Ma zui xue za zhi = Anaesthesiologica Sinica最新文献

The efficacy of morphine by either lumbar extradural route or caudal extradural route and their adverse effects for postoperative analgesia were studied by comparing with the control group without morphine administration. 105 patients, 79 males and 26 females, aged 18 to 70 years, scheduled for hemorrhoidectomy surgery were selected. They were randomly assigned into three groups, i.e group I: without morphine use as control group (n = 35), group II: lumbar extradural morphine group (n = 35) and group III: caudal extradural morphine group (n = 35). Patients in group I received general anesthesia by face mask after induction by intravenous anesthetics and maintained with potent halogenated inhalation agents (isoflurane) through face mask. Patients in group II received lumbar extradural blockade through the L4-L5 intervertebral space, and those in group III received caudal extradural blockade through the sacrococcygeal junction (sacral hiatus) for intraoperative anesthesia and analgesia. Drugs included 0.5% bupivacaine 10ml + 2% xylocaine 10ml + 2mg morphine HCl + 0.1mg epinephrine were given either into the lumbar extradural space or into the caudal extradural space. No more narcotic has been given throughout the whole intraoperative course. All of these patients were followed up 24 hours later after the end of anesthesia. There were 11 patients (31.4%) in the control group, 26 patients (74.3%) in the lumbar extradural morphine group, and 25 patients (71.4%) in the caudal extradural morphine group who did not need additional narcotic for pain relief for more than 24 hours postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Endotoxic shock is presented with a complex pathophysiology and is associated with high mortality. Recently, it has been reported that endogenous opioids play an important role in endotoxic shock. Pressor effect of naloxone in shock may be mediated through antagonism of endogenous opioid inhibition of the sympatho-adrenal catecholaminergic system. In endotoxemic animal, circulating catecholamine levels were not elevated by naloxone. It is possible that naloxone acts upon opiate receptors to enhance catecholamine actions at the receptor level or post-receptor level. We investigated endotoxic shock using a rat model. The animals anesthetized with phenobarbital were infused with E. coli LPS for 30 minutes. They were divided into 5 groups. After an endotoxin i.v. infusion of 15 mg/kg (LD 60), a significant fall in mean arterial pressure (MAP), heart rate and pH occurred in all groups. Treatment with naloxone or buprenorphine or naloxone + epinephrine resulted in significant improvement in MAP, pH and base excess. Treatment with morphine resulted in a decrease in MAP and an increase in heart rate. The pressor response to epinephrine 10, 30, 60 microgram/kg i.v. caused an increase of 62%, 48% and 17% of control values respectively in endotoxic treated rats. The duration of the pressor response to epinephrine was significantly increased by naloxone, although no significant effects on survival were seen at 4 hours after the start of treatment. These findings suggest that the buprenorphine may prove to be an alternative to naloxone, the co-administration of naloxone and epinephrine may be of benefit in the management of septic shock.

Blood loss in patients on cardiopulmonary bypass is tremendously large after surgery due to platelet dysfunction. Desmopressin acetate (a synthetic analogue of vasopressin) has been shown to improve blood coagulation in a variety of platelet disorders especially in patients with hemophilia, von Willebrand's disease and uremia. Recent years, it has been used to treat patients with severe platelet dysfunction and profuse hemorrhage after cardiopulmonary bypass. We have investigated the effect of desmopressin acetate administration in randomized trials of 48 adult patients placed on cardiopulmonary bypass during cardiac surgery. Twenty four patients received intravenous infusion 0.3 microgram/kg desmopressin acetate one hour after cardiopulmonary bypass and other patients only received a placebo. Comparing with the control group, patients receiving desmopressin had shortened bleeding time (3.4 +/- 0.6 vs 5.1 +/- 1.6 mins, 8 hrs post bypass), lessened blood loss (482 +/- 258 ml vs 1430 +/- 733 ml, 24 hrs post bypass) and received fewer blood component therapy (pack RBC 2.7 +/- 2.2 vs 6.6 +/- 3.2 units, FFP 4.3 +/- 2.4 vs 11.7 +/- 5.7 units, platelet 3.8 +/- 5.0 vs 8.4 +/- 7.2 units). We conclude that desmopressin acetate can improve blood coagulation ability with safety and in reducing blood loss in patients after cardiopulmonary bypass.

The patients with preeclampsia undergoing emergent cesarean section is always a challenge to an anesthesiologist, because severe hypertensive response after laryngoscopy and tracheal intubation may result in life-threatening complication such as cerebral hemorrhage. Most of these patients receive magnesium sulfate for the prevention of convulsion. An ideal anti-hypertensive drug for preeclampsia should be effective, limited fall in blood pressure, rapid onset, maintaining uteroplacental blood flow, and less maternal and fetal side effects. We studied the efficacy of 10 mg sublingual nifedipine in attenuating the pressor response to intubation. We were also concerned about whether this calcium antagonist may inhibit uterine contraction and increase intra and postpartum hemorrhage when it is used with magnesium sulfate and general anesthesia. There were thirty-three patients in our study (16 in nifedipine group and 17 in control group). This study revealed that nifedipine attenuate the hypertensive response effectively. Uterine contraction response to oxytocic drugs was quite well in both groups. There was no significant difference in blood loss between nifedipine and control group. And no severe maternal and fetal adverse effect.

It is fairly widespread clinical practice to administer large doses of corticosteroids to patients in cases of shock; doses of hydrocortisone as high as 50 mg/kg given intravenously have been proposed and used; especially in cases of Myasthenia Gravis. Its effects on neuromuscular transmission is not yet fully understood. In order to determine the mechanism of this interaction, we undertook this investigation. The neuromuscular effects of Dexamethasone, at single dose of 100 micrograms/kg intravenously or intraperitoneally, were studied by electromyographical quantification of the tibialis-anterior muscle evoked by sciatic nerve stimulation in 21 rats anesthetized with Urothane 1.25 g/kg given intraperitoneally. Intravenous Dexamethasone (n = 7) had no obvious effect on the blockade of tibialis-anterior muscle produced by the cumulative doses of Vecuronium (ED50 = 180 +/- 24 micrograms/kg), as compared with the control group (n = 7) (ED50 = 201 +/- 18 micrograms/kg). In contrast, intraperitoneal Dexamethasone (n = 7) produced a significant (P < 0.05) change (ED50 = 240 +/- 28 micrograms/kg), when compared with control group. The results showed that in tibialis-anterior muscle sciatic nerve preparation of rats, intraperitoneal Dexamethasone had antagonism effect on Vecuronium. However, there was no obvious influence on Vecuronium in the intravenous Dexamethasone group.

Despite vast clinical experience and success with intravenous regional anaesthesia (IVRA), the site and mode of action of the local anesthetic agents remains controversial. Many investigations have been published, but conclusions are variable. The principal site of action of lidocaine in IVRA was studied using 15 ASA I-II patients receiving surgical operation on the hands and forearms. A 22 gauge plastic cannula was inserted into the median cubital vein at the elbow. A double cuff tourniquet was secured on the upper arm, as described by Bier and modified by Homes. Another single tourniquet was then applied on the forearm as near the plastic catheter as possible. Two different concentrations of lidocaine (0.5% and 2%) in a total dose of 3 mg kg-1 was slowly injected into the vein via the catheter after the limb was exsanguinated and the tourniquets were inflated. The results showed that 0.5% lidocaine produced analgesia only on the intercuff area; there was no analgesic response noted on the forearm distal to the third tourniquet after a 15 minutes observation. However patients who received 2% lidocaine experienced in analgesia rapidly on the intercuff area and also slowly on the forearm and hand. The anesthesia developed from the fingertips upward. Based on this evidence, we concluded that the principal site of action of lidocaine in IVRA depends on concentration. The lower concentration acts on the sensory nerve endings and the small nerves. Whereas, the higher concentration acts on both nerve trunks and nerve endings.

Toxicity of local anesthetics is a serious concern by anesthesiologists while performing regional anesthesia. The toxicity includes convulsion, respiratory difficulty, or sometimes cardiac arrest. Total dose of local anesthetic usually cannot predict the occurrence of toxic effects because these effects are directly correlated to the plasma concentration. The plasma concentration is dependent not only on total dose given, but also on the routes of administration, volume of distribution, plasma protein binding and the rate of local absorption. This study is to examine the plasma concentration of lidocaine during spinal or epidural anesthesia in geriatric patients. 12 ASA physical status class II-III patients, age over 65 years old, were selected in this study. They were randomly divided into two groups. Group A patients (n = 6) were anesthetized with 3 mL 2% lidocaine intrathecally and Group B patients (n = 6) were anesthetized with 15 mL 2% lidocaine epidurally. Plasma concentration of lidocaine was examined every 15 minutes after drug administration. The peak level in group A was reached at 90 minutes and group B 105 minutes after drug administration. Peak level in Group A was 1.12 +/- 0.08 micrograms/mL and the plateau was reached at 45 minutes after drug administration. In Group B, peak level was 4.70 +/- 0.74 micrograms/mL and the plateau was reached at 15 minutes. The results also indicated that the absorption of the drug in spinal is much lower than in epidural.

Intravenous meperidine 25mg has been employed effectively to treat shivering following regional anesthesia and general anesthesia. The study was designed to evaluate the effectiveness of intramuscular meperidine for the prevention of shivering in spinal anesthesia. The series consisted of 60 patients who were divided into 2 groups with 30 patients in each, undergoing lower abdominal or lower extremity surgery. All patients were given diazepam 0.1mg/kg i.v. for anxiolysis when they came to the operating room. In a double blind and randomized fashion, patients in the study (meperidine) group received meperidine 25mg IM (= 0.5ml). In the control group 0.9% N/S 0.5ml IM was given instead. All patients received spinal anesthesia 15 minutes later. Measurement of the levels of sensory loss to pinprick was made. The ambient temperature and the rectal temperature were continuously monitored to evaluate the effect of the change in body temperature on shivering during operation. The degree and the occurrence of shivering were carefully evaluated and recorded by a blind-trust observer. There was no significant difference in maximal analgesic level, ambient temperature and change of rectal temperature during operation between the groups. Shivering occurred in 17 patients (56.7%) in the saline group with an onset time of 7.9 +/- 2.5min following spinal anesthesia. In the meperidine group, shivering occurred only in 3 patients (10%) with an onset time of 54 +/- 29.5min after spinal anesthesia. There was a significantly lower incidence of shivering in the meperidine group than in the saline group (p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)