四氯化碳中毒及其解救对家兔呼吸作用的影响

四氯化碳耳静脉注入家兔并实施解救，描记呼吸曲线，结果表明，家兔注射四氯化碳后，呼吸频率减少，幅度加深，解救后呼吸频率回升，高度回落。     

叶下珠生物碱对兔离体肠肌的舒张作用

目的:以兔离体小肠平滑肌为研究对象,研究叶下珠生物碱对兔离体肠肌收缩的影响,并探讨其作用机制。方法:利用BL-420E生物机能系统,观察叶下珠生物碱对兔离体肠肌自发性收缩和工具药乙酰胆碱、阿托品、新斯的明、组胺作用下离体肠肌活动的影响,观察并记录收缩频率和振幅。结果:叶下珠生物生物碱可显著抑制兔离体肠肌自发性收缩的频率和振幅(P0.05);可显著或极显著抑制由乙酰胆碱、新斯的明和组胺引起的离体肠肌挛缩,加强阿托品对离体肠肌的舒张作用。结论:叶下珠抗腹泻作用可能与抑制小肠蠕动有关,叶下珠生物碱抑制肠肌运动可能与促进肠上皮细胞释放钙离子、阻断H1受体促进胞外钙离子内流相关。     

3种麻醉药对家兔麻醉效果的观察

将25只家兔随机分成5组,每组5只,各组分别为耳缘静脉注射生理盐水[3 mL/(kg·BW)]组、耳缘静脉注射25%乌拉坦[4 mL/(kg·BW)]组、耳缘静脉注射3%戊巴比妥钠[1 mL/(kg·BW)]组、耳缘静脉注射陆眠宁[0.2 mL/(kg·BW)]组、肌肉注射陆眠宁[0.2 mL/(kg·BW)]组。观察试验过程中动物麻醉诱导时间、麻醉维持时间及外科麻醉期一般状况;外科麻醉期0 h、外科麻醉期0.5 h与苏醒时的呼吸和心率。结果显示,陆眠宁效果较好,尤以陆眠宁肌肉注射麻醉维持时间较长,麻醉时家兔的呼吸、心率变化较小,提示对家兔进行麻醉时宜采取肌肉注射陆眠宁的方式,剂量为0.2 mL/kg。     

内皮素对哈萨克公羊生理生化指标的影响

为探究内皮素(ET)对羊生理生化指标的影响,选取5只新疆哈萨克公羊,采用不完全拉丁方试验设计,每只羊一次性静脉注射0.7nmol/kg ET-1或ET-3,对照组注射1g/L BSA生理盐水。结果显示,注射ET-1或ET-3后同对照组比,心率降低21%~36%(P0.01),红细胞总数增加10%~14%(P0.01),血红蛋白含量增加14%~17%(P0.05),红细胞比容增加14%~16%(P0.05);血糖含量增高27%~53%(P0.05),而且从这些指标改变的幅度和持续时间看,ET-1比ET-3作用强。在整个试验过程中未观察到羊呼吸频率、白细胞总数及分类计数和血浆蛋白浓度的影响(P0.05)。研究结果提示,ET可调控反刍动物心血管活动、红细胞比容,并参与血糖稳态调节,而且这些作用可能主要是通过内皮素A受体(ET-A)介导的。     

禁食、急性冷暴露和外源性注射Ghrelin对羔羊生理指标的影响

为了探究禁食、急性冷暴露和注射外源性生长激素释放肽Ghrelin对羔羊生理指标的影响,本研究监测了室温禁食24h后继续禁食并冷冻(-24.7℃±0.2℃)2h羔羊基本生命体征、血液生理指标和血糖浓度的变化,同时探究了外源性Ghrelin对于冷冻的禁食羔羊以上指标的影响。结果显示,在禁食后8、16、24h羔羊呼吸频率、心率和血糖浓度均较禁食前显著降低(P0.05),在禁食后16h和24h直肠温度均较禁食前极显著降低(P0.01),而血液生理指标变化不明显(P0.05);在冷冻1.5h和2.0h后羔羊呼吸频率较保温组显著减慢(P0.05),心率和血糖浓度在冷冻后1.0、1.5、2.0h显著增加(P0.05),冷冻过程中羔羊直肠温度差异不显著(P0.05);冷冻2h后颈静脉一次性注射Ghrelin未发现对羔羊以上指标的影响(P0.05)。以上研究结果提示,羔羊在禁食和低温情况下可通过调整自身活动,以维持机体稳态,并且Ghrelin可能并未参与该调整过程。     

高温条件下温湿度指标对生长肥育猪体温调节的影响

夏季高温条件下选择６０－７５公斤生长肥育猪２１头，每天测定室温、相对湿度、气流、体温、呼吸频率和心率各项生理指数的变化，计算温湿度指标，研究ＴＨＩ对其体温调节的影响。结果表明，ＴＨＩ、室温与体温、呼吸频率和心率的变化呈现强正直线相关，且都达到极显著水平（ｐ＜０．０１），ＴＨＩ估计炎热程度比单一因素准确性要高，随着ＴＨＩ的提高，体温、心率随之升高，但均属正常范围，而呼吸频率极显著升高，由于气流的作用     

舒泰与盐酸右美托咪定对兔复合麻醉效果的研究

为了探讨用舒泰与盐酸右美托咪定对实验兔进行复合麻醉在小型手术和试验中使用的可行性,试验在兔的耳缘静脉分别按体重注射舒泰(0.3 mL/kg)和盐酸右美托咪定(0.02 mL/kg),记录麻醉诱导时间、麻醉时间、苏醒时间,麻醉前(0分钟)及麻醉后5,10,15,20,25,30分钟的镇痛、镇静和肌松作用效果及体温(T)、呼吸频率(RR)、心率(HR)、血氧饱和度(SpO₂)等生理指标;分别在麻醉前(0小时)及麻醉后1,2,24小时时耳缘静脉采血,测定血常规和血液生化指标。结果表明：该复合麻醉方案的麻醉诱导时间为(2.6±0.4)min,麻醉时间为(31.2±5.2)min,苏醒时间为(8.5±2.6)min。麻醉后5分钟大多数实验兔进入良好的镇静状态,并持续至麻醉后第25分钟;麻醉后5分钟大多数实验兔进入良好的镇痛状态,并持续至麻醉后第20分钟;麻醉后15分钟大多数实验兔肌松状态良好,并持续至麻醉后第20分钟。与麻醉前相比,实验兔T、RR、HR、SpO₂均呈现先下降后上升趋势。T在麻醉后10分钟显著下降(P<0.05);随后逐渐升高,基本...     

右美托咪啶与舒泰复合用药对犬生理指标的影响

右美托咪啶是一种新型、强效、高选择性的α2-肾上腺素受体激动剂[1].近几年来该药因作用快,所需量少与可明显减少其他麻醉剂需求量等特点,被广泛应用在欧美兽医临床中,但在国内尚无完整的兽医临床相关数据可供参考.本文的主要目的就是为了监测低剂量右美托咪啶和舒泰联合用药,对犬心率、呼吸频率、体温生理指标的影响,为临床应用提供有价值的资料.     

复合麻醉剂KMT对八眉猪呼吸和循环系统的影响

为探讨复合麻醉剂氯胺酮-美托嘧啶-曲马多(KMT)对八眉猪呼吸和循环系统的影响。8只8~10周龄的八眉猪,肌肉注射KMT 0.1m L/kg,并在注药前及注射药后5、10、15、20、30、45、60、90及120 min测定呼吸频率、脉搏血氧饱和度、心率、无创血压及体温等。试验结果表明:注射KMT后,呼吸频率开始增加,10 min时达到最高值,之后开始下降,到45 min时降至最低;动脉血氧饱和度在整个监测过程中均在90%以上;心率与血压在注射KMT后10 min时达到最高值,之后开始下降,到60 min时降至最低;体温从注药后开始下降,在整个监测过程中体温下降幅度在2℃以内。提示:KMT对八眉猪呼吸和循环系统的影响短暂且轻微,证明KMT组方科学合理,临床使用安全。     

电针麻醉对绵羊生理生化指标的影响

针刺绵羊百会、三台二穴，研究电针麻醉对心率、呼吸频率、体温、血糖、血清谷转氨酶（ＧＯＴ）、谷丙转氨酶（ＧＰＴ）等生理生化指标的影响。结果表明，电针麻醉使心率略有下降，体温、呼吸频率有所上升；电针麻醉过程中血糖含量上升；ＧＯＴ、ＧＰＴ含量变化不显著。     

Respiratory and pulmonary haemodynamic changes during experimental organophosphate poisoning in goats

Five French Alpine goats received 2 mg kg^–1 of dichlorvos (DDVP) by intravenous injection and 0.15 mg kg^–1 of atropine sulphate 5–10 min later. Ventilatory mechanics, gas exchanges, pulmonary haemodynamics and pulmonary vascular resistance (PVR) were measured before treatment, 5 min after DDVP injection and 5 min after atropine injection.Within 2 min of DDVP administration, all the goats showed acute respiratory distress, excitation and slight muscle fasciculations. A post-inspiratory pause was recorded in 3 goats. Hypersecretion of saliva or nasal discharge was not observed. Dynamic compliance and heart rate decreased significantly and total pulmonary resistance, pulmonary artery and wedge pressures increased significantly. On the other hand, minute ventilation, arterial oxygen and carbon dioxide tensions were not significantly altered by DDVP.Atropine treatment reversed all the clinical and functional parameters, with the exception of the central nervous and muscular signs, which disappeared within 12 h.It was concluded that experimental DDVP toxicosis induced changes in the mechanics of breathing and pulmonary haemodynamics associated with diffuse bronchoconstriction and cardiac insufficiency respectively.     

Effect of romifidine and romifidine-butorphanol for sedation in dogs

The sedative and physiological effects of intravenous romifidine at 120 μg/kg were compared with intravenous romifidine (120 μg/kg) followed immediately by intravenous butorphanol (01 mg/kg) in 18 clinically normal adult beagles in a blinded randomised change-over study. Following the injection of romifidine alone the dogs became recumbent and there was an increase in a subjective score awarded to the degree of sedation. Heart rate and respiratory rate decreased and minor bradyarrhythmias were noted. The romifidine-butorphanol combination produced a significant decrease in the time to the onset of sedation and increase in the sedative effect and duration of action compared with romifidine alone. With the exception of a further decrease in heart rate and respiratory rate, there were no additional side effects following the use of the romifidine-butorphanol combination. The marked sedative effect associated with this combination would appear to be useful in the clinical situation where an increased degree of sedation is required.     

Pulmonary function changes induced by experimental dichlorvos toxicosis in calves

Clinical and pulmonary function changes induced by intravenous dichlorvos (2,2-dichlorvinyldimethyl phosphate) (DDVP) toxicosis, and reversibility of these changes after atropine treatment were investigated in six Friesian calves one to three months old. From one minute after dosage, all animals showed severe respiratory distress, excitation, weakness, muscle fasciculation and cholinesterase inhibition. Decrease in dynamic lung compliance and arterial oxygen tension and increase in total pulmonary resistance, viscous work of breathing and alveolar arterial oxygen gradient were highly significant (P less than 0.01). On the other hand, body secretions, heart rate, respiratory rate, tidal volume and arterial carbon dioxide tension were not significantly affected by DDVP injection. Atropine promptly and completely reversed these changes, except for muscle fasciculations, central depression and cholinesterase inhibition which disappeared progressively within 24 hours.     

Observations on the use of glyceryl guaiacolate as an adjunct to general anaesthesia in horses

Twenty-one horses undergoing clinical surgery and diagnostic procedures received 15% glyceryl guaiacolate followed by a rapid intravenous injection of a thiobarbiturate for induction of anaesthesia. Premedication was with atropine and acepromazine. Induction was smooth and free from problems apart from transient apnoea in some horses. Maintenance of anaesthesia was with oxygen and halothane administered by means of a closed circle system with soda-lime absorber and with the vaporiser out of circuit. During the period immediately following induction, the heart rate increased and the respiratory rate fell. Blood gas estimations were carried out on 6 horses during anaesthesia. These horses showed respiratory acidosis. Arterial blood oxygen tension values were above those reported in conscious horses. Use of glyceryl guaiacolate in this way provides a safe induction and enables transition to a stable maintenance period which is followed by a quiet and uneventful recovery.     

Hemodynamic Effects of Atropine and Glycopyrrolate in Isoflurane-Xylazine-Anesthetlzed Dogs

Alterations in parasympathetic tone are partially responsible for xylazine's hemodynamic effects. The purpose of this study was to evaluate and compare the hemodynamic changes caused by the administration of intravenous (IV) atropine or glycopyrrolate after IV xylazine in isoflurane-anesthetized dogs. Six healthy beagles (8.2 to 10.7 kg) were used in two trials separated by 7 days. Anesthesia was induced and maintained with isoflurane in 100% oxygen with controlled ventilation. Once constant end-tidal isoflurane (1.8%) and arterial partial pressure of carbon dioxide (35 to 45 mm Hg) values were reached, baseline data were recorded and xylazine (0.5 mg/kg, IV) was given. In trial 1 atropine (0.1 mg/kg, IV) was given 5 minutes after xylazine, and in trial 2 glycopyrrolate (0.025, mg/kg, IV), was given 5 minutes after xylazine. Hemodynamic variables were recorded 3 minutes after xylazine and 3 minutes after anticholinergic administration. In trial 2, bilateral vagotomies were performed 10 minutes after glycopyrrolate, and hemodynamic variables were recorded 3 minutes later. Heart rate, cardiac index, and stroke index decreased; arterial pressure and systemic vascular resistance increased after xylazine. Heart rate, cardiac index, and rate pressure product increased after anticholinergic administration. Significant differences between atropine and glycopyrrolate were not observed in any of the hemodynamic parameters. Similarly, significant differences between glycopyrrolate and bilateral vagotomy were not observed. The authors conclude that intravenous atropine and glycopyrrolate have equivalent hemodynamic actions during the increased pressure phase after IV xylazine in isoflurane-anesthetized dogs; that intravenous atropine and glycopyrrolate produce comparable increases in heart rate and that both may increase the risk of myocardial hypoxia associated with an increase in rate pressure product; and that vagal blockade produced by high-dose glycopyrrolate (.025 mg/kg, IV) is similar to that produced by bilateral vagotomy.     

The effects of atropine and methotrimeprazine on the epinephrine-induced arrhythmias in halothane-anesthetized dogs.

The effects of atropine and methotrimeprazine on epinephrine-induced ventricular arrhythmias were evaluated in halothane-anesthetized dogs. Ten mixed-breed dogs were assigned to 3 treatments (saline, atropine, and methotrimeprazine) in a randomized complete block design. Anesthesia was induced and maintained with halothane (1.5 minimum alveolar concentration) in oxygen. Controlled ventilation was used throughout to maintain eucapnia. Saline, atropine (0.05 mg/kg, i.v.) or methotrimeprazine (0.5 mg/kg, i.v.) were administered and, 5 minutes later the arrhythmogenic dose of epinephrine (ADE) was measured by i.v. infusion of progressively increasing infusion rates of epinephrine, until the ventricular arrhythmia criterion was met (at least 4 ectopic ventricular contractions (EVCs) during a 15-second period). Data were analyzed using a student's t-test for ADE values and multivariate profile analysis for heart rate (HR), arterial blood pressure (ABP), and rate pressure product (RPP). The ADE increased in atropine- and methotrimeprazine-treated groups, whereas 1 and 4 animals from these groups did not develop any ventricular arrhythmia, respectively. Epinephrine induced multiform premature ventricular contractions (PVCs) in the atropine group, whereas ventricular escape beats were observed in the control and methotrimeprazine groups. Heart rate and RPP decreased, and ABP increased at the time of ADE observation in the control group. Epinephrine infusion in the atropine group caused marked increases in HR, ABP, and RPP, which were associated with pulsus alternans in 2 animals. It was concluded that 1) the presence of cholinergic blockade influences the type of ventricular arrhythmia induced by epinephrine; 2) increased ADE values recorded following atropine administration must be cautiously interpreted, since in this situation the PVCs were associated with signs of increased myocardial work and ventricular failure; and 3) the use of a broader arrhythmia criterion (EVCs instead of PVCs) may not allow a direct comparison between ADE values, since it includes ventricular arrhythmias mediated by different mechanisms.     

Cardiovascular and allied actions of xylazine and atropine in the unanaesthetized goat

The cardiovascular effects of xylazine and atropine, separately and in combination, were studied in goats. Methylatropine was used to distinguish between the central and peripheral effects of atropine. Mean arterial blood pressure and heart rate were recorded, and the sedative effect and changes in respiration and salivation noted. Intravenous infusion of xylazine (2.4-80.0 micrograms/kg) decreased mean arterial blood pressure and heart rate in a dose-dependent manner. Single intravenous injections of both atropine sulphate (0.1 mg/kg) and methylatropine bromide (0.05 mg/kg) increased blood pressure and heart rate. After methylatropine, tachycardia lasted twice as long as after atropine. Following atropinization, a potentiated rise in mean arterial blood pressure was present during the infusion of xylazine (80 micrograms/kg). Xylazine-induced bradycardia was reversed by both atropine and methylatropine. The action of atropine is presumed to be primarily peripheral because of the similar effects with methylatropine. Xylazine-induced sedation was dose dependent. At the highest dose the goats were unable to stand for 30-60 min, respiration became irregular with periods of apnoea, and saliva started to drip a few minutes after infusion without increased salivation. Atropine had no visible effect on the sedation, pattern of respiration or saliva dripping effect of xylazine.     

Sedative and cardiorespiratory effects of acepromazine or atropine given before dexmedetomidine in dogs

To test the hypothesis that acepromazine could potentiate the sedative actions and attenuate the pressor response induced by dexmedetomidine, the effects of acepromazine or atropine were compared in six healthy adult dogs treated with this alpha2-agonist. In a randomised block design, the dogs received intravenous doses of either physiological saline, 0.05 mg/kg acepromazine or 0.04 mg/kg atropine, 15 minutes before an intravenous dose of 5 microg/kg dexmedetomidine. The dogs' heart rate was reduced by 50 to 63 per cent from baseline and their mean arterial blood pressure was increased transiently from baseline for 20 minutes after the dexmedetomidine. Atropine prevented the alpha2-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the alpha2-agonist, except for a slight reduction in the magnitude and duration of its pressor effects. The dexmedetomidine induced moderate to intense sedation in all the treatments, but the dogs' sedation scores did not differ among treatments. The combination of acepromazine with dexmedetomidine had no obvious advantages in comparison with dexmedetomidine alone, but the administration of atropine before dexmedetomidine is contraindicated because of a severe hypertensive response.