摘要:

The effect of isoflurane alone (Group 1) and isoflurane following thiopental (Groups 2 and 3) on baroreflex control of heart rate in humans was investigated in this study. Phenylephrine (the pressor test) and sodium nitroprusside (the depressor test) were used to induce moderate changes in arterial blood pressure and to alter the stimulation of baroreceptor sites. In addition, graded neck suction was employed to examine carotid baroreflex control of heart rate. In Group 3 subjects, phenylephrine was infused continuously during anesthesia to maintain mean arterial blood pressure near control levels. The pressor- and neck-suction-derived baroreflex slopes were decreased progressively from awake to 1.0 and 1.5 MAC isoflurane. The slopes of the depressor responses were decreased at 1.0 MAC but showed little further depression at 1.5 MAC. For each method, the depression of baroreceptor slopes from control to 1.0 MAC and 1.5 MAC was similar among the three groups. Maintenance of arterial blood pressure (Group 3) and the utilization of thiopental (Group 2) did not significantly alter the depression of baroreflex responses during increasing levels of isoflurane anesthesia. Neck suction derived slopes compared favorably with the pressor test slopes (r = 0.75,P< 0.001). This study indicates that the depression of arterial baroreflex heart rate responses under isoflurane anesthesia are less pronounced than the depression of baroreflex responses noted by other investigators for halothane or enflurane. The neck suction technique appears to be a sensitive method useful in assessing the carotid sinus reflex in awake and anesthetized humans.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The effect of high-dose fentanyl on the cerebral vascular response to alterations in mean arterial blood pressure, arterial O2tension (PaO2), and arterial CO2tension (PaCO2) was studied in 28 mongrel dogs using the cerebral venous outflow technique. In 13 animals anesthetized with sodium pentobarbital (30 mg/kg, iv), bolus injection of fentanyl (25 μ/kg, iv) decreased mean arterial blood pressure (MABP) without a change in cerebral blood flow (CBF). In these animals, the response of the cerebral circulation to changes in PaO2, PaCO2, and MABP was determined before and after fentanyl administration. Fentanyl did not alter the increase in CBF caused by hypoxic hypoxia or hypercapnia. The lower and upper limit of cerebral autoregulation determined by hypovolemic hypotension and norepinephrine infusion, respectively, also were unaltered by fentanyl administration. The CBF response to alterations of MABP, PaO2, and PaCO2were studied in another group of 15 dogs anesthetized with fentanyl (100 μ/kg) plus small doses (3–5 mg/kg) of pentobarbital. The CBF response to PaO2, and PaCO2in these animals was not different from that observed in animals anesthetized with barbiturates only. The lower and upper limit of cerebral autoregulation also were not different from that observed in animals anesthetized with barbiturates only. These data suggest that fentanyl in doses sufficient to cause profound analgesia and anesthesia did not alter cerebral responsivity to changes in PaO2, and PaCO2, and MABP.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The effects of thiopental sodium on the adrenergic neuroeffector junction were studied in isolated rabbit pulmonary arteries. Basal tension was not altered by thiopental (2 X 10-5and 10-4M) but was increased by high concentrations of thiopental (5 X 10-4M). Thiopental (10-4and 5 X 10-4M) potentiated contractions induced by transmural electrical stimulation. Contractile responses to exogenously applied low concentrations of norepinephrine (NE) were potentiated by thiopental (2 X 10-5, 10-4and 5 X 10-4M), whereas those to high concentrations were not altered. In strips previously incubated in 1-[7,8-3H]-NE (10-7M), the release of [3H] induced by transmural stimulation (5 Hz) was not altered by thiopental (10-4and 5 X 10-4M). Potentiation by thiopental (10-4M) of the responses to transmural stimulation was not affected by prior application of cocaine or hydrocortisone. Contractions induced by alpha receptor agonists (phenylephrine and methoxamine) were potentiated by thiopental (10-4M), while those induced by acetylcholine were not altered. Contractile responses to potassium chloride were attenuated by thiopental (10-4M). Amobarbital sodium and pentobarbital sodium (10-4M, respectively) attenuated contractions induced by NE. It may be concluded that thiopental specifically increases the responsiveness of postsynaptic alpha receptors to NE.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Using the open ventriculocisternal perfusion method, the rate of cerebrospinal fluid (CSF) production was examined in dogs anesthetized with isoflurane (1.4%) and nitrous oxide (66%) in oxygen. In one group (n = 6) the rate of CSF production did not change significantly when the expired concentration was decreased from 1.4% to <0.15%. In a second group (n = 6) maintained at isoflurane 1.4%, the rate of CSF production decreased by ∼8%/h, similar to the time effect previously reported in controls with this model (a decrease of 4–9%/h). These data suggest that isoflurane causes no significant change in the rate of CSF production and that an increase in CSF volume does not occur during prolonged isoflurane anesthesia. In patients at risk due to increased intracranial pressure, isoflurane may be preferred to anesthetics that may increase intracranial volume,e.g., enflurane or ketamine.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The differential effects of exposure to a moderately hypoosmotic hyponatric solution (0.35 isoosmotic, Na+36 mmol/l) on conduction in myelinated (A) and unmyelinated (C) axons were studiedin vitroon compound action potentials of rabbit vagus nerves in which the perineurial sheath had remained undisturbed. Controls were incubated at 37° C in isoosmotic isonatric solution for 5 h (Group 1a, n = 7) or 7 h (Group 3, n = 3). Other controls were incubated in isoosmotic isonatric solution for 2 h followed by 3 h in isoosmotic hyponatric (Na+36 mmol/l) solution (Group 1b, n = 6); experimental nerves were incubated in isoosmotic isonatric solution for 2 h followed by 3 h in hypoosmotic hyponatric solution (Group 2, n = 7) and, to study recovery, a further 2 h in isoosmotic isonatric solution (Group 4, n = 8). In Group 1b, isoosmotic hyponatric exposure approximately doubled the latency of the A-component (A-CAP) and decreased the A-CAP amplitude to 44 ± 8% of control; the amplitude of the C-component decreased to 65 ± 15% of control. Hypoosmotic hyponatric exposure increased the latency of the A-CAP by 82 ± 10% (mean ± SE,P< 0.001) and extinguished A-CAP within 20 min, whereas the latency increase of the C-component (C-CAP) was more than twice as great and extinction slower and often incomplete; neural wet weight increased 34 ± 4% and neural sodium and potassium contents decreased 55 and 42%, respectively. Recovery in isoosmotic isonatric solution (Group 4) was absent or very small in the case of A-CAP, as regards latency and amplitude but was complete for C-CAP amplitude. Neural wet weights and sodium content also recovered fully, but neural potassium content recovered only about 45%. Electron microscopy revealed hypoosmotic hyponatric structural damage to the larger myelin sheaths; the axons themselves were unaffected. It is concluded that it is probably inadvisable to attempt selective conduction block of sensory C-fibers by application of hypoosmotic solutions to peripheral nerves.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The exact role of calcium in nerve conduction in neurons that have been blocked by local anesthetics remains controversial. Recently, attention has been drawn to the importance of examining both frequency-dependent and nonfrequency-dependent conduction block, since it is felt that frequency-dependent block provides a model that more closely approximates the normal physiologic state. The present study was designed to examine the effects of calcium on both the nonfrequency-dependent and frequency-dependent components of lidocaine nerve block. Desheathed, whole sciatic nerves from frogs were placed in a sucrose gap chamber and stimulated by trains of 20 impulses at frequencies from 3 to 90 Hz at supramaximal intensity for activation of the compound action potential. After control studies, the nerve was bathed by a frog Ringer's solution containing calcium concentrations, which increased from 0.0 mM to the physiologic value of 2.0 mM with or without 0.5 mM lidocaine. Compound action potentials were measured, and both frequency-dependent block and nonfrequency-dependent block were compared in each solution. Low calcium concentrations significantly enhanced both nonfrequency- and frequency-dependent lidocaine block. The effect of low concentrations of calcium was greater at higher frequencies of stimulation.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The authors are studying the molecular details of the process that begins with hepatic metabolism of halogenated inhalation anesthetics and ends with hepatic necrosis. In previous studies they have shown that the halothane-free radical produced by UV-irradiation is identical to that produced during reductive metabolism of halothane by hepatic cytochrome P-450. In the present study, the authors have examined a mechanism by which free radicals may propagate damage in the endoplasmic reticulum of liver cells. The 1-chloro-2,2,2-trifluoroethyl free radical produced by UV-irradiation of halothane can abstract a hydrogen radical from arachidonic acid to yield 2-chloro-1,1,1-trifluoroethane and an arachidonic acid-free radical. The arachidonic acid-free radical reacts with molecular oxygen to form 5− and 15-hydroperoxyeicosatetraenoic acid. There is considerable evidence that the peroxidation process that we studied in the model system will be similar when the arachidonic acid is an acyl chain on a membrane phospholipid and the free radicals are generated metabolically. The authors suggest that these hydroperoxides may be toxic by acting as intermediates in the pathway of leukotriene production as well as by direct oxidation of membrane components.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

If further sympathetic stimulation is neither possible nor desirable during moderate hypovolemia, anesthetic agents capable of sympathetic stimulation would not be advantageous for induction of anesthesia during hypovolemia. To test this hypothesis, 21 swine were studied during normovolemia and after 30% of their estimated blood volume was removed. Swine were divided randomly into three equal groups to receive no anesthetic or the minimal anesthetic dose of ketamine (6.65 ± 0.38 mg/kg, iv) or thiopental (5.77 ± 0.21 mg/kg, iv). After the initial response to hypovolemia, animals given no drug did not exhibit further changes during the hypovolemic period. Five minutes after induction of anesthesia in the hypovolemic state, ketamine, but not thiopental, caused large increases in plasma epinephrine, norepinephrine, and renin activity. Despite these differences, both anesthetics equally depressed systemic vascular resistance, mean systemic arterial blood pressure, heart rate, and cardiac output. Ketamine, but not thiopental, decreased stroke volume. Neither anesthetic affected oxygen consumption. Both anesthetics caused similar increases in blood lactate concentration. Thirty minutes after induction of anesthesia, plasma epinephrine, norepinephrine, and renin activity remained higher in animals given ketamine than in those given thiopental. Stroke volume, systemic vascular resistance, cardiac output, and oxygen consumption did not differ among groups; however, only the animals given ketamine showed further increase in blood lactate concentration and base-deficit. Thirty minutes after infusion of shed blood, cardiac output and blood lactate concentration were greater in the animals given ketamine than in those given thiopental or no anesthetic. Ninety minutes after infusion of shed blood, no differences existed among groups. The authors conclude that after moderate hemorrhage, further increase in circulating catecholamines is possible but that the levels achieved either exceed the maximal effective concentration at site(s) of action or their effects are overwhelmed by the depressant effects of ketamine. This study failed to document any advantage of ketamine over thiopental when used in the minimal anesthetic dosage for induction of anesthesia during hypovolemia.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

To study the metabolic effects of anesthesia, whole-body oxygen consumption (VO2) was compared on 242 occasions in six dogs under standard conditions while awake, sleeping, or anesthetized. The dogs were trained to lie unrestrained in the lateral position for the measurement of VO2(STPD) in the unanesthetized state. Arterial blood gas tensions,pH, heart rate, and blood pressure also were determined. The maximum VO2of the alert resting and the minimum of the drowsy resting state averaged (±SE) 5.57 ± 0.48 and 3.97 ± 0.41 ml · kg-1· min-1, respectively. VO2was lowest and least fluctuating during natural sleep (2.46 ± 0.2 ml · kg-1· min-1). During deep anesthesia with methohexital, thiopental, and etomidate, VO2averaged (±SE) 4.68 ± 0.26, 4.26 ± 0.28, and 4.77 ± 0.35 ml · kg-1· min-1during spontaneous ventilation (open-circuit flow-through technique) and 3.54 ± 0.27 ml · kg-1· min-1during controlled ventilation (open-circuit collection technique) with 2% halothane. Anesthesia reduces VO2relative to the resting values of the alert state but increases it relative to that of natural sleep. Accordingly, anesthetics should not be considered general metabolic depressants without qualification.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID