Objective—To determine the cardiopulmonary effects of 3 doses of isoflurane, with and without controlled mechanical ventilation and noxious stimulation, in healthy adult New Zealand white rabbits. Animals—6 adult female rabbits. Procedures—Each rabbit was administered isoflurane in oxygen at each of 3 anesthetic doses (1.0, 1.5, or 2.0 times the published minimum alveolar concentration of 2.07%). At each anesthetic dose, blood gas and cardiopulmonary measurements were obtained before and during application of a supramaximal noxious stimulus. Effects of spontaneous and mechanical ventilation were assessed during separate anesthetic episodes. Results—Mean ± SEM isoflurane concentrations used were 2.11 ± 0.04%, 3.14 ± 0.07%, and 4.15 ± 0.06%. During spontaneous ventilation, the rabbits’ Paco2 and mixed venous Pco2 significantly increased with concomitant reductions in both arterial and mixed venous pH as isoflurane concentration increased. Cardiac output and vascular resistance did not change significantly. Noxious stimulation minimally affected measured cardiopulmonary variables. During mechanical ventilation, significant reductions in arterial blood pressures and cardiac output occurred with increasing isoflurane dose. Systemic vascular resistance index at the highest anesthetic dose was significantly lower than the value at the lowest anesthetic dose. During noxious stimulation, systolic arterial blood pressure and cardiac output significantly increased at the 2 lower isoflurane concentrations, but not at the highest concentration. Conclusions and Clinical Relevance—In rabbits, isoflurane-induced dose-dependent cardiopulmonary depression was attributable to vasodilation and negative inotropy. At an isoflurane concentration of 4.15% with mechanical ventilation, cardiovascular depression was severe; use of unnecessarily high isoflurane concentrations in this species should be avoided.

Objective: This study aimed to reveal the coronary veins and the branches that join it to provide venous drainage of the heart in Southern Karaman sheep. Material-Method: Eight Southern Karaman sheep’s heart tissues were used in the study. Latex injection techniques were used to determine the coronary veins and the branches that join it for providing venous drainage of the heart.Result: In the study, vena cordis magna, vena cordis media, and vv. cordis dextra was observed as venous drainage providing vessels. The vena cordis magna began in the lower third of the sulcus interventricularis paraconalis, called vena interventricularis paraconalis. This vein reached the sulcus coronarius and continued as vena circumflexus sinister. Vena cordis media was named as vena interventricularis subsinosus in sulcus interventricularis subsinosus. The vv. cordis dextra was responsible for the venous drainage of the facies atrialis of the heart.Conclusion: In the evaluation of the study findings, it was determined that the coronary veins and the branches joined it of Southern Karaman sheep were mainly similar to other sheep breeds in the literature. Still, there were some anatomical differences, for example; vena distalis ventriculi sinistri was opening into vena circumflexus sinister, vena apicis cordis was absent, vena semicircumflexa dextri was present.

Ischemic preconditioning (IPC), i.e., a preliminary brief episode of ischemia and reperfusion, has been shown to reduce the cell damage induced by long ischemia and reperfusion. Superoxide radical which is produced during reperfusion after ischemia was recongnized as a factor of the ischemic injury and it is dismutated into H2O2 and O2 by two types of intracellular superoxide dismutase (SOD), Cu,Zn-SOD in cytoplasm and Mn-SOD in mitochondria. Recently oxygen free radicals are suggested to induce the apoptosis, however mechanism of the reduced apoptosis by ischemic precondition was unknown, while many studies performed in mammalian heart indicated that ATP-sensitive K+(K atp) channel activation related with the protective effects. The aim of present study is toinvestigate 1)whether IP upregulate the Cu,Zn-SOD and Mn-SOD activities, and 2)whether ischemic preconditioning decreases apoptosis via K atp channel activation in timely reperfused skeletal muscle after long ishemia. The experimental animals, Sprague-Dawley rats weighing 250~300g, were divided into 8 group; 1)control group, 2)ischemic preconditioning only groups, 3)pinacidil, a K atp channel opener, treatment only groups, 4)glibenclamide, a K atp channel blocker, treatment only groups, 5)ischemia groups, 6)ischemia after IPC groups, 7)ischemia and pinacidil treatment groups, and 8)IP and ischemia after glibenclamide pretreatment groups. Animals of the control group were administered with the vehicle (DMSO) alone. Pinacidil (1mg/kg) was administred intravenously 5 minutes after initiation of ischemia, and glibenclamide(0.5mg/kg) was injected intravenously 20 minutes before IPC. In rats that were ischemic preconditioned, the left common iliac artery was occluded for 5 minutes followed by 5 minutes of reperfusion by three times usign vascular clamp. Ischemia was done by occlusion of the same artery for 4 hours. The specimens of left rectus femoris muscle were obtained immediately (0 hours), 12 hours, 24 horus after drug administrations, IP or ischemia and reperfusion. The immunoreactivities of SOD and its alterations were observed by use of sheep antihuman Cu,Zn-SOD and Mn-SOD antibodies onthe 10 micro meter cryosections. The incidencies of apoptosis were observed by TUNEL methods with in situ apoptosis detection kit on 6 micro meter paraffine section. The results obtained were as follows: 1. After IPC, immunoreactivities of Cu,Zn-SOD mainly in the small-sized fibers were increased by 24 hours, that of Mn-SOD at 0 hour and 24 hours. 2. No significant changes in immunoreactivities of SDO was observed in the pinacidil and in the glibenclamide treatment only groups, and in the ischemia only groups. 3. The immunoreactivities of the Cu,Zn-SOD were incresed in the ischemia after IPC groups and the ischemia and pinacidil treatment groups. 4. The immunoreactivities of the Cu,Zn-SOD in the IPC and ischemia after glibenclamide pretreantment groups were not increased except for the 12 hours reperfusion group. But, Mn-SOD immunoreactivities were incresed in to 0 hours, 12 hours and 24 hours after reperfusion. 5. In the control group, the IPC only groups, and the pinacidil treatment only groups, negative or trace apoptotic reactions were observed, but the positive apoptotic reaction occured in the glibenclamide treatment groups. 6. Moderate or many number of apoptosis were revealed in the ischemia groups, and also the IPC and ischemia after glibenclamide pretreatment group except for 12 hours and 24 hours after reperfusion. However, the incidence of apoptosis was decreased in the ischemia after IPC groups and in theischemia and pinacidil treatment groups. 7. There is a coincidence between the increase of Cu,Zn-SOD immunoreactivities and the decrease of apoptosis in thepresence of ischemia and reperfusion. These results suggest that the protective effects of ishemic preconditioing may related to the SOD activation, and the ischemic preconditioning decreases the apoptosis partially via K atp channel activation in timely reperfused rat skeletal muscle. It is also suggested that inhibition of apoptosis by IPC may related with the SOD activation.

Objective—To compare responses of equine digital arteries (EDAs) and veins (EDVs) to human-acalcitonin gene-related peptide (hαCGRP), evaluate effect of the endothelium, and characterize receptors and sources of endogenous CGRP. Sample—Palmar digital vessels (5 to 9/experiment) from healthy adult horses killed at an abattoir. Procedures—Vessel rings were mounted under tension in organ baths containing Krebs-Henseleit solution at 30°C, with relaxation responses examined in vessels preconstricted with a thromboxane-mimetic (3 × 10(−8)M). Responses of endothelium-intact (+e) and -denuded (−e) EDAs and EDVs to hαCGRP C10−10 to 3 × 10(−7)M) were compared. Following incubation with an hαCGRP receptor antagonist (hαCGRP8–37; 1μM), responses of EDA(−e) and EDV(−e) to hαCGRP (10(−7)M) were obtained. Responses of endothelium-intact and -denuded arteries and veins to hαCGRP (3 × 10(−7)M) or capsaicin (10(−5)M) were evaluated as well as responses of endothelium-intact and -denuded EDA and EDV to hαCGRP (10(−10) to 10(−6)M) after incubation with endothelin-1 (ET-1; 10(−12)M). Results—hαCGRP resulted in nonendothelium, concentration-dependent relaxation in EDAs and EDVs, with greater responses in EDAs. Treatment with hαCGRP8–37 had minimal effect on responses to hαCGRP in either vessel type. Capsaicin induced relaxation in both vessel types. There were no differences between responses to hαCGRP for vessels pretreated with ET-1 or vehicle. Conclusions and Clinical Relevance—Both hαCGRP and capsaicin induced digital vasodilation unaffected by a functional endothelium. This suggested that endogenous CGRP likely emanates from sensory-motor nerves and may contribute to digital vasodilation.

The purpose of this study was to evaluate the relationship between the results of laboratory examinations and ultrasonographic findings, especially portal vein hemodynamics in experimentally bile duct ligated dogs. Biliary obstruction was accomplished by surgically occluding the common bile duct in five dogs. All the dogs became visibly jaundiced within 24 hours after surgery. The total protein and albumin/globulin ratio showed a gradual decrease throughout the examination period, while blood urea nitrogen reached its peak in the 6th week and decreased to pre ligation values by the 10th week. Similar trends were noted in the alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and direct and total bilirubin. Total cholesterol and fasting serum bile acid levels rapidly increased after surgery to peak values between the 2nd and 4th week, and then gradually decreased, but still remained high throughout the experiment period. The portal flow volume and velocity significantly (p0.05) decreased while only a slight increase was noted in the congestion index after bile duct ligation. The cross sectional area of the portal vein changed insignificantly. Bile duct and gallbladder distention was evident within the 1st week after ligation but there was little change in the echogenicity of the liver parenchyma. The results of this study suggest that the determination of Doppler ultrasound parameters of hepatic hemodynamics, especially the portal vein flow indices, may contribute to a better noninvasive assessment of the canine patient with biliary obstructive disease