摘要:

BackgroundUpper abdominal surgery (UAS) induces diaphragmatic dysfunction. Thoracic extradural block (TEB) using 0.5% bupivacaine improves some pressure and motion indices of diaphragmatic function. However, no direct information on diaphragmatic activity is available after UAS. The aim of this study was to assess diaphragmatic electrical activity (Edi) after UAS before and after TEB.MethodsA postoperative electromyogram was obtained, using intramuscular electrodes inserted by the surgeon in the costal and crural parts of the diaphragm, in 14 patients undergoing abdominal aortic surgery. Tidal changes in abdominal (VAB) and rib-cage (VRC) volumes, and gastric (ΔPgas), esophageal (ΔPes), and transdiaphragmatic (ΔPdi) pressures were used to measure tidal volume (VT) and respiratory rate and to provide indirect indices of diaphragmatic activity from the two ratios VAB/VTand ΔPgas/ΔPdi. These respiratory variables were obtained preoperatively. Postoperatively, measurements including Edi were obtained before and after a seg-mental epidural block, reaching a T4 level was achieved with 0.5% plain bupivacaine.ResultsUpper abdominal surgery induced an increase in respiratory rate (+28 ± 15%; P <.01), associated with a decrease in VAB/VT(from 0.75 ± 0.11 to 0.07 ± 0.08; P <.01), ΔPgas/ΔPdi (from 0.3 ± 0.08 to 0.01 ± 0.19; P <.05), and VT(30 ± 14%; P<.01). After surgery, all patients exhibited electrical diaphragmatic activity that increased with TEB by 48 ± 28% (P <.01) and 60 ± 22% (P <.001) for the cural and costal segments, respectively. The ratio ΔPdi/Edi, used to evaluate diaphragmatic contractility, was not modified by TEB. Tidal volume, respiratory rate, and ΔPgas/ΔPdi returned to preoperative levels, whereas VAB/VTincreased but remained different from preoperative values.ConclusionsThis study demonstrates that TEB produces an increase in diaphragmatic activity, identical for the two segments of the muscle. Interruption of afferents that produce an inhibitory effect on diaphragmatic activity appears the most attractive hypothesis to explain the consequences of TEB after UAS.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundCirculating vasoactive hormones (e.g., vasopressin) play an important role in the regulation of blood flow to the choroid plexus and the rate of cerebrospinal fluid (CSF) production. We tested the hypothesis that halothane decreases CSF production through a vasopressin-related mechanism and examined the related changes in blood flow to the choroid plexus.MethodsUsing ventriculocisternal perfusion, CSF production was measured in chloralose anesthetized, normothermic rabbits whose lungs were mechanically ventilated. Rabbits received either 0.5 minimum alveolar concentration (MAC; end-tidal) of halothane (added to a preestablished chloralose anesthetic), 0.5 MAC of halothane in the presence of a vasopressin V1antagonist (iv), or the V1antagonist alone. In addition, we examined animals in which no intervention was made (time control) and animals subjected to a 25% decrease in mean blood pressure produced by hemorrhage, with and without the V1-antagonist. In a separate series of rabbits, regional and total blood flows to the brain and the choroid plexus were measured using radioactive microspheres. These studies were carried out under similar conditions, except that the effects of end-tidal 0.25, 0.5, and 1 MAC of halothane were examined in each rabbit (each added to a preestablished chloralose anesthetic).ResultsUnder control conditions, blood flow to the choroid plexus averaged 351 ± 198 ml. min−1. 100 g−1(mean ± SD) and CSF production averaged 10.1 ± 1.9μl.min.−1. Halothane (0.25, 0.5, and 1 MAC) did not alter choroid plexus blood flow but decreased CSF production by 28 ± 6% at 0.5 MAC (P <.05). In contrast, 1 MAC of halothane increased total blood flow to the brain by 20 ± 25% (P <.05). The V, antagonist, which did not affect production of CSF when given alone, prevented the decrease in CSF production in response to halothane. Hemorrhage decreased blood flow to the choroid plexus but not to the brain, and the V1antagonist attenuated the decrease in the rate of CSF production by hemorrhage (34 ±11% vs. 48 ± 18%, P<.05).ConclusionsHalothane decreases CSF production with no net change in the blood flow to the choroid plexus. Decrease in CSF production appears to be mediated through a vasopressin-related mechanism and not to the blood pressure decrease seen during halothane anesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundEtomidate has been shown to induce no significant inotropic effect on normal myocardium, but its effects on diseased myocardium remain unknown.MethodsThe effects of etomidate (1 and 5 μg/ml) on the intrinsic contractility of left ventricular papillary muscle from normal hamsters and those with cardiomyopathy (strain BIO 82.62, 6 months old) were investigated in vitro (Krebs-Henseleit solution, 29°C, pH 7.40, Ca++2.5 mM, stimulation frequency 3/min).ResultsThe contractility of papillary muscles from hamsters with cardiomyopathy was less than that of controls, as shown by the decrease in maximum shortening velocity (-25%, P <.001), isometric active force (-45%, P <.01), peak power output (-57%, P <.01), and sarcoplasmic reticulum function (P <.01). Etomidate did not induce a significant inotropic effect, as shown by the absence of changes in maximum shortening velocity and active isometric force, except at 5 μg/ ml in cardiomyopathic hamsters (+8 ± 10%, P <.05). The effects of etomidate on these inotropic parameters were not different in normal and cardiomyopathic hamsters. Etomidate impaired contraction-relaxation coupling under low load in both groups, suggesting that etomidate decreased sarcoplasmic function. This impairment was less (P <.02) pronounced in cardiomyopathic muscles. The effects of etomidate on contraction-relaxation coupling under heavy load were not different between groups. In both groups, etomidate had no effect on the peak power output and the curvature of the total force-velocity curve, suggesting that it did not modify the muscle myothermal economy.ConclusionsEtomidate had only a slight effect on the intrinsic mechanical properties of hamster cardiac papillary muscles, and these effects did not depend on the pathophys-iologic state of the myocardium. These results may be clinically useful as, unlike etomidate, most anesthetics depress myocardial contractility.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundHyperventilation frequently is employed to reduce carbon dioxide partial pressure in patients in the operating room and intensive care unit. However the effect of hypocapnia on oxygenation is complex and may result in worsening in patients with preexisting intrapulmonary shunt. To better define the interplay between hypocapnia and oxygenation, the effects of hypocapnia and hypercapnia on the matching of ventilation (VA) and perfusion (Q) were studied in dogs with oleic acid-induced pulmonary edema, using the multiple inert gas elimination technique.MethodsEight pentobarbital-anesthetized, closed-chested dogs were administered 0.06 ml/kg of oleic acid at least 150 min prior to study. Ventilation was set with an F1o2;of 0.90, a tidal volume of 20 ml/kg, and a respiratory rate of 35 breaths/ min. The arterial carbon dioxide tension (PaCo2) was varied in a randomized order to three levels (26, 38, and 50 mmHg) by altering the amount of CO2in the inspired gas mixture. Gas exchange was assessed by true shunt, dead space, the log standard deviation of the perfusion (log SDQ) and the ventilation (log SDv) distributions, and the tracer inert gas arterial-alveolar difference ([a-A]D) area.ResultsCardiac output (4.1 ± 0.4 I./min), mean pulmonary artery pressure (25 ± 1 mmHg), inert gas shunt (22 ± 3%), and dead space (38 ± 4%) during normocapnia were not different from that during hypocapnia and hypercapnia. Hypocapnia increased (P <.05) the alveolar-arterial oxygen tension difference (P[A-a]o2) and decreased (P <.05) the arterial blood oxygen tension (Pao2181 ± 33 mmHg vs. 221 ± 35 mmHg with normocapnia). P[A-a]o2and Pao2were unaffected by hypercapnia. During hypocapnia, VA/Q inequality increased, demonstrated by an increase (P <.05) in log SDQ (1.60 ± 0.15 vs. 1.35 ± 0.19 with normocapnia) and in the [a-A]D area (0.63 ± 0.09 vs. 0.50 ± 0.09 with normocapnia) indexes of VA/Q heterogeneity. During hypercapnia, the [a-A]D area (0.63 ± 0.11) and log SDv (1.13 ± 0.10 compared to 0.97 ± 0.12 with normocapnia) also were increased (P <.05). With hypocapnia, there was a small but insignificant increase in blood flow to shunt and low VA/Q areas (29 ± 4% compared to 26 ± 4% with normocapnia). In the presence of a high F1o2this small increase in shunt and low VA/Q may result in a significant decrease in Pao2.ConclusionsBoth hypocapnia and hypercapnia were associated with an increased VA/Q inequality. However, PaOidecreased and P[A-a]o2increased with only hypocapnia. These results suggest that hyperventilation to reduce PaCo2may be detrimental to arterial Po2in some patients with lung disease.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundPropofol anesthesia often is associated with marked decreases in arterial blood pressure. Previous investigations in vivo have provided conflicting reasons for this clinical finding, including propofol-induced decreases in preload or afterload and/or direct myocardial depressant effects. Interpretation of the results of these studies is complicated by use of indices of myocardial contractility that may only indirectly indicate changes in inotropic state or are significantly dependent on ventricular loading conditions.MethodsEight experiments were performed using dogs chronically instrumented for measurement of aortic and left ventricular pressure, the peak rate of increase of left ventricular pressure (dP/dtmax). subendocardial segment length, in-trathoracic pressure, and cardiac output. Myocardial contractility was evaluated in conscious and anesthetized dogs using the preload recruitable stroke work (PRSW) relationship, a sensitive, easily quantified, and relatively load-independent index of contractile function in normal canine myocardium in vivo. The relationship was derived from ventricular pressure-segment length loops generated by abrupt vena caval constriction. Respiratory variation in ventricular pressure was reduced by calculation of transmural pressure via instantaneous subtraction of Intrathoraclc pressure from corresponding left ventricular pressure. Systemic hemodynamics and myocardial contractility were recorded and evaluated in the conscious state and after a bolus of 5 mg/kg and a propofol infusion for 15 min at 15, 30, 60, and 120 mg. kg−1. h−1.ResultsA significant (P <.05) and dose-dependent decrease in PRSW slope (106 ± 7 during control to 54 ± 3 mmHg at the 120 mg.kg−1.h−1infusion) was observed, demonstrating a direct depression of contractility. Concomitant decreases in left ventricular dP/dtmaxand percent segment shortening also were observed. In addition, a significant decrease in systemic vascular resistance occurred at the two largest infusions.ConclusionsThe results indicate that the significant decrease in systemic arterial blood pressure observed during continuous propofol anesthesia in dogs is a result of direct negative inotropic actions of propofol along with its direct effects upon arterial and venous vascular tone.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundAlthough ketamine has been administered splnally in humans, previous neurotoxicity studies have shown that it can induce spinal cord lesions in various animal models. The aim of this work was to evaluate by histologic and blood-brain barrier studies whether different components of the commercial ketamine solution might be responsible for the microscopic lesions observed.MethodsForty white New Zealand rabbits were randomly assigned to four groups of 10. One-percent preservative-free ketamine (0.3 ml), 1% d ketamine, 0.05% chlorobutanol, and 1% lidocaine were intrathecally injected through the atlantooccipital membrane. Laminectomy was performed on day 8, and the dura was preserved using paraformaldehyde-glutaraldehyde fixative. Light and fluorescence microscopy were performed on transverse spinal cord sections by a neuropathologist unaware of injected agents used. Specimens were then graded as normal or abnormal as compared with a control group receiving lidocaine.ResultsIsomers of ketamine did not induce spinal cord lesions in either study, but chlorobutanol (the preservative used in the ketamine solution) induced significant severe spinal cord lesions in both studies.ConclusionsThe appearance of spinal cord lesions after intrathecal chlorobutanol strongly suggests that this preservative is responsible for apparent toxicity of ketamine and therefore should not be used in any solution intrathecally injected into humans.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundThere is increasing interest among anesthesiologists in the use of continuous infusion of intravenous drugs. The therapeutic effect of most drugs is a function of the concentration at the site of drug effect, which in turn is determined by the plasma concentration. Constant plasma concentrations can be maintained by computer-controlled infusion pumps. However, such equipment is not yet widely available and will be expensive.MethodsA technique is presented to enable the anesthesiologist to maintain approximately a desired plasma concentration after an arbitrary bolus dose by using a series of infusions with rates decreasing in a stepwise fashion. The algorithm is based on approximating the exact infusion needed to maintain the target plasma concentration by producing this concentration at discrete, specific times. Equations are derived for calculating the sequential rates of the infusion scheme. The equations assume linear pharmacokinetics, and the starting point for derivation of the equations is the assumption that the plasma concentration is given by the convolution of the drug infusion and the unit dose-response function.ResultsThe accuracy of the technique was assessed by simulating the infusion of fentanyl and midazolam. By using an infusion scheme of three steps, the error was no greater than 38% for fentanyl and no greater than 10% for midazolam.ConclusionsOther than the assumption of linear kinetics, the algorithm is independent of pharmacokinetic models. Implementation does not require computer-based numerical analysis.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundThe spinal mechanisms underlying the hyper-esthetic state during inflammation are little understood. To gain a better understanding of these mechanisms, this study evaluated the effects of intrathecal morphine; MK-801, an N-methyl-D aspartic (NMDA) antagonist; and CP-96,345, an NK1 antagonist, on the hyperesthesia observed after carageenan injection of the rat paw.MethodsIn rats injected with 2 mg carageenan, the paw withdrawal latency (PWL) for the injected paw was typically 5–6 s less than that for the untreated paw, at 2 h after the carageenan injection. Drugs were administered 2 h after the carageenan injection. The magnitude of hyperesthesia was evaluated with the difference score (OS), which was calculated by subtracting the PWL of the untreated paw from the PWL of the injected paw.ResultsIntrathecal morphine increased PWLs of both the injected and the untreated paws equally in a dose-dependent manner, but intrathecal morphine did not affect the level of DS. Intrathecal MK-801 increased PWLs of the injected paw to the level of the untreated paw in a dose-dependent manner and increased the DS levels. Intrathecal CP-96,345 had no effect on PWLs of either the injected or the untreated paw. Coad-ministration of MK-801 with morphine reduced the DS for each dose of morphine.ConclusionsThese data indicate that (1) an NMDA receptor, but not an NK1 receptor, plays an important role in maintaining the hyperesthesia after carageenan injection; and (2) NMDA antagonism has a simple additive interaction with morphine in the carageenan model of inflammatory hyperesthesia.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundBecause the effect of hypocapnia on distribution of cerebral blood flow during focal cerebral ischemia is controversial, this investigation was performed in rats to determine whether hypocapnia, instituted immediately after the onset of focal cerebral ischemia, produces a favorable redistribution of blood flow (an “inverse steal”) toward the ischemic territory.MethodsAfter surgical preparation during normocapnic isoflurane anesthesia, middle cerebral artery occlusion (MCAO) was performed. Animals were randomized to either immediate institution of hypocapnia (n 9; PaCo223 ± 2 mmHg) or continued normocapnia (n-8; PaCo240 ± 2 mmHg). Thirty minutes thereafter, local cerebral blood flow (1-CBF) was determined autoradiographically using14C-iodoantipyrine. Local cerebral blood flow was determined in four coronal brain sections spanning the distribution of the middle cerebral artery. For the hemisphere ipsilateral to MCAO, the areas of cortex in which CBF fell within three specified CBF ranges (0–6, 6–15, and 15–23 ml/100 g/min) were measured and expressed as a percentage of the total area of cortex in that section. In the hemisphere contralateral to MCAO, to confirm the presence of normal CO2reactivity in non-ischemic brain in this model, average 1-CBF was determined for the cortex, the subcortex, and the entire hemisphere in each coronal section.ResultsHypocapnia resulted in significantly lower 1-CBF in the cortex, subcortex, and entire hemisphere in all coronal sections of brain contralateral to MCAO. In the hemisphere ipsilateral to MCAO, a favorable redistribution of CBF was not observed. For the three more anterior coronal sections (1–3), a significantly larger percentage of the cortex had 1-CBF in the range of 15–23 ml.100 g−1. min−1in the hypocapnia group animals. In sections 2 and 3, significantly larger areas of cortex had 1-CBF in the range of 6–15 ml.100 g−1.min−1in the hypocapnia group than in the normocapnia group. For all sections, there were no significant differences between hypo-capnic and normocapnic groups in the area of cortex with 1-CBF in the range of 0–6 ml. 100 g−1.min−1.ConclusionsThe current study does not provide evidence for the occurrence of a hypocapnia-induced inverse steal phenomenon during acute focal cerebral ischemia of 30 min duration in the rat. The data suggest that, rather than reducing the area of the critically ischemic brain, hypocapnia may increase the size of the region at risk. The data do not support the use of hypocapnia as a therapeutic measure to produce a favorable redistribution of CBF during focal cerebral ischemia of acute onset.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

BackgroundVolatile anesthetics depress global left ventricular function by altering intracellular calcium (Ca2+) homeostasis at several sites within the myocyte. Although extracellular Ca2+partially reverses the negative inotropic effects of volatile anesthetics, the actions of extracellular Ca2+on anesthetic-induced diastolic dysfunction are unexplored. This investigation examined and compared the direct effects of extracellular Ca2+on left ventricular systolic and diastolic function in conscious and anesthetized dogs.MethodsExperiments were conducted in the presence of pharmacologic blockade of the autonomic nervous system because autonomic nervous activity may significantly influence the hemodynamic actions of anesthetics and Ca2+in vivo. Three groups comprised a total of 27 experiments conducted using nine dogs chronically instrumented for measurement of aortic and left ventricular pressure, left ventricular dP/dt, subendocardial segment length, and cardiac output. Myocardial contractility was evaluated using the preload recruitable stroke work relationship slope (Mw). Diastolic function was assessed using a time constant of isovolumic relaxation (β), a regional chamber stiffness constant (Kp), and maximum segment lengthening velocity during rapid ventricular filling (dI./dtE) and atrial systole (dL/dtA). On 3 separate days, a CaCl2infusion at 1.25, 2.5, or 5 mg.kg−1. min−1was administered. Hemodynamics and ventricular pressure-length loops were recorded after a 20-min equilibration at each dose in the conscious state or during halothane or isoflurane anesthesia.ResultsIn conscious dogs, CaCl2produced a significant (P <.05) and dose-dependent increase in contractility as evaluated by Mw. In the presence of halothane anesthesia, CaCl2increased contractility (Mwof 26 ± 5 mmHg to 78 ± 10 mmHg during the high dose of CaCl2), enhanced isovolumic relaxation (T of 57.9 ± 4.2 ms to 41.1 ± 1.9 ms during the high dose of CaCl2), improved rapid ventricular filling (dL/dtEof 11.8 ± 1.4 mm/s to 20.2 ±1.6 mm/s during the high dose of CaCl2), and reduced regional chamber stiffness (Kpof 0.70 ± 0.18 mm−1to 0.38 ± 0.04 mm−1during the high dose of CaCl2). Similar findings were observed when CaCl2was administered to dogs anesthetized with isoflurane.ConclusionsAlthough CaCl2produced positive inotropic effects in both the conscious and anesthetized states, CaCl2did not alter diastolic function in conscious dogs. In contrast, CaCl2reversed halothane- and isoflurane-induced negative lusitropic actions. The results of the present investigation suggest that improvement of left ventricular performance by CaCl2during volatile anesthesia may be related to actions in diastole as well as systole.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID