The hemodynamic effects of medetomidine continuous rate infusions in the dog

ObjectiveTo characterize the hemodynamic effects of continuous rate infusions (CRI) of medetomidine administered at doses ranging from 0 to 3 μg kg^?1 hour^?1.Study designProspective, blinded, randomized experimental trial.AnimalsSix adult purpose-bred mongrel dogs.MethodsAnesthesia was induced with sevoflurane for placement of arterial and venous catheters. Dogs recovered from anesthesia after which baseline hemodynamic measurements were obtained via lithium dilution cardiac output (CO) determination, with subsequent measurements via pulse power analysis to provide continuous CO determinations. Medetomidine, 1, 2, or 3 μg kg^?1 hour^?1 or a volume equivalent placebo, was administered via CRI for 60 minutes. Systolic, mean, and diastolic arterial pressure, heart rate (HR), CO and stroke volume were measured and stroke index (SI), cardiac index (CI), total peripheral resistance (TPR), and total peripheral resistance index (TPRI) were calculated at 3, 7, 10, 20, 30, 45, 60, 90, and 120 minutes from the start of the infusion.ResultsIncrease in dose decreased SI by 25%, 19%, and 30%, HR by 33%, 57%, and 60%, CI by 50%, 65%, 70% and increased TPRI by 109%, 235%, and 222% from baseline to the 60-minute measurement for the 1, 2, and 3 μg kg^?1 hour^?1 doses, respectively. HR, TPRI, and CI all showed significant differences over the duration of the study from the placebo treatment.ConclusionsMedetomidine CRI produces clinically relevant changes in CO, TPR, and HR. The demonstrated decrease in CO is largely because of bradycardia and the degree of cardiovascular depression appears to be dose-dependent. These findings are consistent with previously described hemodynamic changes with single bolus administration of medetomidine.Clinical relevanceLow-dose medetomidine CRIs produce clinically relevant hemodynamic depression at doses as low as 1 μg kg^?1 hour^?1 and should be used cautiously in dogs.     

Fibrinous pericarditis and cardiac tamponade in a 3‐week‐old pony foal

A 3‐week‐old Pony of the Americas foal presented with a history of respiratory distress presumed to result from Actinobacillus equuli pleuropneumonia and septic arthritis. Failure of transfer of passive colostral immunity was suspected, but not confirmed, based on a history of the foal being separated from its dam shortly after parturition. Transient improvement was noted following thoracocentesis and removal of approximately 600 ml of pleural fluid but progressive clinical signs of congestive heart failure developed. Fibrinous pericarditis with evidence of cardiac tamponade was subsequently diagnosed via thoracic ultrasonography. Early clinical signs of cardiogenic shock were identified and fibrinopurulent exudate removed through a catheter placed with ultrasound guidance into the pericardium. The foal experienced cardiorespiratory arrest during the procedure and died despite resuscitative efforts. Post mortem examination identified extensive hypertrophy of the pericardium, septic arthritis, mild pleural effusion and focal bronchopneumonia. This report details the clinical evaluation, haematology, treatment and post mortem pathology of a foal with Actinobacillus equuli associated fibrinous pericarditis, as well as a brief review of cardiac tamponade.     

Lack of agreement between thermodilution and echocardiographic determination of cardiac output during normovolemia and acute hemorrhage in clinically healthy, anesthetized dogs

Objective and hypothesis: To determine whether or not there is agreement between the thermodilution and echocardiographic measurement of cardiac output (CO) during normovolemia and acute hemorrhage. The hypothesis was that there will be agreement between echocardiographic measurement of CO (ECO) and thermodilution measurement of CO (TDCO) during normovolemia and acute hemorrhage. Design: CO was measured by both thermodilution and echocardiography during α‐chloralose anesthesia in dogs before and 15 and 30 minutes following acute arterial hemorrhage. Setting: Laboratory investigation. Animals: Eighteen clinically healthy dogs, weighing 20–25 kg, anesthetized with α‐chloralose. Interventions: Acute arterial hemorrhage of approximately 50% of the total blood volume. CO was measured by thermodilution and echocardiography before and 15 and 30 minutes following hemorrhage. Measurements and main results: Acute hemorrhage resulted in a significant decrease in CO. There was a lack of agreement between the 2 methods to measure CO at each time and at all anatomic points of measurement in the aorta and pulmonary artery. Conclusion: There is a lack of agreement between the 2 methods; thus, determination of CO by echocardiography may not be a clinically useful tool following hemorrhage in dogs.     

牛心型α肌动蛋白基因的进化及表达研究

试验旨在对鲁西黄牛心型α肌动蛋白的进化及表达进行研究,为研究该基因的功能提供依据。试验采用生物信息学方法对心型α肌动蛋白的进化进行了分析,利用Western blotting和免疫荧光的方法分析了牛心型α肌动蛋白的表达模式。结果显示,心型α肌动蛋白除在鲁西黄牛心脏组织中有强表达外,在骨骼肌中也检测到该蛋白的表达。推测心型α肌动蛋白除在成体鲁西黄牛的心脏发育过程中起作用外,在骨骼肌发育过程中也起作用。     

TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION IN A FOAL

An 8-day-old Arabian-Morgan cross colt underwent cardiac evaluation. The foal was tachycardic, tachypneic, exercise intolerant and had a loud right-sided heart murmur and cyanotic mucous membranes. Total anomalous pulmonary venous connection was diagnosed with echocardiography and confirmed at postmortem examination. Total anomalous pulmonary venous connection is a very rare congenital cardiac abnormality that has not been reported before in the horse.     

双氢睾酮诱导大鼠心肌细胞肥大模型的建立

应用胰蛋白酶分次消化法分离乳鼠心肌细胞,以差速贴壁法纯化心肌细胞,α-sarconme-actin抗体免疫细胞化学染色鉴定心肌细胞。心肌细胞在无血清无酚红培养基中培养48h后,用双氢睾酮(DHT)诱导心肌细胞肥大,建立心肌细胞肥大模型。24h后检测心肌细胞肥大的指标心肌细胞表面积;BCA法测定心肌细胞蛋白含量;半定量RTPCR两步法检测心肌细胞肥大的特征性基因—心房利钠因子(atrial natriuretic factor,ANF,β-肌球蛋白重链(β-myosin heavy chain,β-MHC)mRNA的表达。结果显示免疫细胞化学染色显示培养的心肌细胞纯度达到90%以上,心肌细胞分离良好。与对照组相比,10-8 mol/L的DHT能显著的增加心肌细胞表面积、蛋白质含量、ANP和β-MHC基因表达的增加(P0.01),心肌细胞肥大模型建立成功。     

埋藏式心脏起搏器术后起搏阈值的动态变化

目的:观察埋藏式心脏起搏器术后电极成熟期前后起搏阈值的变化规律。方法:对30例接受埋藏式心脏起搏治疗的患者分别于术中、术后1周、2周、1个月、2个月、3个月、6个月测定起搏阈值。结果:16例应用Medtronic CAPSURESP系列(激素洗提)心房电极的患者心房起搏阈值术后升高,本后1周达峰值,后逐渐降低,术后2个月开始趋于稳定,除术后6个月外,其余各时间点与术中比较差异均有非常显著性(P<0.01);24例应用MCSP系列心室电极的患者心室起搏阚值术后均明显高于术中(P<0.01);9例应用BIOTRONIK SYNOX SX系列(高阻抗非激素洗提)电极的患者心房、心室平均起搏阈值具有与MCSP系列起搏电极类似的术后演变趋势.其急性期起搏阈值呈明显峰化现象,且具有较高的慢性期阚值,与40条MCSP系列电极比较,两者急、慢性期起搏阈值差异均有非常显著性(P<0.01)。结论:埋藏式心脏起搏器术后6个月内,起搏阈值明显升高;激素洗提电极能明显降低急性期和慢性期阚值。     

Anesthetic management of an off-pump open-heart surgery in a dog

ObservationsA 9 year-old, 40 kg, female spayed Bouvier des Flandres was anesthetized for surgical removal of an intra-cardiac mass. Pre-anesthetic work-up included thoracic radiographs, which revealed moderate pleural effusion, and cardiac ultrasound, which identified a mass attached to the wall of the right ventricular outflow tract (RVOT). The mass caused dynamic obstruction of the RVOT during systole. The dog was pre-medicated with intravenous (IV) hydromorphone (0.05 mg kg^?1). Following pre-oxygenation, anesthesia was induced with ketamine (3.75 mg kg^?1, IV) and diazepam (0.18 mg kg^?1, IV). Anesthesia was maintained with isoflurane in oxygen, an intravenous constant rate infusion (CRI) of fentanyl (10–30 μg kg^?1 hour^?1) and a CRI of lidocaine (50–200 μg kg^?1 minute^?1). A right lateral thoracotomy was performed. The heart was stopped transiently with a cold cardioplegic solution for 7.83 minutes to allow the removal of the mass through an open-heart procedure. No cardiopulmonary bypass was used. The heart was successfully restarted after cardiopulmonary resuscitation with internal cardiac massage and internal defibrillation. The dog recovered uneventfully from anesthesia without any apparent neurological sequelae. Post-operative analgesia consisted of intercostal nerve blocks with bupivacaine, CRIs of fentanyl (2–5 μg kg^?1 hour^?1) and lidocaine (40 μg kg^?1 minute^?1) and with oral meloxicam (0.1 mg kg^?1). Five days following surgery, the dog was discharged from the hospital. Histopathology and immunohistochemistry of the mass identified an ectopic thyroid carcinoma.ConclusionsThis case showed the feasibility of whole body hypothermia and using a cold cardioplegic solution to induce cardiac arrest for a short open-heart procedure.