No abstract

The purpose of this study was to establish the feasibility of laparoscopy in embalmed cadavers to teach abdominal gross anatomy. One cadaver was selected based on body habitus and absence of previous abdominal operations. A standard trocar was used to enter the abdomen at the umbilicus. Two trocars were placed in the left upper quadrant. Pneumoperitoneum was achieved with continuous CO(2) pressure. Liver retraction was achieved percutaneously, exposing the porta hepatis and the gallbladder. The dissection was done with four first-year medical students using standard laparoscopic equipment. Following this, the demonstration was projected over multiple monitors so that all students could participate. Laparoscopic dissection in an embalmed cadaver is feasible and an excellent educational tool for both the medical student and the dissector. The dissector has the opportunity to manipulate laparoscopic tools in a human model closely paralleling operative experience, and the students have an opportunity to learn abdominal anatomy from a clinical perspective. Laparoscopic examination and dissection of fresh cadavers has been used for training surgeons on new procedures such as colon resection, antireflux procedures, and cholecystectomy. There is no report of this same technology used in embalmed cadavers to teach basic anatomy. This approach allows first-year medical students to learn the anatomy while exposing them to the technology currently used in surgical practice, and it affords surgical residents and students additional opportunities to practice laparoscopic skills.

After distal bypass grafting, men and women have similar rates of patency and limb salvage, but women have a higher incidence rate of perioperative myocardial infarction and a decreased 5-year survival rate. These data suggest that women have unrecognized cardiac disease that affects them adversely in the perioperative period and the long term when compared with men who undergo the same operation.

Isoflurane mimics the cardioprotective effect of acute ischemic preconditioning with an acute memory phase. We determined whether isoflurane can induce delayed cardioprotection, the involvement of ATP-sensitive potassium (KATP) channels, and cellular location of the channels. Neonatal New Zealand White rabbits at 7-10 days of age (n ϭ 5-16/group) were exposed to 1% isoflurane-100% oxygen for 2 h. Hearts exposed 2 h to 100% oxygen served as untreated controls. Twenty-four hours later resistance to myocardial ischemia was determined using an isolated perfused heart model. Isoflurane significantly reduced infarct size/area at risk (means Ϯ SD) by 50% (10 Ϯ 5%) versus untreated controls (20 Ϯ 6%). Isoflurane increased recovery of preischemic left ventricular developed pressure by 28% (69 Ϯ 4%) versus untreated controls (54 Ϯ 6%). The mitochondrial KATP channel blocker 5-hydroxydecanoate (5-HD) completely (55 Ϯ 3%) and the sarcolemmal KATP channel blocker HMR 1098 partially (62 Ϯ 3%) attenuated the cardioprotective effects of isoflurane. The combination of 5-HD and HMR-1098 completely abolished the cardioprotective effect of isoflurane (56 Ϯ 5%). We conclude that both mitochondrial and sarcolemmal KATP channels contribute to isoflurane-induced delayed cardioprotection. ischemia; heart; infarct size; volatile anesthetics; myocardial preconditioning BRIEF PERIODS OF ISCHEMIA lead to a reduced severity of cardiac injury following a second sustained period of ischemia. This cardioprotective effect has been termed ischemic preconditioning and has been demonstrated in all species studied. Certain pharmacological agents can mimic the cardioprotective effect of ischemic preconditioning. Recent clinical and experimental data indicate that volatile anesthetics also exert acute protective effects on the myocardium.The protective effects of volatile anesthetics on ischemic myocardium have been termed anesthetic-induced preconditioning because of its remarkable similarity to ischemic preconditioning. Isoflurane improves functional recovery of stunned myocardium in chronically or acutely instrumented dogs after brief periods of coronary artery occlusion and reperfusion (25,26,44). Low doses of the ATP-sensitive K (K ATP ) channel blocker glibenclamide completely abolished the cardioprotective effects of isoflurane (25). These results indicate that K ATP channels are activated by isoflurane and mediate the beneficial effects of isoflurane in stunned myocardium in animal models that respond to acute ischemic preconditioning in a similar fashion to the human heart (5, 45).K ATP channel openers mimic early ischemic preconditioning, whereas K ATP channel blockers prevent ischemic preconditioning. These effects were initially attributed to opening and closing of sarcolemmal K ATP channels, respectively. New evidence suggests, however, that mitochondrial K ATP channels might very well have even a greater influence on preconditioning (35, 37). For instance, diazoxide, an opener of mitochondrial K ATP channels, was demonstrated to exert ca...

Many infants who undergo cardiac surgery have a congenital cyanotic defect where the heart is chronically perfused with hypoxemic blood. Infant hearts adapt to chronic hypoxemia by activation of intracellular protein kinase signal transduction pathways. However, the involvement of heat shock protein 70 in adaptation to chronic hypoxemia and its role in protein kinase signaling pathways is unknown. We determined expression of message and subcellular protein distribution for inducible (Hsp70i) and constitutive heat shock protein 70 (Hsc70) in chronically hypoxic and normoxic infant human and rabbit hearts and their relationship to protein kinases. In chronically hypoxic human and rabbit hearts message levels for Hsp70i were elevated 4-to 5-fold compared with normoxic hearts, Hsp70i protein was redistributed from the particulate to the cytosolic fraction. In normoxic infants Hsp70i protein was distributed almost equally between the cytosolic and particulate fractions. Hsc70 message and subcellular distribution of Hsc70 protein were unaffected by chronic hypoxia. We then determined if protein kinases influence Hsp70i protein subcellular distribution. In rabbit hearts SB203580 and chelerythrine reduced Hsp70i message levels, whereas SB203580, chelerythrine, and curcumin reversed the subcellular redistribution of Hsp70i protein caused by chronic hypoxia, with no effect in normoxic hearts, indicating regulation of Hsp70i message and subcellular distribution of Hsp70i protein in chronically hypoxic rabbit hearts is influenced by protein kinase C and mitogen-activated protein kinases, specifically p38 MAPK and JNK. We conclude the Hsp70 signal transduction pathway plays an important role in adaptation of infant human and rabbit hearts to chronic hypoxemia.