Differential depressant effects of general anesthetics on the cardiovascular response to cocaine in mice.

In recent years, murine models have gained increasing importance for studies of cardiovascular physiology and pharmacology, largely due to the development of transgenic strains with specific alterations in phenotype. Differential effects of general anesthetic agents on the cardiovascular responses to cocaine have been reported in larger mammals; therefore, we studied the effects of commonly used anesthetics on heart function and on blood pressure responses to cocaine in Swiss Webster mice. We positioned a polyethylene catheter (PE-10) in the right carotid artery or left ventricle of mice anesthetized with equivalent anesthetic dose of either ketamine-xylazine (KX, 40 mg/kg + 5 mg/kg), pentobarbital (PEN, 40 mg/kg) or alpha-chloralose-urethane (CU, 80 mg/kg + 100 mg/kg). Cocaine (0.3 mg/kg, 1 mg/kg and 3 mg/kg) was administrated via the left jugular vein by bolus injection. In the KX group, the basal mean arterial pressure (MAP) and systolic left ventricular pressure (LVP) were 110 +/- 12 and 120 +/- 13 mmHg, respectively, close to conscious values. However, PEN and CU significantly decreased the basal parameters (P < 0.01 compared to the KX group). The lowest dose of cocaine (0.3 mg/kg) elicited minimal changes. Significant responses were obtained with a 1-mg/kg dose of cocaine (P < 0.01 compared to baseline). However, at 3 mg/kg, a toxic effect of cocaine appeared in all three anesthetic groups. Compared to published conscious animal data, anesthetic agents attenuated the cardiovascular effects of cocaine. Taken together, our results indicate that minimally effective doses of general anesthetics may significantly alter the basal hemodynamic state and the responses to sympathomimetic agents in the murine model, as has been reported in larger mammalian species. We concluded that anesthesia with ketamine-xylazine provides baseline hemodynamic values close to reported values in conscious animals, but also attenuates the hemodynamic response to cocaine.     

The effects of prolonged ketamine-xylazine intravenous infusion on arterial blood pH, blood gases, mean arterial blood pressure, heart and respiratory rates, rectal temperature and reflexes in the rabbit

The prolonged and safe maintenance of general anesthesia in rabbits with commonly used injectable agents is difficult. Protracted, stable anesthesia with short recovery time has been described in humans using continuous intravenous infusion of ketamine with or without sedatives, muscle relaxants and paralytics. This study evaluated the anesthetic plane achieved and respiratory and cardiovascular effects produced with a ketamine-xylazine intravenous infusion in New Zealand White rabbits. Ten female rabbits were anesthetized with intramuscularly administered ketamine hydrochloride (35 mg/kg) and xylazine hydrochloride (5 mg/kg) after the preanesthetic, baseline measurements of arterial blood pO2, pCO2 and pH and heart and respiratory rates were recorded. The above parameters as well as mean arterial blood pressure, righting, palpebral, pedal, and jaw reflexes were monitored ten minutes after the intramuscularly administered dosage and throughout 4 hours of infusion. Results showed moderate hypotension (21.2% deviation from normal, p less than 0.008) and profound hypoxemia (45% deviation from baseline, p less than 0.001) 10 minutes after the intramuscularly administered induction dosage. Then, the 4 hour infusion of ketamine (1 mg/minute) and xylazine (0.1 mg/minute) was started. Hypotension progressed (49.1% deviation from normal, p less than 0.008), but hypoxemia and hypercarbemia gradually improved with no resultant change (p greater than 0.1) in arterial pH. There was no significant change (p greater than 0.1) in respiratory rate but varying qualities of respiration were observed. Both mean arterial pO2 and pCO2 values returned to baseline within 20 minutes after completion of infusion. Heart rate and rectal temperature remained stable during the trial. The righting reflex was abolished in all rabbits throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of pentobarbital, fentanyl-droperidol, ketamine-xylazine and ketamine-diazepam on noxious stimulus perception in adult male rats

The increased use of rats for laboratory studies has increased the urgency for a better understanding of their perception of painful or noxious stimuli and the means of obtunding such stimuli. Four different injectable drugs, pentobarbital, fentanyl-droperidol (Innovar-Vet), ketamine-xylazine and ketamine-diazepam, were evaluated in this study. Unlike previous studies in rodents, this study has quantitated noxious stimulus perception following a temporal sequence of observations. Results showed the greatest inhibition of noxious stimulus perception with Innovar-Vet, lesser inhibition with ketamine-xylazine and ketamine-diazepam, and the least obtunding of nociception with pentobarbital. Results of this study also suggested that a spatial orientation, similar to that present in man, exists within the CNS of rats for receipt of noxious stimulation.     

Susceptibility of rats to corneal lesions after injectable anesthesia

Corneal injury is not a commonly reported side effect after injectable or inhalation anesthesia in rats, but a number of surgery studies at our facility resulted in a high incidence of these injuries. To explore the potential association of various anesthetic protocols with the development of corneal lesions in rats, we retrospectively evaluated clinical records and sections of eyes from 215 male and 187 female Wistar rats used in eight intravenous infusion toxicology studies. None of the studied compounds was associated with eye toxicity. For placement of jugular vein vascular access ports, rats were anesthetized with enflurane, isoflurane, ketamine-xylazine, or Hypnorm-midazolam. Histologically, corneal changes were scored from 0 to 4 in light of degree of mineralization, leukocytic infiltrates, neovascularization, fibrosis, and ulceration. Prestudy (postsurgical) ophthalmic examination findings of corneal opacities were correlated with mineralization of the anterior limiting membrane and corneal ulceration. Corneal lesions were more severe in animals anesthetized with ketamine-xylazine, and minimal changes occurred after anesthesia with either enflurane or isoflurane. The results of further analysis suggest that corneal lesions can be observed within 24 h after injectable anesthetic administration and are not reversible. The severity of corneal changes was reduced when ketamine-xylazine anesthesia was reversed with yohimbine. Compared with Sprague-Dawley and Lewis rats, Wistar, Long-Evans, and Fischer 344 rats had increased incidence and severity of corneal lesions after anesthesia with ketamine-xylazine, suggesting that these three strains are at increased risk for developing postanesthetic corneal lesions with this regimen.     

Respiratory sinus arrhythmia in freely moving and anesthetized rats.

Heart rate increases during inspiration and slows during postinspiration; this respiratory sinus arrhythmia helps match pulmonary blood flow to lung inflation and maintain an appropriate diffusion gradient of oxygen in the lungs. This cardiorespiratory pattern is found in neonatal and adult humans, baboons, dogs, rabbits, and seals. Respiratory sinus arrhythmia occurs mainly due to inhibition of cardioinhibitory parasympathetic cardiac vagal neurons during inspiration. Surprisingly, however, a recent study in anesthetized rats paradoxically found an enhancement of cardiac vagal activity during inspiration, suggesting that rats have an inverted respiratory sinus arrhythmia (Rentero N, Cividjian A, Trevaks D, Pequignot JM, Quintin L, and McAllen RM. Am J Physiol Regul Integr Comp Physiol 283: R1327-R1334, 2002). To address this controversy, this study examined respiratory sinus arrhythmia in conscious freely moving rats and tested whether the commonly used experimental anesthetics urethane, pentobarbital sodium, or ketamine-xylazine alter respiratory sinus arrhythmia. Heart rate significantly increased 21 beats/min during inspiration in conscious rats, a pattern similar to the respiratory sinus arrhythmia that occurs in other species. However, anesthetics altered normal respiratory sinus arrhythmia. Ketamine-xylazine (87 mg/kg and 13 mg/kg) depressed and pentobarbital sodium (60 mg/kg) abolished normal respiratory sinus arrhythmia. Urethane (1 g/kg) inverted the cardiorespiratory pattern so that heart rate significantly decreased during inspiration. Our study demonstrates that heart rate normally increases during inspiration in conscious, freely moving rats, similar to the respiratory sinus arrhythmia pattern that occurs in other species but that this pattern is disrupted in the presence of general anesthetics, including inversion in the case of urethane. The presence and consequences of anesthetics need to be considered in studying the parasympathetic control of heart rate.     

Effect of desflurane-induced preconditioning following ischemia-reperfusion on nitric oxide release in rabbits

Nitric oxide (NO) is the mediator of ischemic preconditioning against myocardial infarction. Desflurane produces anesthetic preconditioning to protect the myocardium against infarction. In the model of myocardial ischemia-reperfusion injury in rabbits, we evaluated desflurane-induced ischemic preconditioning and studied its mechanism of NO synthesis. Thirty-two male adult New Zealand white rabbits were anesthetized with intravenous (IV) 30 mg/kg pentobarbital followed by 5 mg/kg/hr infusion. All rabbits were subjected to 30 minutes (min) long lasting left anterior descending coronary artery (LAD) occlusion and three hours (hr) of subsequent reperfusion. Before LAD occlusion, the rabbits were randomly allocated into four groups for preconditioning treatment (eight for each group). The control group did not receive any preconditioning treatment. The desflurane group received inhaled desflurane 1.0 MAC (minimal end-tidal alveolar concentration) for 30 min that was followed by a 15 min washout period. The L-NAME-desflurane group received L-NAME (NG-nitro-L-arginine methyl ester; non-selective Nitric Oxide Synthetase (NOS) inhibitor) 1 mg/kg IV 15 min before 1.0 MAC inhaled desflurane for 30 min. The L-NAME group received L-NAME 1 mg/kg IV. Infarct volume, ventricular arrhythmia, plasma lactate dehydrogenase (LDH), creatine kinase (CK) activity and myocardial perfusion were recorded simultaneously. We have found that hemodynamic values of the coronary blood flow before, during, and after LAD occlusion were not significantly different among these four groups. For the myocardial ischemia-reperfusion injury animals, the infarction size (mean +/- SEM) in the desflurane group was significantly reduced to 18 +/- 3% in the area at risk as compared with 42 +/- 7% in the control group, 35 +/- 6 in the L-NAME group, and 34 +/- 4% in the L-NAME-desflurane group. The plasma LDH, CK levels, and duration of ventricular arrhythmia were also significantly decreased in the desflurane group during ischemia-reperfusion injury. Our results indicate that desflurane is an anesthetic preconditioning agent, which could protect the myocardium against the ischemia-reperfusion injury. This beneficial effect of desflurane on the ischemic preconditioning is probably through NO release since L-NAME abrogates the desflurane preconditioning effect.     

Comparison of xylazine with tiletamine-zolazepam (Telazol) and xylazine-ketamine anesthesia in rabbits

Although widely used to provide short term anesthesia, ketamine-xylazine does not always produce satisfactory anesthesia. We compared the efficacy of ketamine-xylazine to tiletamine-zolazepam-xylazine for producing surgical anesthesia in rabbits. Four of six rabbits receiving ketamine-xylazine and all of the 12 animals given tiletamine-zolazepam-xylazine were anesthetized successfully. The mean surgical anesthesia time in the ketamine-xylazine group was 35 +/- 6 minutes as compared to the tiletamine-zolazepam-xylazine group, 72 +/- 8 minutes (p less than 0.05). There was no significant difference in the interval between the injection of the different anesthetic mixtures and the loss of either the righting reflex, the jaw reflex or the toe web pinch reflex. Respiratory rates and arterial oxygen partial pressure were higher in the ketamine-xylazine group (p less than 0.05). However, in both groups arterial blood pressure and arterial PO2 were lowered, while arterial PCO2 was elevated. No nephrotoxicity occurred. Tiletamine-zolazepam-xylazine provides effective surgical anesthesia in rabbits and in many cases may be preferable to conventional ketamine-xylazine regimen.     

Effects of Anesthetics on the Renal Sympathetic Response to Anaphylactic Hypotension in Rats

The autonomic nervous system plays an important role in rat anaphylactic hypotension. It is well known that sympathetic nerve activity and cardiovascular function are affected by anesthetics. However, the effects of different types of anesthesia on the efferent renal sympathetic nerve activity (RSNA) during anaphylactic hypotension remain unknown. Therefore, we determined the renal sympathetic responses to anaphylactic hypotension in anesthetized and conscious rats and the roles of baroreceptors in these responses. Sprague-Dawley rats were randomly allocated to anesthetic groups that were given pentobarbital, urethane, or ketamine-xylazine and to a conscious group. The rats were sensitized using subcutaneously injected ovalbumin. The systemic arterial pressure (SAP), RSNA and heart rate (HR) were measured. The effects of sinoaortic baroreceptor denervation on RSNA during anaphylaxis were determined in pentobarbital-anesthetized and conscious rats. In all of the sensitized rats, the RSNA increased and SAP decreased after antigen injection. At the early phase within 35 min of the antigen injection, the antigen-induced sympathoexcitation in the conscious rats was significantly greater than that in the anesthetized rats. Anaphylactic hypotension was attenuated in the conscious rats compared to the anesthetized rats. The anesthetic-induced suppression of SAP and RSNA was greater in the order ketamine-xylazine >urethane = pentobarbital. Indeed, in the rats treated with ketamine-xylazine, RSNA did not increase until 40 min, and SAP remained at low levels after the antigen injection. The baroreceptor reflex, as evaluated by increases in RSNA and HR in response to the decrease in SAP induced by sodium nitroprusside (SNP), was suppressed in the anesthetized rats compared with the conscious rats. Consistent with this finding, baroreceptor denervation attenuated the excitatory responses of RSNA to anaphylaxis in the conscious rats but not in the pentobarbital-anesthetized rats. RSNA was increased markedly in conscious rats during anaphylactic hypotension. Anesthetics attenuated this antigen-induced renal sympathoexcitation through the suppression of baroreceptor function.     

The effects of pentobarbital, fentanyl-droperidol, ketamine-xylazine and ketamine-diazepam on core and surface body temperature regulation in adult male rats

Many commonly used anesthetics cause hypothermia by inhibiting central and peripheral thermoregulatory mechanisms. Although it is probable that a loss of thermal homeostasis contributes directly to the high mortality frequently reported following anesthesia of laboratory rodents, this adverse effect has been investigated rarely in the past. This study compared the effects of three parenteral anesthetics (pentobarbital, ketamine-xylazine and ketamine-diazepam) and a neuroleptanalgesic (fentanyl-droperidol) on core and surface body temperature regulation in rats. Results showed a profound hypothermia with all dosages of pentobarbital, while ketamine-xylazine and ketamine-diazepam caused a dose-dependent depression in core and surface body temperature. All dosages of fentanyl-droperidol (Innovar-Vet) caused minimal depression in thermoregulation, suggesting that it is the drug which requires the least external thermal support. Results of this study also suggested that inability to compensate for heat loss, particularly from the body core, may profoundly influence anesthetic toxicity and the safety of anesthetic procedures.     

Blood pressure and other physiological responses in awake and anesthetized guinea pigs

The effect of combinations of injectable anesthetics on mean arterial blood pressure, blood gases, heart rate and respiration of the guinea pig (NIH Outbred strain) was investigated. After a 30 minute period in which baseline resting cardiorespiratory measurements were obtained, five groups of six pigmented animals having indwelling carotid cannulas were anesthetized with (a) ketamine hydrochloride (30 mg/kg, im)/xylazine (5 mg/kg, im); (b) sodium pentobarbital (15 mg/kg, ip)/fentanyl-droperidol (0.4 mg/kg, im); (c) diazepam (5mg/kg, ip)/fentanyl citrate (0.32 mg/kg, im); (d) diazepam (5 mg/kg, ip)/alphaxalone-alphadolone acetate (45 mg/kg, im); or (e) 1% alpha-chloralose-40% urethane (0.8 ml/100g, ip). Animals were not respirated artificially and no supplemental doses of anesthetic were given. Resting blood pressure in awake animals was measured over time for as long as cannulas remained patent (109 measurements). Mean resting blood pressure, for this strain of guinea pigs, was determined to be 53.1 +/- 4.2 mmHg. There was no indication that mean arterial blood pressure changed with age in animals varying in weight from 215 g to 550 g. Under diazepam/fentanyl, blood pressure rose significantly above resting level to a mean of 71.1 +/- 6.1 mmHg. With the other four combinations, blood pressure stabilized near, but below pre-anesthesia levels (ketamine/xylazine 47.1 +/- 6.8 mmHg; pentobarbital/fentanyl-droperidol, 46.9 +/- 3.2 mmHg; diazepam/alphaxalone-alphadolone, 47.8 +/- 4.8 mmHg; chloralose-urethane, 51.0 +/- 1.2 mmHg). Under diazepam/alphaxalone-alphadolone and chloralose-urethane, respiration was depressed and blood gas levels deviated from normal to the extent that artificial ventilation would be necessary to maintain an adequate physiological state.     

Reversal of ketamine/xylazine anesthesia in the rabbit with yohimbine

Ketamine and xylazine used in combination have been shown to be effective, easily administered, cost efficient agents for surgical anesthesia in the rabbit. The effect of xylazine on the central nervous system has been shown to be mediated through alpha-2 adrenergic receptors. Yohimbine, an alpha-2 adrenergic antagonist has been shown to reverse xylazine induced depression and partially antagonize ketamine in other species. We evaluated the antagonistic effect of yohimbine on ketamine/xylazine anesthesia in the rabbit. Six New Zealand White rabbits were anesthetized with intramuscular ketamine (50 mg/kg) and xylazine (10 mg/kg) to establish baseline parameters including respiratory rate, heart rate, and palpebral, pedal and postural reflex activity. Fourteen days later each rabbit was subjected to the same anesthetic regimen followed 30 minutes later by the intravenous administration of yohimbine (0.2 mg/kg). The duration of anesthesia estimated by the time elapsed between the loss and return of the palpebral reflex was reduced in the yohimbine treated trial (means = 29.7 +/- 1.9 minutes) compared to the control trial (means = 67.0 +/- 13.5 minutes). The palpebral reflex returned within 5 minutes following yohimbine treatment. Our results indicated that yohimbine is an effective antagonist of ketamine/xylazine anesthesia in the rabbit. Yohimbine decreases anesthetic duration after intravenous administration and also may aid in the control of undesirable anesthetic effects and overdosage.     

Comparison of the ability of opioid analgesics to increase endogenous opioid-like activity in the cerebrospinal fluid of rabbits

We have previously demonstrated that the acute administration of morphine increases the level of endogenous substances, which have antinociceptive activity, in cerebrospinal fluid (CSF). The present study was conducted to determine whether other opioid analgesics exert a similar effect. CSF was withdrawn from the cisterna magna of anesthetized rabbits before and after s.c. injections of meperidine, pentazocine, levorphanol and methadone, and was bioassayed for opioid-like activity in the mouse tail-flick and phenylquinone writhing tests. The opioid-like activity of CSF taken 60 min after meperidine (50 mg/kg) was significantly increased in both bioassays, and the CSF level of meperidine was insufficient to account for this effect. Pentazocine (25-75 mg/kg) also significantly increased opioid-like activity in rabbit CSF, but the effects of methadone (5-10 mg/kg) and levorphanol (20 mg/kg) were less marked. Dextrorphan (20 mg/kg), diazepam (10 mg/kg) and pentobarbital (20 mg/kg) administration did not significantly increase opioid-like activity in CSF. It is concluded that the antinociceptive action of some opioid analgesics in rabbits may be mediated in part by the release of endogenous antinociceptive substances.     

Effects of anesthetic agents on systemic critical O2 delivery

The present study tested the hypothesis that anesthetic agents can alter tissue O2 extraction capabilities in a dog model of progressive hemorrhage. After administration of pentobarbital sodium (25 mg/kg iv) and endotracheal intubation, the dogs were paralyzed with pancuronium bromide, ventilated with room air, and splenectomized. A total of 60 dogs were randomized in 10 groups of 6 dogs each. The first group served as control (C). A second group (P) received a continuous infusion of pentobarbital (4 mg.kg-2.h-2), which was started immediately after the bolus dose. Three groups received enflurane (E), halothane (HL), or isoflurane (I) at the end-tidal concentration of 0.7 minimum alveolar concentration (MAC). The sixth group received halothane at the end-tidal concentration of 1 MAC (HH). Two groups received intravenous alfentanil at relatively low dose (AL) or high dose (AH). The last two groups received intravenous ketamine at either relatively low dose (KL) or high dose (KH). In each group, O2 delivery (Do2) was progressively reduced by hemorrhage. At each step, systemic Do2 and O2 consumption (VO2) were measured separately and the critical point was determined from a plot of Vo2 vs. Do2. The critical O2 extraction ratio (OER) in the control group was 65.0 +/- 7.8%. OER was lower in all anesthetized groups (P, 44.3 +/- 11.8%; E, 47.0 +/- 7.7%; HL, 45.7 +/- 11.2%; I, 44.3 +/- 7.1%; HH, 33.7 +/- 6.0%; AL, 56.5 +/- 9.6%; AH, 43.5 +/- 5.9%; KH, 57.7 +/- 7.1%), except in the KL group (78.3 +/- 10.0%). The effects of halothane and alfentanil on critical OER were dose dependent (P less than 0.05), whereas critical OER was significantly lower in the KH than in the KL group. Moreover, the effects of anesthetic agents on critical Do2 appeared related to their effects on systemic vascular resistance. Anesthetic agents therefore alter O2 extraction by their peripheral vascular effects. However, ketamine, with its unique sympathetic stimulant properties, had a lesser effect on OER than the other anesthetic agents. It could therefore be the anesthetic agent of choice in clinical situations when O2 availability is reduced.     

Pretreatment with catalase or dimethyl sulfoxide protects alloxan-induced acute lung edema in dogs.

We tested the preventive effects of catalase, an enzymatic scavenger of hydrogen peroxide, or dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, on intravenous alloxan-induced lung edema in four groups of pentobarbital sodium-anesthetized, ventilated dogs for 3 h: saline (20 ml.kg-1.h-1) infusion alone (n = 5), alloxan (75 mg/kg) + saline infusion (n = 5), catalase (150,000 U/kg) + alloxan + saline infusion (n = 5), or DMSO (4 mg/kg) + alloxan + saline infusion (n = 5). Catalase or DMSO significantly prevented the increase in plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha over 3 h after alloxan and the accumulation of extravascular lung water after 3 h [3.95 +/- 0.52 (SE) g/g with catalase, 3.06 +/- 0.42 g/g with DMSO] but not early pulmonary arterial pressor response. An electron microscopic study indicated that catalase or DMSO significantly reduced the endothelial cellular damages after alloxan. These findings strongly suggest that hydrogen peroxide and hydroxyl radical are major mediators responsible for intravenous alloxan-induced edematous lung injury in anesthetized ventilated dogs.     

Cardiopulmonary,hematological, serum biochemical and behavioral effects of sevoflurane compared with isoflurane or halothane in spontaneously ventilating goats

This study compares cardiopulmonary, hematological, serum biochemical and behavioral effects of sevoflurane, isoflurane or halothane anesthesia in spontaneously breathing, conventionally medicated goats. Six male adult goats were anesthetized repeatedly at 2-week intervals with three anesthetics. Goats were administered atropine (0.1 mg/kg) intramuscularly, and 10 min later, induced to anesthesia by an intravenous infusion of thiopental (mean 14.3 mg/kg). After intubation, goats were anesthetized with halothane, isoflurane or sevoflurane in oxygen and maintained at surgical depth of anesthesia for 3 h. Recovery from anesthesia with sevoflurane was more rapid than that with isoflurane or halothane. Time-related hypercapnia and acidosis were observed during halothane anesthesia, but not observed during sevoflurane or isoflurane anesthesia. Both hypercapnia and acidosis during sevoflurane anesthesia did not differ from isoflurane anesthesia, but were less during halothane anesthesia, especially at prolonged maintenance period. There were no significant differences between anesthetics in respiration and heart rates, arterial pressures, hematological and serum biochemical values. It was concluded that sevoflurane is an effective inhalant for use in goats showing the most rapid recovery from anesthesia, and that cardiopulmonary effects of sevoflurane are similar to isoflurane than halothane.     

戊巴比妥钠联用速眠新Ⅱ对西藏小型猪麻醉效果观察

目的观察联合应用速眠新Ⅱ和戊巴比妥钠对西藏小型猪的麻醉效果。方法采用速眠新Ⅱ（0.1mL/kg）肌内注射和3%戊巴比妥钠生理盐水溶液（0.2 mL/kg）静脉注射联合麻醉方法对15头行胚胎移植术的西藏小型猪进行麻醉,观察动物麻醉维持时间、镇痛效果、呼吸频率和心率变化及术后苏醒情况。结果80%（12头/15头）西藏小型猪初始量麻醉状态维持45 min以上,20%（3头/15头）西藏小型猪手术过程中追加麻醉。麻醉期间肌肉松弛效果好,动物呼吸和心率平稳。手术过程中西藏小型猪呼吸频率为（12-22）次/min,心率为（63-85）次/min,麻醉过程中未出现麻醉死亡,术后苏醒时间为30-60 min。结论速眠新和戊巴比妥钠混合麻醉效果好,且麻醉剂量较以往大幅减少,术后苏醒快。戊巴比妥钠联用速眠新复合麻醉对西藏小型猪是一种较理想的麻醉方法,且动物麻醉安全性高。     

Use of two anesthetic combinations for semen collection by electroejaculation from captive coatis (Nasua nasua)

The objective was to compare the effects of ketamine-xylazine or tiletamine-zolazepam combinations as anesthetic protocols for captive coatis (Nasua nasua) for semen collection by electroejaculation. Five mature male coatis were physically restrained and then anesthetized by im injections of ketamine (10 mg/kg) plus xylazine (1 mg/kg) or a tiletamine-zolazepam combination (8 mg/kg). For the two combinations, additional quarter-doses of ketamine or the tiletamine-zolazepam combination were administered when necessary. Semen was collected by electroejaculation and immediately evaluated for color, volume, pH, sperm motility, vigor, morphology, acrosomal integrity, and percentage of live cells. Overall, collection of nine ejaculates was attempted from five animals for each treatment. Regardless of the anesthetic combination, all animals developed an erection during each attempt to collect semen. Ejaculates were obtained in all (9 of 9) attempts that used ketamine-xylazine for anesthesia, but in only 3 of 9 attempts (P < 0.05) when tiletamine-zolazepam was used. All ejaculates contained sperm, with no significant differences in semen characteristics between the two anesthetic combinations. Recovery was smooth in all animals. In conclusion, semen collection by electroejaculation in coatis was significantly more successful with the use of a ketamine-xylazine combination than with tiletamine-zolazepam.     

Cortico-Cardio-Respiratory Network Interactions during Anesthesia

General anesthetics are used during medical and surgical procedures to reversibly induce a state of total unconsciousness in patients. Here, we investigate, from a dynamic network perspective, how the cortical and cardiovascular systems behave during anesthesia by applying nonparametric spectral techniques to cortical electroencephalography, electrocardiogram and respiratory signals recorded from anesthetized rats under two drugs, ketamine-xylazine (KX) and pentobarbital (PB). We find that the patterns of low-frequency cortico-cardio-respiratory network interactions may undergo significant changes in network activity strengths and in number of network links at different depths of anesthesia dependent upon anesthetics used.     

Time-dependent change in baroreflex control capacity of arterial pressure by pentobarbital anesthesia in rabbits.

The present study is designed to investigate the time-dependent effect of pentobarbital anesthesia on the baroreflex arterial pressure (AP) control system in rabbits. The overall AP control capacity of the baroreflex system was assessed with mean arterial pressure (MAP) responses to the rapid mild hemorrhage (2 ml/kg body weight) and an overall open-loop gain (G) of the system. The G value was determined by means of the following formula: G = delta API/delta APS-1, where delta APl is an immediate MAP fall and delta APS a steady-state fall after the rapid hemorrhage. Prior to the experiment, two catheters for AP measurement and hemorrhage were chronically in-dwelt in the aortic arch via the left subclavian and left common carotid arteries, respectively. Control mean arterial pressure averaged for 30 sec before the rapid hemorrhage (CMAP), delta API and delta APS significantly increased and reached the maximal value at 14 min (CAMP: p < 0.01) and 28 min (delta API: p < 0.01 and delta APS: p < 0.01) after the intravenous injection of sodium pentobarbital in a 25.0 mg/kg dose, respectively. These values gradually decreased in the course of time and tended to recover to near the preanesthetic level at 77-98 min after the anesthesia. The G value significantly decreased from 7.3 in the conscious state to 1.5 at 28 min after the anesthesia (p < 0.001), gradually increased with lapse of time and recovered to near the preanesthetic level at 77-98 min after the anesthesia. No significant difference in G was observed between in the conscious and anesthetized states beyond 70 min after the anesthesia (p > 0.05). These findings suggest that pentobarbital sodium exerts a time-dependent inhibitory effect on the baroreflex system but does not significantly affect the overall AP control capacity of the baroreflex system itself at least 70 min after the intravenous administration at a dose of 25.0 mg/kg.     

Kinetics of chylomicron triglyceride removal from plasma in rats: a comparison of the anesthetized and the unanesthetized states

The kinetics of chylomicron-TG removal were studied using an experimental method which allows measurements to be made under optimal physiological conditions. Chylomicrons, labeled with palmitic acid-(14)C, were constantly infused at a rate of 0.5 mg total lipid per min into chronically cannulated, unanesthetized, unrestrained rats which had been fasted for 18 hr. Serial blood samples were withdrawn from an arterial cannula during a 20 min infusion period and for 10 min following the infusion. Plasma lipoproteins were separated into two fractions in the ultracentrifuge, and the lipids were extracted. Radioactivity in the low-density fraction (d<1.006) was taken to represent chylomicron-TG radioactivity. Using this method we studied the influence of anesthesia on the kinetics of removal of chylomicron-TG. The following three phases of the radioactivity-time curve were plotted: (a) the increase in (14)C during infusion of chylomicrons, (b) the steady-state phase during the infusion, and (c) the decay of (14)C after chylomicron infusion was stopped. The values for the anesthetized rats failed to reach a steady-state phase during the course of the experiment. From the disappearance of (14)C following the end of the infusion, the apparent half time of removal of chylomicron-TG was estimated to be 2.8 +/- 0.37 min in unanesthetized rats, 4.5 +/- 0.37 min in rats anesthetized with sodium pentobarbital, and 4.4 +/- 0.44 min in rats anesthetized with halothane. Thus, two anesthetics with different physical properties markedly slowed the removal of chylomicron-TG from the circulation. The reduced rate may have resulted from alterations in cardiac output or distribution of blood flow induced by the anesthetic agents.