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PubMed1999

Time dependency of the ratio of umbilical vein/maternal artery concentrations of vecuronium in caesarean section.

BACKGROUND: The ratio of umbilical vein (UV) and maternal artery (MA) concentrations of vecuronium may more accurately determine the placental transfer ratio during caesarean section. This ratio potentially correlates with the time from induction of anaesthesia to delivery (I-D time). The aim of this study was to determine the UV/MA ratio of vecuronium and its relationship with the I-D time. METHODS: Eighteen pregnant women at full term undergoing caesarean section were studied. The parturient was given intravenously 0.01 mg/kg vecuronium as a priming dose, followed 180 s later by 0.11 mg/kg vecuronium as an intubation dose and 4 mg/kg thiamylal. The time from the injection of the intubation dose to the clamping of the umbilical cord was regarded as the I-D time. At the time of clamping the umbilical cord, blood samples were collected and the UV and MA of vecuronium were measured. RESULTS: The UV/MA ratio and the I-D time, expressed as the mean (SD), were 0.056 (0.016) and 280 (57) s, respectively. The regression equation indicated y = 0.0083 + 0.00017 x (R2 = 0.381, r = 0.617, P = 0.0063, I-D time (s) = x, UV/MA = y). CONCLUSION: The present study demonstrated that the UV/MA ratio of vecuronium as an index of the placental transfer becomes smaller as the delivery time after injection of this drug becomes shorter during caesarean section.

Adult↗
PubMed1996

Temperatures measured by a deep body thermometer (Coretemp) compared with tissue temperatures measured at various depths using needles placed into the sole of the foot.

Continuous monitoring of body temperature during anaesthesia is a widely accepted clinical practice for which a variety of techniques are used. In this study, the accuracy of the deep body thermometer (Coretemp) was compared with temperatures measured by needle thermocouples. With IRB approval and informed consent, seven ASA physical status I and II patients undergoing otolaryngeal surgery were studied. General anaesthesia and neuromuscular blockade were induced with thiamylal and vecuronium. Anaesthesia was maintained with isoflurane at an end-tidal concentration of 1.0-2.0% and 66% nitrous oxide in oxygen. After induction of general anaesthesia, subcutaneous temperature was measured at the sole of the left foot using a Coretemp. Additionally 8-, 18-, and 38-mm-long needle thermocouples were inserted into the the sole of the left foot close to Coretemp and skin-surface temperature was also recorded adjacent to the needles. The Coretemp measurement (Tc) correlated best with 18-mm-deep needle temperature (r2 = 0.87). There was also a good correlation between Tc and 38-mm-deep needle temperature (r2 = 0.83). Skin and 8-mm-deep needle temperatures correlated poorly or only moderately with Tc (r2 = 0.67, 0.75, respectively). These results indicate that temperatures measured by Coretemp well reflect the temperatures at a depth of 18 mm or more from the skin into the foot.

Anesthesia, General↗
PubMed1999

Effects of propofol anesthesia on cognitive recovery of patients undergoing electroconvulsive therapy.

The effects of different doses of propofol on post-electroconvulsive therapy (ECT) cognitive recovery were evaluated together with the effects on seizure duration and hemodynamic changes during ECT in 15 depressive patients. Propofol attenuated the increase in arterial blood pressure and heart rate in a dose-dependent manner compared with thiamylal. Propofol showed a clinically significant anticonvulsant effect during ECT in a dose-dependent manner. There were no significant differences among the four different induction groups in the mean recovery time from anesthesia, however, a low dose of propofol suppressed the early recovery of cognitive function. For early cognitive recovery after ECT, a deep anesthetic level is necessary when the traditional ECT apparatus is used which produces sine curve wave stimuli.

Adult↗
PubMed1996

Thiobarbiturates suppress depolarization-induced contraction of vascular smooth muscle without suppression of calcium influx.

We have studied the effects of barbiturates on vascular smooth muscle tension and cytosolic calcium concentrations ([Ca2+]i) in endothelium-denuded rat aortic rings, preloaded with fluo-3. Changes in [Ca2+]i were estimated by the fluorescence intensity of the calcium-bound form of fluo-3. In aortic rings under basal conditions, thiobarbiturates (thiopentone and thiamylal 100-300 mumol litre-1) increased [Ca2+]i, concomitantly with an increase in tension, although oxybarbiturates (pentobarbitone and secobarbitone up to 300 mumol litre-1) had no effect. Thiopentone (300 mumol litre-1)-induced increases in tension and fluorescence intensity were mean 25.1 (SD 3.2)% and 55.0 (6.0)%, respectively, of those induced by KCl 30 mmol litre-1 (n = 8, each). In KCl (30 mmol litre-1)-precontracted aortic rings, thiopentone decreased tension without reduction of [Ca2+]i, whereas pentobarbitone decreased tension and [Ca2+]i, KCl (30 mmol litre-1)-induced contraction was suppressed by pretreatment with all barbiturates (100-300 mumol litre-1); thiopentone 300 mumol litre-1 suppressed contraction to 64.8 (2.5)% (n = 6) and pentobarbitone 300 mumol litre-1 to 57.5 (2.2)% (n = 9). However, the increase in [Ca2+]i was suppressed by oxybarbiturates (pentobarbitone 300 mumol litre-1 to 77.9 (5.2) %; n = 9), but not altered by thiobarbiturates. These results suggest that thiobarbiturates and oxybarbiturates affect vascular smooth muscle differently and that the affected site in thiobarbiturate-induced vasodilatation is distal to regulation of [Ca2+]i.

Anesthetics, Intravenous↗
PubMed2000

Complete recovery of consciousness in a patient with decorticate rigidity following cardiac arrest after thoracic epidural injection.

A 46-yr-old man with dysaesthesia (burning sensation) following herpes zoster in the left upper chest region was treated with a single thoracic (T2/T3) epidural injection (1.0% lidocaine 3 ml + 0.125% bupivacaine 3 ml) as an outpatient. Twenty minutes after the injection, a nurse noticed the patient to be unconscious with dilated pupils, apnoea and cardiac arrest. Following immediate cardiopulmonary resuscitation, the patient was treated with an i.v. infusion of thiamylal sodium 2-4 mg kg-1 h-1 and his lungs were mechanically ventilated. When the patient developed a characteristic decorticate posture, mild hypothermia (oesophageal temperature, 33-34 degrees C) was induced. On the 17th day of this treatment, after rewarming (35.5 degrees C) and discontinuation of the barbiturate, the patient responded to command. Weaning from the ventilator was successful on the 18th day. About 4 months after the incident, the patient was discharged with no apparent mental or motor disturbances. We suggest that mild hypothermia with barbiturate therapy may have contributed to the successful outcome in this case.

Analgesia, Epidural↗
PubMed1975

Presynaptic inhibition in man during anesthesia and sleep.

The slow positive (P2) wave of the evoked electrospinogram was recorded from the dorsal epidural space in man. The waveform characteristics of the P2 wave were similar to those of the dorsal cord positive wave (P wave), which is believed to be caused by the primary afferent depolarization (PAD) and to be related to presynaptic inhibitory action in animals. The "second" component of the P2 wave appeared during excitement or following strong stimulation and disappeared after thiamylal administration and during natural slow-wave sleep. The second component, also demonstrated in the P wave of rabbits during ketamine anesthesia, was abolished by spinal transection. Therefore, these second components in man and rabbits may originate from a feedback loop via supraspinal structures. Thus, supraspinal influences might play an important role in the regulation of presynaptic inhibition in the spinal cord of man during wakefulness and anesthesia.

Afferent Pathways↗
PubMed1978

Cerebral effects of nitrous oxide in the dog.

The cerebral effects of nitrous oxide, 60 per cent, were examined in 27 dogs. During administration of halothane, 0.2 per cent, nitrous oxide increased cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMR02) to a maximum of 203 and 121 per cent of control, respectively. Cerebrospinal fluid pressure paralleled the change in CBF. The electroencephalogram (EEG) showed low-voltage slow-wave activity. With halothane, 0.8 per cent, nitrous oxide increased CBF and CMR02 to maximum values of 164 and 108 per cent of control, respectively. After administration of thiamylal, 8 mg/kg, intravenously, nitrous oxide did not increase CBF or CMR02 for the first 30-min period, but thereafter, CMR02 increased to 11 per cent above control. Pretreatment with reserpine, 0.5 mg/kg, intramuscularly, for two days did not modify the cerebral circulator and metabolic responses to nitrous oxide. These results indicate that nitrous oxide causes cerebral metabolic stimulation accompanied by an increase in CBF and slowing of the EEG. Sympathoadrenal stimulation would appear not to be the mechanism for the increases in CBF and CMR02. The cerebral effects of nitrous oxide are modified by the background anesthesia.

Animals↗
PubMed1984

Anesthetics and excitatory/inhibitory responses of midbrain reticular neurons.

The effects of nitrous oxide, halothane, ether, isoflurane, thiopental, and thiamylal on the excitatory as well as inhibitory responses of single neurons in the midbrain reticular formation (MRF), believed to be one of the most important sites for the regulation of wakefulness, were studied by long-term, extracellular microelectrode recording in cats and rats. All anesthetics except nitrous oxide suppressed the excitatory responses of MRF neurons evoked by somatosensory stimulation. The inhibitory responses markedly were potentiated by both barbiturates but variously affected by other inhalation anesthetics. Blockade of the inhibitory responses (disinhibition) was observed more frequently with the inhalation agents during the light state of anesthesia. Thus, suppression of excitatory responses is likely to be a general feature of the anesthetic state in terms of the behavior of MRF neurons. Further, potentiation of the inhibitory responses might be characteristic of barbiturate anesthesia.

Anesthetics↗
PubMed1986

Prolonged hyporesponsiveness of airway smooth muscle to histamine following general anesthesia.

The prolonged effect of barbiturates and inhalation anesthesia on airway response to histamine was studied in five groups of dogs. Group B (n = 10), H24 (n = 5), and H72 (n = 5) were anesthetized with sodium thiamylal (B) or halothane and N2O (H24, H72) for 3 h, during which a dose-response curve to histamine was obtained. The animals were then allowed to recover; 24 h (B and H24) or 72 h later, the animals were killed and an in vitro dose-response curve to histamine was obtained on a tracheal smooth muscle (TSM) specimen. Group C (n = 5), the control group, had no prolonged exposure to anesthesia. The dogs were immediately killed and the in vitro histamine response of the TSM was measured. The results (mean +/- SE) showed that the smooth muscle contractile properties (i.e., the maximum contraction to electrical field stimulation) were comparable in all four groups: 111 +/- 12 g (B); 168 +/- 23 g (H24); 106 +/- 32 g (H72); and 107 +/- 31 g (C). The maximum response (mean +/- SE) to histamine (as % of maximum electrical contraction) was: 15 +/- 6% (B), 30 +/- 9% (H24), 32 +/- 12% (H72), and 50 +/- 8% (C). Statistical analysis of the data showed that the histamine response of Group B and Group H24 was significantly decreased compared to Group C (P less than 0.01 and less than 0.05, respectively); in Group H72 the results were not significantly different from Group C (0.1 greater than P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1987

Differential effects of isoflurane on human median nerve somatosensory evoked potentials.

The effect of isoflurane on median nerve somatosensory evoked potentials (MN-SSEPs) was studied in 15 patients. Anesthesia was induced with thiamylal and maintained with oxygen and isoflurane. MN-SSEPs were recorded in awake patients and after achieving 0.5, 1.0, 1.5, and 2.0% stable end-tidal concentrations of isoflurane. Peak latencies and amplitudes of EP, N13, and N20 and conduction times EP-N13, N13-N20, and EP-N20 were measured. Peak latencies of all components increased after all concentrations of isoflurane compared with control values. N20 peak latencies after 1% and 1.5% isoflurane differed significantly, whereas EP and N13 latencies showed no significant difference. No significant change in conduction time EP-N13 resulted from 1% and 1.5% concentrations of isoflurane compared with control values. Isoflurane increased conduction time N13-N20 significantly when compared with control values, and this increase was dose related. Amplitude of EP and N13 did not show significant change with 1% and 1.5% isoflurane when compared with control values. Amplitude of N20 decreased significantly following isoflurane anesthesia compared with control values, and the difference between 1% and 1.5% isoflurane recordings was also statistically significant. N20 was not discernible in one out of 14 patients after 1.5% and in three out of ten patients after 2% isoflurane. These results indicate that subcortical potentials are less affected by isoflurane anesthesia than cortical potentials. Amplitude reduction of cortical potentials was more noticeable than either prolongation of peak latency or conduction time.(ABSTRACT TRUNCATED AT 250 WORDS)

Evoked Potentials, Somatosensory↗
PubMed1978

Intravenous procaine for general anesthesia in dogs: a new look at an old technic.

New anesthetics have been introduced during the last 25 years which are not without inherent disadvantages. They are expensive, and some produce nephrotoxicity and possibly hepatotoxicity. Although the use of procaine intravenously as an anesthetic has been discarded, probably because of a convulsive effect, it is believed this disadvantage can be controlled by concomitant use of other drugs. Hence procaine, preceded by thiamylal, was administered to dogs to test its anesthetic capability, reversibility, and effects on the cardiovascular and central nervous systems. Blood levels of procaine were measured and correlated with these physiologic responses. Convulsive doses were ten times those producing anesthesia. There were no detrimental effects which would preclude a reevaluation in humans. Intravenous procaine produces definite general anesthesia, and it has the additional advantages of being rapidly hydrolyzed and providing antiarrhythmic effects. It may prove useful in modern anesthesia.

Anesthesia, General↗
PubMed1981

Naloxone does not antagonize the anesthetic-induced depression of nociceptor-driven spinal cord response in spinal cats.

The effects of several anaesthetics on spinal cord nociceptive neural mechanisms and their interactions with the opiate antagonist, naloxone, were studied in acute, spinal cord transected cats. Intra-arterial injection of bradykinin was used as the noxious test stimulus. Spontaneous activity and the neural response induced by bradykinin were recorded by the multi-unit activity technique in the lateral funiculus of the spinal cord. Naloxone, 0.1 or 2.0 mg/kg i.v. had little effect on the bradykinin-induced response, but enhanced the spontaneous firing of the lateral funiculus significantly. Fentanyl, 30 micrograms/kg i.v., depressed both the bradykinin-induced response and spontaneous firing. These effects of fentanyl were antagonized completely by naloxone, 0.1 mg/kg i.v. Nitrous oxide, thiamylal, halothane and ether depressed the bradykinin-induced response considerably, but it was not antagonized by naloxone, 0.1-2.0 mg/kg i.v. Enflurane had little effect on the bradykinin-induced response. The effects of these anesthetics on spontaneous firing were divergent: nitrous oxide enhanced it while other drugs depressed it, to various degrees. All these data suggest that the neural and/or neurochemical mechanisms of anesthetic-induced analgesia differ from mechanisms related to opioids.

Anesthetics↗
PubMed1993

Combined effects of adrenergic and intravenous anesthetic agents on inositol monophosphate levels in rat liver prisms.

Combined effects of adrenergic and intravenous anesthetic agents on phosphatidylinositol (PI) turnover were studied using rat liver prisms incubated with [3H]myo-inositol. Rat liver prisms responded to epinephrine, norepinephrine and phenylephrine dose-dependently with an increase in inositol monophosphate (IP1) formation but they did not respond to ephedrine. Dopamine-induced effects were seen only at concentrations as high as 10(-4) mol.l-1. The enhancement of IP1 formation induced by epinephrine was potentiated by thiamylal at concentrations of 10(-5) mol.l-1 and 10(-4) mol.l-1, remained unaffected by ketamine, fentanyl or midazolam, but was dose-dependently inhibited by droperidol. The present results from in vitro studies of liver cell metabolism suggest that alpha-adrenergic agents in combination with barbiturates may potentiate liver cell damage by activation of PI turnover and interrelated intracellular Ca++ accumulation.

Anesthesia, Intravenous↗
PubMed2001

Anesthesia rapidly suppresses insulin pulse mass but enhances the orderliness of insulin secretory process.

Induction of anesthesia is accompanied by modest hyperglycemia and a decreased plasma insulin concentration. Most insulin is secreted in discrete pulses occurring at approximately 6- to 8-min intervals. We sought to test the hypothesis that anesthesia inhibits insulin release by disrupting pulsatile insulin secretion in a canine model by use of direct portal vein sampling. We report that induction of anesthesia causes an abrupt decrease in the insulin secretion rate (1.1 +/- 0.2 vs. 0.7 +/- 0.1 pmol. kg(-1). min(-1), P < 0.05) by suppressing insulin pulse mass (630 +/- 121 vs. 270 +/- 31 pmol, P < 0.01). Anesthesia also elicited an approximately 30% higher increase in insulin pulse frequency (P < 0.01) and more orderly insulin concentration profiles (P < 0.01). These effects were evoked by either sodium thiamylal or nitrous oxide and isoflurane. In conclusion, anesthesia represses insulin secretion through the mechanism of a twofold blunting of pulse mass despite an increase in orderly pulse frequency. These data thus unveil independent amplitude and frequency controls of beta-cells' secretory activity in vivo.

Anesthesia↗
PubMedDate not supplied

Inhibitory effect of barbiturates and local anaesthetics on protein kinase C activation.

A calcium- and phospholipid-dependent protein kinase C subspecies purified from rat brain was inhibited by thiamylal, thiopentone, pentobarbitone, mepivacaine and bupivacaine. This was attributed to the inhibition of the activation process rather than to direct interaction with the active site of the enzyme. It is well established that unsaturated diacylglycerol markedly increases the affinity of protein kinase C for calcium ions. Kinetic analysis suggested that pentobarbitone brought about the inhibition by competing with the diacylglycerol diolein and that mepivacaine and bupivacaine competed with the phospholipid phosphatidylserine used in the assay. The possibility exists that the effects of local anaesthetics on the function of various tissues are due, in part, to an inhibitory action on protein kinase C.

Anesthetics, Local↗
PubMed1986

Multisystem degeneration: drugs and square wave jerks.

We studied a 55-year-old woman with macrosquare wave jerks and macrosaccadic oscillations with a vertical component. The oscillations almost completely disappeared after administration of diazepam, clonazepam, thiamylal, or phenobarbital. A disorder of GABAergic tonic inhibitory system from the substantia nigra to superior colliculus probably plays an important the pathogenesis of these abnormal ocular movements. role in the pathogenesis of these abnormal ocular movements.

Clonazepam↗
PubMedDate not supplied

Heart-rate slowing and junctional rhythm following intravenous succinylcholine with and without intramuscular atropine preanesthetic medication.

The incidence of heart-rate slowing (greater than 15 percent) and junctional rhythm after two injections of succinylcholine (1 mg/kg), separated by 5 minutes, was determined in adult patients. All patients received intramuscular morphine as preanesthetic medication 60 to 90 minutes before intravenous thiamylal anesthetic induction. Intramuscular atropine (mcg/kg) 60 to 90 or 15 to 20 minutes before anesthetic induction did not alter the incidence of first or second succinylcholine dose heart-rate slowing or junctional rhythm as compared with patients receiving only morphine premedication.

Anesthesia, Endotracheal↗
PubMed1990

Effects of thiobarbiturates on smooth muscle reactivity in isolated aortas from spontaneously hypertensive rats.

The direct effects of thiobarbiturates on helical strips of aortas from spontaneously hypertensive (SH) rats were compared with those from Wistar-Kyoto (WKY) rats. At 5-6 wk of age, the arterial pressure of SH and WKY rats did not differ, and the effects of thiobarbiturates on aortic strips from SH and WKY rats were similar. By contrast, at the age of 10-12 or 20-21 wk arterial pressure was higher in SH than in WKY rats, and responses to thiobarbiturates differed in aortic strips from SH and WKY rats: contractile responses were greater in WKY than in SH rats, and relaxing effects were greater in SH than in WKY rats. Responses to sodium nitroprusside did not differ in the aortas of SH and WKY rats, but the effects of nifedipine were greater in strips from SH rats than from WKY rats at the age of 10-12 wk. Ca2(+)-induced contractions of strips exposed to Ca2(+)-free media and depolarized by high K+ were inhibited by treatment with thiamylal; the inhibition was greater in SH than in WKY rats. The increase in smooth-muscle relaxation induced by thiobarbiturates in strips from SH rats may be due to increased sensitivity to the Ca2(+)-channel blocking action of thiobarbiturates.

Animals↗