Effects Of Lumbar Epidural Anesthesia Research Articles

Effects of lumbar epidural anesthesia on cell apoptosis in rat kidneys with ischemia-reperfusion injury

Objective To investigate the influence of lumbar epidural anesthesia on cell apoptosis in rat kidneys with ischemia-reperfusion injury. Methods Thirty male Wistar rats were divided into three groups at random, including a sham-operated group, a model group, and an anesthesia group. Then the local norepinephrine, local angiotensin Ⅱ, plasma superoxide dismutase, plasma malondialdehyde and cell apoptosis index were observed at the 24 h after the reperfusion in rat kidneys of ischemia 60 min. Results Compared to the sham-operated group, ischemia-reperfusion of kidney caused a significant increase in contents of local norepinephrine, local angiotensin Ⅱ, and malondialdehyde in the model group and anesthesia group as well as increasing in the cell apoptosis index (P<0.05), and those parameters above were lower in the anesthesia group than those in the model group (P<0.05). Meanwhile, the activities of plasma superoxide were higher than those in model group (P<0.05). Conclusions The lumbar epidural anesthesia can reduce the excessive accumulation of neuroendocrine hormone in kidney, alleviate oxidative stress, which plays an important role in restraining the ischemia-reperfusion injury and cell apoptosis. Key words: Anesthesia, epidural; Reperfusion injury; Kidney/CY/PA; Apoptosis

Regional anesthesia: sympathectomy-mediated vasodilation

To the Editor, I read with interest the recent study concerning autonomic, sensory, and motor effects of lumbar epidural anesthesia in patients randomized to receive varying bupivacaine doses and concentrations. At lower concentrations, sensory block was observed in the mid-thoracic dermatomes with little change in the temperature or pulse oximeter perfusion index of the upper and lower extremities despite a concomitant decrease in systemic arterial pressure. These data were interpreted to suggest that sensory neural function may, in some cases, ‘‘be more susceptible than sympathetic neural function to local anesthetic blockade’’, in contrast to widely accepted dogma that the reverse is the case. As alluded to in the Discussion, these data must be interpreted in the context of direct (sympatholysis secondary to local anesthetic effects on spinal sympathetic outflow) and indirect (e.g., baroreceptor-mediated sympathetic activation secondary to fall in systemic arterial pressure) effects on autonomic tone. Thus, the response of sympatho-target organs, as described in this report, will reflect the balance of these opposing effects. A further confounding variable rarely addressed in the literature is that a dermatome may not reflect the segmental organization of sympathetic outflow to that area. A simple example to consider is the thumb, which has sensory innervation from spinal segments C6, but sympathetic preganglionic neurons are not found rostral to T1. In fact, there is extensive convergence and divergence of input from sympathetic preganlionic axons onto postganglionic cells contained in the sympathetic chain, and sympathetic target organs may receive input from numerous spinal cord segments. This may be one mechanism to facilitate a ‘‘widespread diffusion of nervous impulses’’ associated with the sympathetic response to stress. Of note, vasoconstriction of the upper extremity is mediated by sympathetic preganglionic neurons from the middle to the caudal thoracic spinal segment, the axons of which course in the sympathetic chain before synapsing onto sympathetic (vasoconstrictor) postganlionic neurons in the stellate ganglion. Thus, neuraxial anesthesia producing a sensory deficit in dermatome T8 may indeed be accompanied by vascular resistance changes in the upper extremity simply on the basis of anatomy: both afferent activity and autonomic outflow are blocked at the same segmental level. To conclude that this is a result of extraordinary sensitivity of sympathetic outflow to local anesthetic action, as has been decided previously, ignores these anatomical features that have been known for more than a century. A further consideration involves the unique physiological properties of sympathetic preganglionic neurons, such as tonic activity, refractory period, and axonal fibre diameter, which distinguish them from spinal sensory and motor neurons. These properties may account, in part, for the differential blocking effects of local anesthetics on specific types of spinal neurons. Moreover, functionally specific subgroups of sympathetic neurons may themselves be differentiated on the basis of their physiological properties that are particularly matched to the behaviour (e.g. frequency-response characteristics) of their sympathotarget organs. The above points may be relevant when contemplating the differential effects of neuraxial (spinal or epidural) anesthesia on autonomic, sensory, and motor responses.

Abstracts of literature

Abstracts of literature

The effect of lumbar epidural anesthesia on maternal middle cerebral artery blood flow in normal pregnancy: A prospective, randomized, double-blind comparison study

Objective: Lumbar epidural anesthesia is associated with a transient elevation in intracranial pressure in both animals and humans and decreased cerebral blood flow in animals. We sought to determine the effect of medium-onset and slow-onset local anesthetic lumbar epidural anesthesia on maternal cerebral blood flow in normal human pregnancy. Study Design: In an Institutional Review Board–approved, double-blind study, 24 healthy, normotensive, nonlaboring, term gravida women undergoing elective cesarean section were prospectively placed into random groups to receive either 2% lidocaine with 8.4% sodium bicarbonate (1:10) or 0.5% bupivacaine lumbar epidural anesthesia. After prehydration with 20 mL/kg crystalloid and 15-degree left-wedged supine positioning with 15-degree head tilt, transcranial Doppler ultrasound (Nicolet Pioneer EME) and simultaneous electrocardiogram, automatic blood pressure (Dinamap), and end-tidal CO 2 (SAR-Trans) monitoring were performed. Pulse, blood pressure, respiratory rate, end-tidal CO 2 , middle cerebral artery blood flow velocity, and pulsatility index were measured at (1) baseline (once supine positioning was assumed); (2) immediately after administration of 20 mL local anesthetic; and (3) every 5 minutes for 25 minutes. Timing of the attainment of a T4 dermatome anesthetic level was noted. Comparisons were made by t test, rank sum tests, χ 2 , and repeated measures analysis of variance. P < .05 was considered significant. Results: Maternal heart rate, blood pressure, respiratory rate, and end-tidal CO 2 were not significantly different within or between groups. No significant difference was found in baseline middle cerebral artery blood flow velocity or pulsatility index values between groups. Neither middle cerebral artery blood flow velocity nor pulsatility index changed significantly within or between groups up to 25 minutes after institution of epidural anesthesia. Conclusions: Maternal middle cerebral artery blood flow velocity, as measured by transcranial Doppler ultrasonography, is maintained in normotensive, nonlaboring term gravida women receiving either lidocaine or bupivacaine lumbar epidural anesthesia, which supports intact cerebrovascular autoregulation in normal pregnancy. (Am J Obstet Gynecol 1998;179:1237-40.)

Effect of lumbar epidural anesthesia on ventilatory response to hypercapnia in young and elderly patients

Study Objective: To examine the influence of age on resting ventilation, arterial blood gas tensions, and the ventilatory response to hypercapnia in lumbar epidural anesthesia. Design: Clinical study using groups of young and elderly patients. Setting: Surgical operation center of a university hospital. Patients: Seven young (average age 39 years) and seven elderly (average age, 69 years) unpremeditated patients undergoing lower abdominal surgery. Interventions: Patients were administered lumbar epidural anesthesia with 10 ml of 2% lidocaine. Measurements and Main Results: Resting ventilation, arterial blood gas tensions, and ventilatory response to hypercapnia were measured before and 20 minutes after the block. Regarding the ventilatory response to hypercapnia, the mean slope of the hypercapnic response curve (change in minute ventilation (V̇E) divided by change in end-tidal partial pressure of carbon dioxide (P ET CO 2)] increased significantly following the epidural block, by 16% in the young patients. and by 23% in the elderly patients, and the mean V̇E at a P ET CO 2 of 55 mmHg (V̇E 55) also increased significantly,, by 16% in the young subjects and by 26% in the older subjects. These changes in ΔV̇E/ΔP ET CO 2 and V̇E 55 were statistically equivalent between the two age-groups. Conclusions: The effects of lumbar epidural anesthesia on resting ventilation, arterial blood gas tensions, and ventilatory response to hypercapnia were not affected by age.

Abnormalities in Myocardial Segmental Wall Motion during Lumbar Epidural Anesthesia

The effect of lumbar epidural anesthesia on myocardial wall motion was compared in two groups of patients using precordial two-dimensional echocardiography (2DE). All patients were scheduled to undergo lower abdominal or peripheral surgery. Group 1 included five healthy ASA PS 1 subjects and group 2 included 10 patients with coronary artery disease (CAD). In all patients 12.5 ml of 2% lidocaine HCl was injected into the lumbar epidural space, and systolic and diastolic blood pressures, and heart rate were continuously monitored. 2DE evaluation was performed before and at 10, 20, 30, and 60 min (T10-T60) after epidural lidocaine injection. The left ventricular wall was divided into 16 segments for parasternal long-axis, short-axis and apical four-chamber views. The wall motion of each segment was graded on a scale from 1 (dyskinesia) to 6 (hyperkinesia), with 5 representing normal motion. A decrease in segmental wall motion greater than or equal to 2 grades was considered indicative of ischemia. Plasma lidocaine and catecholamine levels were measured before and 10, 20, and 60 min after epidural lidocaine injection. Peak plasma lidocaine levels in groups 1 and 2 were 2.79 +/- 1.06 micrograms/ml (mean +/- SD) and 2.58 +/- 1.48 micrograms/ml at 10 min, respectively (NS). Plasma epinephrine and norepinephrine levels were unchanged from baseline. Systolic pressures decreased significantly in group 2 from T10 to T60. Diastolic pressure decreased significantly in the same group from T20 to T60, and in group 1 only at T10. Mean arterial pressure decreased significantly in both groups at T30, without change in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Severe Preeclampsia

The hemodynamic effects of lumbar epidural anesthesia (LEA) were evaluated in 11 patients with severe preeclampsia. All patients were receiving magnesium sulfate upon entry into the study. Hemodynamic measurements were obtained before and after LEA, at delivery, and 2 hr postpartum. Lumbar epidural anesthesia significantly reduced mean arterial pressure from 121.4 mm Hg to 97.7 mm Hg, without altering cardiac index, pulmonary vascular resistance, central venous pressure (CVP), or pulmonary capillary wedge pressure (PCWP). There was a slight but statistically insignificant decrease in systemic vascular resistance from 1078 to 900.7 dynes X sec X cm-5. Cardiac index and left ventricular stroke work index were elevated in these patients, suggesting hyperdynamic left ventricular function. There was poor correlation between PCWP and CVP in several patients. We conclude that LEA may be used safely in severe preeclamptic patients and that pulmonary arterial catheters may help guide appropriate therapy in preeclamptic patients with cardiac failure or oliguria refractory to modest fluid challenges.

Motor Blockade During Epidural Anesthesia

The effects of lumbar epidural anesthesia (LEA) on a previously described test of function of the rectus abdominalis muscle (the RAM-test) were compared with the effects of LEA on the Bromage test of muscle power in the hips and legs in 20 women having elective cesarean sections under LEA using 0.5% bupivacaine with epinephrine 1:200,000. The results showed no statistically significant correlation between the two tests. We conclude that zones of differential somatic motor blockade are present during LEA and that in obstetrics the RAM-test is the more appropriate test for evaluating the effects of LEA on somatic motor function. Use of the RAM-test is suggested in situations where one is interested in motor function of the abdominal wall muscles under LEA.

Severe Preeclampsia

The hemodynamic effects of lumbar epidural anesthesia (LEA) were evaluated in 11 patients with severe preeclampsia. All patients were receiving magnesium sulfate upon entry into the study. Hemodynamic measurements were obtained before and after LEA, at delivery, and 2 hr postpartum. Lumbar epidural anesthesia significantly reduced mean arterial pressure from 121.4 mm Hg to 97.7 mm Hg, without altering cardiac index, pulmonary vascular resistance, central venous pressure (CVP), or pulmonary capillary wedge pressure (PCWP). There was a slight but statistically insignificant decrease in systemic vascular resistance from 1078 to 900.7 dynes X sec X cm-5. Cardiac index and left ventricular stroke work index were elevated in these patients, suggesting hyperdynamic left ventricular function. There was poor correlation between PCWP and CVP in several patients. We conclude that LEA may be used safely in severe preeclamptic patients and that pulmonary arterial catheters may help guide appropriate therapy in preeclamptic patients with cardiac failure or oliguria refractory to modest fluid challenges.