Resuscitation after hemorrhagic shock: the effect on the liver--a review of experimental data.

The liver is currently considered to be one of the first organs to be subjected to the hypoxic insult inflicted by hemorrhagic shock. The oxidative injury caused by resuscitation also targets the liver and can lead to malfunction and the eventual failure of this organ. Each of the various fluids, vasoactive drugs, and pharmacologic substances used for resuscitation has its own distinct effect(s) on the liver, and the anesthetic agents used during surgical resuscitation also have an impact on hepatocytes. The aim of our study was to identify the specific effect of these substances on the liver. To this end, we conducted a literature search of MEDLINE for all types of articles published in English, with a focus on articles published in the last 12 years. Our search terms were "hemorrhagic shock," "liver," "resuscitation," "vasopressors," and "anesthesia." Experimental studies form the majority of articles found in bibliographic databases. The effect of a specific resuscitation agent on the liver is assessed mainly by measuring apoptotic pathway regulators and inflammation-induced indicators. Apart from a wide range of pharmacological substances, modifications of Ringer's Lactate, colloids, and pyruvate provide protection to the liver after hemorrhage and resuscitation. In this setting, it is of paramount importance that the treating physician recognize those agents that may attenuate liver injury and avoid using those which inflict additional damage.

Effect of long-term calcitonin administration on steroid-induced osteoporosis after cardiac transplantation.

BACKGROUND: Early, rapid bone loss and fractures after cardiac transplantation are well-documented complications of steroid administration; therefore, we undertook this study on the effects of long-term calcitonin on steroid-induced osteoporosis. METHODS: Twenty-three heart transplant recipients on maintenance immunosuppression with cyclosporine, mycophenolate mofetil and prednisone were retrospectively studied. All patients received long-term prophylactic treatment with elemental calcium and vitamin D. Twelve (52.2%) patients also received long-term intranasal salmon calcitonin, whereas 11 (47.8%) received none. Bone mineral density and vertebral fractures were assessed at yearly intervals. Statistical comparisons between each group's bone loss during the first year and in the early (1 to 3 years), intermediate (4 to 6 years) and late (7+ years) post-transplantation periods were done. RESULTS: Lumbar spine bone loss was significant during the early follow-up period in the group not receiving calcitonin (0.744 +/- 0.114 g/cm(2) vs 0.978 +/- 0.094 g/cm(2) [p = 0.002]). The calcitonin group showed bone mineral density (BMD) levels within normal average values throughout the study period. BMD increased in the no-calcitonin group during the intermediate (4 to 6 years) and late (7+ years) follow-up periods, with values approaching normal average and no significant difference between the 2 groups (0.988 +/- 0.184 g/cm(2) vs 0.982 +/- 0.088 g/cm(2) [p = 0.944] and 0.89 +/- 0.09 g/cm(2) vs 1.048 +/- 0.239 g/cm(2) [p = 0.474], respectively). CONCLUSIONS: Prophylactic treatment with intranasal salmon calcitonin prevents rapid bone loss associated with high-dose steroids early after cardiac transplantation. Long-term administration does not seem warranted in re-establishing BMD.