|
1. |
Enflurane Causes a Prolonged and Reversible Increase in the Rate of CSF Production in the Dog |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 255-260
Alan Artru,
Michael Nugent,
John Michenfelder,
Preview
|
PDF (501KB)
|
|
摘要:
Using the open ventriculocisternal perfusion method, rates of cerebrospinal fluid (CSF) production and reabsorption by bulk flow were examined in dogs anesthetized with either enflurane (2.2%) in nitrogen (60–70%) and oxygen, or nitrous oxide (60–70%) and enflurane (<0.2%) in oxygen (controls). The mean rate of CSF production increased significantly with enflurane (2.2%), from 0.055 ± 0.020 ml/min (mean ± SD) in controls to 0.082 ± 0.033 ml/min (n = 12). After this initial increase of approximately 50%, the production rate decreased significantly by about 7.4%/h. When the expired concentration of enflurane was decreased from 2.2% to <0.2%, the mean rate of CSF production decreased to control values at 45–50 min. An intracerebral accumulation of CSF resulting from this enflurane-induced increase in CSF production may contribute in part to increased intracranial pressure when the dura is intact.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
2. |
EdrophoniumDuration of Action and Atropine Requirement in Humans during Halothane Anesthesia |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 261-266
Roy Cronnelly,
Robert Morris,
Ronald Miller,
Preview
|
PDF (447KB)
|
|
摘要:
Edrophonium's onset and duration of antagonism (n = 26) and atropine requirement (n = 24) were determined under conditions ofd-tubocurarine (dTc) neuromuscular blockade and halothane, nitrous oxide anesthesia. Results are compared with previous work in our laboratory on neostigmine and pyridostigmine under similar conditions.dTc was administered by continuous infusion to maintain a 90% depression of muscle twitch tension. Edrophonium (0.03–1.0 mg/kg) was injected as an iv bolus in combination with atropine (0.5 mg).dTc infusion was continued until a stable 90% depression of muscle twitch tension was reestablished. Time-to-peak effect (onset of action), duration, and magnitude of antagonism were recorded. The atropine requirement was determined during spontaneous recovery fromdTc (0.3 mg/kg) and stable halothane, nitrous oxide anesthesia. Edrophonium (0.5 mg/kg) was mixed with 7, 15, or 30 μg/kg of atropine and compared to neostigmine (0.043 mg/kg) and atropine (15 μg/kg). Blood pressure, heart rate, and rhythm were recorded for 60 min following edrophonium administration. The time-to-peak antagonism for edrophonium (0.8–2.0 min) was far more rapid than neostigmine (7–11 min) or pyridostigmine (12–16 min). The ED50for edrophonium was 0.125 mg/kg, however, the dose-response curve was not parallel to those for neostigmine or pyridostigmine. In equiantagonistic doses, the duration of antagonism by edrophonium (66 min) did not differ from neostigmine (76 min), but was shorter than pyridostigmine. Edrophonium required one-half the amount of atropine as did neostigmine to prevent bradycardia. The authors concluded that edrophonium has a more rapid onset than neostigmine and an equivalent duration of antagonism, and requires less atropine to prevent bradycardia.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
3. |
Combined Effects of Sodium Nitroprusside and Propranolol on Hypoxic Pulmonary Vasoconstriction |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 267-271
James Miller,
Jonathan Benumof,
Frank Trousdale,
Preview
|
PDF (405KB)
|
|
摘要:
Recent clinical experience and previous experimental work indicate that propranolol may reverse sodium-nitroprusside-induced inhibition of hypoxic pulmonary vasoconstriction (HPV). Accordingly, the authors decided to test this possibility in an experimental model that allows direct examination of pharmacologic influence on HPV. Six mongrel dogs were anesthetized with pentobarbital and intubated. Following a left thoracotomy, the left lower lobe (LLL) was ventilated independently but synchronously with the rest of the lung. Selective hypoxia of the LLL (95% nitrogen and 5% CO2) caused a 59 ± 6% (mean ± SE) decrease in the electomagnetically measured fraction of the cardiac output perfusing the LLL and a 287 ± 65% increase in the pulmonary vascular resistance of the LLL from their respective prehypoxic values. Propranolol, 1 mg/kg intravenously, caused a 76 ± 5% beta-blockade, as determined by an isoproterenol infusion test, but did not cause a significant change in the LLL HPV response. Sodium nitroprusside (SNP) infusion, caused a 38 ± 4% decrease in systemic arterial pressure, and nearly abolished LLL HPV. Most important, the addition of propranolol to sodium nitroprusside did not significantly change the SNP induced inhibition of LLL HPV. The authors conclude that in acute lung disease, propranolol does not alter lobar HPV and does not reverse sodium nitroprusside inhibition of lobar HPV.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
4. |
Continuous Intravascular Monitoring of Epinephrine‐induced Changes in Plasma Potassium |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 272-278
M. Lim,
R. Linton,
D. Band,
Preview
|
PDF (473KB)
|
|
摘要:
Ion-selective electrode catheters were used for continuous monitoring of epinephrine-induced changes in plasma potassium in different parts of the circulation of anesthetized greyhounds. Bolus injections and continuous infusions of epinephrine produced dose-related changes consisting of an initial transient increase followed by a decrease to levels below control. The latter part of the response was relatively short-lived in the case of bolus injections, but when the epinephrine was administered by continuous infusion, a progressive fall was maintained for the duration of the infusion. During the period when potassium levels were undergoing an acute change, marked differences were seen between concentrations in different parts of the circulation. Further studies are needed to delineate the incidence and extent of similar changes in humans, and their significance in producing dangerous dysrhythmias.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
5. |
Comparative Evaluation of Intravenous Agents for Rapid Sequence Induction—Thiopental, Ketamine, and Midazolam |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 279-284
Paul White,
Preview
|
PDF (452KB)
|
|
摘要:
The pharmacologic effects of ketamine, midazolam, and a midazolam-ketamine combination were compared with thiopental for rapid induction of general anesthesia. Thiopental, 4 mg/kg, 1.5 mg/kg ketamine, 0.3 mg/kg midazolam, or 0.15 mg/kg midazolam, and 0.75 mg/kg ketamine, were administered intravenously in a randomized fashion to 80 patients undergoing emergency surgery. Adequacy of induction, hemodynamic changes, and postoperative effects were assessed during and after a standardized induction-maintenance anesthetic technique. Midazolam had the slowest onset (15–60s) and longest duration of action. During induction, thiopental decreased mean arterial pressure (MAP) by 11%, ketamine increased MAP by 10%, while neither midazolam nor the midazolam-ketamine combination significantly changed MAP. Heart rate (HR) increased during induction in all groups; however, the increase was significantly less in the combination group. After intubation, MAP and HR increased to the same extent in all four groups. Significantly more patients who received ketamine for induction were disoriented during emergence. Midazolam most effectively produced anxiolysis and antegrade amnesia. Significantly more patients who received thiopental felt depressed postoperatively, and 95% required parenteral opiate analgesics in the recovery room. Dreaming was highest after ketamine (55%) and lowest after midazolam (0%) and the combination (5%). Thus, midazolam effectively attenuated both the cardiostimulatory responses and unpleasant emergence reactions associated with ketamine. The author concludes that both midazolam and the midazolam-ketamine combination are safe and effective induction agents for emergency surgery, which may offer an advantage over thiopental in situations where hemodynamic stability is crucial. Furthermore, midazolam effectively attenuates the side effects of ketamine.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
6. |
Potentiation by Thiopental of Halothane–Epinephrine‐induced Arrhythmias in Dogs |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 285-288
John Atlee,
Carol Malkinson,
Preview
|
PDF (366KB)
|
|
摘要:
Epinephrine-induced arrhythmias were studied in 14 dogs (Group 1) anesthetized with halothane alone (1.09% end-tidal), and on another occasion, at the same halothane concentration following intravenous thiopental (20 mg/kg). Surface (Lead II), catheter His bundle and high right atrial electrocardiograms, and airway and femoral arterial pressures were recorded. Graded doses of epinephrine (EPI-least dose 0.25 μg·kg-1·min-1) were infused over five minutes, but terminated sooner if ventricular tachycardia occurred (maximal sensitization). Sensitizing EPI doses (μg·kg-1) were calculated (dose X time to arrhythmia) for: Shift in or wandering atrial pacemaker (SAP-WAP), atrial ectopy (At Ect), A-V dissociation (AVD), and ventricular ectopy, bigeminy, or tachycardia (V Ect, V Bigem, V Tech). With halothane alone, SAP-WAP occurred at the least dose of EPI followed by At Ect, AVD, V Ect, V Bigem, and V Tach in order of increasing EPI dose. Following thiopental, EPI doses for AVD, V Ect, V Bigem, and V Tach were reduced, as well as EPI dose differences for At Ect, AVD, V Ect, and V Bigem.In an additional seven dogs (Group 2), anesthesia was induced with thiopental (20 mg/kg) followed by halothane (1.09% end-tidal). These animals were observed for arrhythmias during graded EPI infusions at 1–2 h and 3–4 h following thiopental. Sensitizing EPI doses for SAP-WAP and V Tach were similar at each time period.The authors concluded that with halothane and increasing EPI dose, sensitization constitutes a spectrum of arrhythmias, beginning with atrial and progressing to severe ventricular arrhythmias. Thiopental reduces the EPI dose needed for AVD and ventricular, but not atrial, arrhythmias. It also reduces the EPI dose discrepancies for atrial and ventricular arrhythmias.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
7. |
Chronotropic Effects of Succinylcholine and Succinylmonocholine on the Sinoatrial Node |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 289-292
Isamu Yasuda,
Toshio Hirano,
Keisuke Amaha,
Hiroto Fudeta,
Shoichi Obara,
Preview
|
PDF (286KB)
|
|
摘要:
The mechanism of bradycardia caused by the administration of succinylcholine has not been fully elucidated. Accordingly, the effects of succinylcholine and succinylmonocholine on the sinoatrial node were studied in 35 mongrel dogs. The sinus node artery was selectively perfused with autologous blood from a femoral artery at a constant pressure of 100 mmHg, and 30 to 1,000 μg of succinylcholine or succinylmonocholine was administered directly into the artery.Succinylcholine caused a transient (63–600 s) dose-related positive chronotropic effect. The heart rate was increased to 14.4 ± 2.1% (mean ± SE) above the control value after the administration of 1,000 μg of succinylcholine. This positive chronotropic effect was inhibited by pretreatment with pindolol or reserpine. By contrast, succinylmonocholine produced a transient (30–248 s) dose-related negative chronotropic effect. The heart rate was decreased to 17.5 ± 1.4% below the control value after administration of 1,000 μg of succinylmonocholine. The negative chronotropic effect was blocked partially by atropine.It was concluded that the positive chronotropic effect of succinylcholine may be mediated through beta-adrenergic receptor stimulation by catecholamine released from the adrenergic nerve endings in the sinoatrial node, and that the negative chronotropic effect of succinylmonocholine may be the result of excitation of cholinergic receptors in the sinus node. However, a direct effect of succinylmonocholine on the sinus node could not be ruled out.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
8. |
Transcutaneous Cranial Electrical Stimulation Increases the Potency of Nitrous Oxide in Humans |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 293-297
Theodore Stanley,
Jean Cazalaa,
Aime Limoge,
Yves Louville,
Preview
|
PDF (395KB)
|
|
摘要:
The potency, amnesic, and postanesthetic analgesic effects of transcutaneous cranial electrical stimulation (TCES) were evaluated during N2O anesthesia in 120 unpremedicated patients, prior to urologic or general surgical operations. The patients were divided into six groups of 20 each with respect to what concentration of N2O in oxygen they were allowed to breathe (75, 62.5, and 50%), and whether they were or were not stimulated with TCES. Recordings of heart and respiratory rates, systolic arterial blood pressure, and minute ventilation were made prior to and after 20 min of N2O, and one minute later following application of a Kocker clamp to the upper inner thigh for one minute. The presence or absence of movement during the painful stimulus, memory of the painful stimulus, and postanesthetic pain at the clamp site (20 min after anesthesia) were also evaluated. Patients who received TCES had significantly lower incidences of movement, memory of the painful stimulus, and postanesthetic pain at the stimulation site at each N2O concentration than patients not getting TCES. TCES did not alter circulatory and respiratory dynamics prior to painful stimulation and prevented an increase in arterial blood pressure during painful stimulation in patients receiving 50% N2O. These data indicate that TCES significantly increases the analgesic potency of N2O and probably also the depth of anesthesia.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
9. |
A Noninvasive In Vivo Method of Assessing the Kinetics of Halothane Metabolism in Humans |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 298-302
Michael Cahalan,
Brynte Johnson,
Edmond Eger,
Lewis Sheiner,
Charles Richardson,
Jeffrey Varner,
John Severinghaus,
Preview
|
PDF (411KB)
|
|
摘要:
The authors describe a noninvasive method of estimating the kinetic constants that characterize metabolism of inhaled anesthetics in humans. Ten healthy male volunteers breathed subanesthetic concentrations of halothane and isoflurane in a fixed inspired ratio of 20:1. Isoflurance served as a marker that identified changes in uptake in nonmetabolizing depots. Each study progressed through nine 30 min levels (numbered 0–8). At each level, inspired concentrations of both halothane and isoflurane were doubled, and alveolar concentrations and uptakes were determined. Clearance (uptake/alveolar concentration) of isoflurane remained constant over a range of concentrations of 0.00006 to 0.008%. In contrast, clearance of halothane decreased as the alveolar concentration increased from 0.0007 to 0.13%. On this basis, the authors assumed that the clearance of halothane was a combination of linear clearance to depots and saturable metabolism, the former proportional to the clearance of isoflurane, and the latter attributable to a Michaelis-Menten process. Applying such a model to halothane, they estimated the mean (±SE) Vmax(the composite maximum rate of metabolism) to be 0.79 ± 0.09 ml·min-1·individual-1, and the Km(the composite concentration at which half-saturation of enzymes occurs) to be 0.029 ± 0.003%. This model provides a significantly better data fit than that provided by two simpler submodels, one of which assumes that all clearance is linear, and the other of which allows a part of clearance to be saturable but ignores the isoflurane marker data.The value of 0.029% for Kmindicates that a wide range of clinical anesthetic concentrations will produce similar rates of metabolism; that metabolism will proceed at near maximum rates during the first several minutes of recovery; and that most metabolism probably occurs after, rather than during, anesthesia.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
10. |
Nitroprusside Increases Cyclic Guanylate Monophosphate Concentrations during Relaxation of Rabbit Aortic Strips and Both Effects Are Antagonized by Cyanide |
|
Anesthesiology,
Volume 57,
Issue 4,
1982,
Page 303-307
Harriet Kruszyna,
Robert Kruszyna,
Roger Smith,
Preview
|
PDF (480KB)
|
|
摘要:
The authors have confirmed previous observations that sodium cyanide (CN-) partially reverses the vasodilator effects of sodium nitroprusside (SNP) on vascular smooth muscle. As tested on rabbit aortic strips contracted by norepinephrine (NE), the final tension is independent of the order of addition of reagents. In the same concentration, CN-alone had no effect on tension also as reported by others. The ED50values for relaxation of aortic strips for a series of directly acting agonists (“nitric oxide vasodilators”) were: sodium azide (N-3) 2.1 X 10-7M;SNP 2.7 X 10-7M;hydroxylamine (H2NOH) hydrochloride 2.5 X 10-6M;human nitric oxide hemoglobin (HbNO) 3.5 X 10-6M;and sodium nitrite (NO-2) 1.2 X 10-4M.In addition to SNP, CN-antagonized the vasodilator effects of N-3and H2NOH, but it failed to reverse relaxation by HbNO, NO gas, NO-2(as observed by us), glyceryl trinitrate, adenosine, or papaverine (as observed by others). The only change noted in cyclic-adenosine monophosphate (c-AMP) concentrations in aortic strips exposed to 1) NE, 2) NE + NO-2or SNP, or 3) NE + NO-2or SNP + CN-was an increase due to NE. The only statistically significant change noted in cyclicguanosine monophosphate (c-GMP) concentrations exposed to 1) NE, 2) NE + NO-2) or 3) NE + NO-2+ CN-was also an increase due to NE. In contrast, SNP resulted in further increases in c-GMP after NE, and when cyanide was added, a significant decrease in c-GMP followed. These results are only partially consistent with a role for c-GMP in relaxation of vascular smooth muscle, but cyanide may become a useful tool for the study of mechanisms of action of the nitric oxide vasodilators.
ISSN:0003-3022
出版商:OVID
年代:1982
数据来源: OVID
|
|