The differences in haemodynamic variables could be attributed to the venule dilatation effect of trimethaphan. We conclude that it was possible to detect the haemodynamic differences between trimethephan and prostaglandin E₁ using TEE.     

Effects of intravenous nicardipine, prostaglandin E1, nitroglycerin, sodium nitroprusside, and epidural lidocaine on hepatic and renal blood flow during hypotensive anesthesia

We studied the effects of intravenous nicardipine (NIC), prostaglandin E1 (PGE1), nitroglycerin (TNG), sodium nitroprusside (SNP) and epidural lidocaine (LID) on hepatic and renal blood flow during general anesthesia (nitrous oxide-oxygen-sevoflurane) in 46 female patients undergoing unilateral total hip arthroplasty. During operations, hepatic blood flow, glomerular filtration rate, renal plasma flow, and renal tubular injury were measured by R 15 ICG (15 minutes retention rate of indocyanine green), CCR (creatinine clearance), CPAH (para-aminohippuric acid clearance), and urinary excretion of NAG and beta 2-microglobulin. Significant elevation of R 15 ICG was observed in the hypotensive state in the TNG group and the elevation of R 15 ICG indicates that blood flow to the liver has decreased during hypotensive anesthesia. Urine volume in the PGE1 group was larger than that in the TNG, SNP or LID group. CCR in the PGE1 group was larger than that in the NIC, TNG or SNP groups. CPAH in the PGE1 group was larger than that in the SNP or LID group. The value of urine NAG in the TNG group was larger than that in the NIC or PGE1 group. The value of urine beta 2-microglobulin in the NIC group was larger than that in the PGE1 or SNP group. The results of urine volume, CCR, CPAH, urine NAG, and urine beta 2-microglobulin indicate that blood flow to the kidneys was greater in the PGE1 group as compared to other groups. This study indicates that prostaglandin E1 is the best hypotensive drug for hepatic and renal blood flow during hypotensive anesthesia.