Treatment of simple elbow dislocation using an immediate motion protocol.

The results of treatment after closed reduction of elbow dislocation vary. Twenty consecutive patients with closed posterior elbow dislocations were treated prospectively on a rapid motion, nonimmobilized functional regimen. This treatment protocol emphasizes immediate active range of motion under close supervision. No slings or splints were employed. Final range of motion averaged -4 degrees to 139 degrees. All patients attained final extension within 5 degrees of the contralateral side. Each patient achieved his final range of motion within an average of 19 days after reduction of the dislocation. Arm circumference returned to normal at an average of 6.5 days. There was one redislocation. After treatment, all patients met qualification for graduation from the U.S. Naval Academy and were able to pursue unrestricted athletic and career options. Our findings suggest that an aggressive immediate motion rehabilitation allows nearly full final elbow motion and an excellent functional outcome.

Progression of meniscal degenerative changes in college football players: evaluation with MR imaging.

Intrameniscal degenerative changes, presumably due to mild repetitive trauma, have been shown in many college and professional athletes, but it is uncertain over what period of time they can develop or significantly progress. To ascertain this period, the authors used magnetic resonance (MR) imaging to examine one knee in each of 20 players in the starting lineup of a major college football team before and after the season. Only asymptomatic knees (right, n = 10; left, n = 10) were examined; the images were reviewed blindly by one experienced observer without reference to the other examination. A significant progression existed in the grade of signal intensity shown in the menisci over the course of the season (P less than .001). Although this is a small study covering only 1 year, these preliminary results suggest that significant degeneration can occur in the menisci of asymptomatic players over a single season.

The effect of estrogen and tamoxifen on hepatocyte proliferation in vivo and in vitro.

We have previously shown that changes in estrogen-hepatocyte interaction occur during liver regeneration. Following 70% hepatectomy, estrogen levels in the blood were elevated, the number of estrogen receptors in the liver was increased and there was an active translocation of estrogen receptors from the cytosol to the nucleus. The injection of tamoxifen, an estrogen antagonist, inhibits hepatocyte proliferation following partial hepatectomy. The administration of 1 microgram tamoxifen per gm body weight at zero time or 6 hr after the operation resulted in a significant inhibition both of DNA synthesis and of the number of cells in mitosis. Injections of tamoxifen 12 hr or later after the operation had no effect. Concomitant injections of equimolar amounts of estrogen abolished the inhibition by tamoxifen. The effects of estrogen and tamoxifen were also tested on hepatocytes in primary culture. Estrogens in the presence of 5% normal rat serum stimulated hepatocyte DNA synthesis as determined by [3H]thymidine incorporation and the labeling index, whereas epidermal growth factor-induced DNA synthesis in the absence of normal rat serum was strongly inhibited. Tamoxifen, in contrast, inhibited DNA synthesis of hepatocytes in the presence of 5% normal rat serum and reversed the stimulatory effect of estrogen in the same system. Attempts to elucidate the mechanism of tamoxifen inhibition in vitro indicated that one effect of tamoxifen is to prevent the amiloride-sensitive Na+ influx necessary to initiate hepatocyte proliferation.

Excision of posterolateral talar dome lesions through a medial transmalleolar approach.

Posterolateral osteochondral fractures of the talus are rare. Although arthroscopy is becoming an increasingly important method of evaluating and treating lesions of the ankle, these techniques may not always be feasible, especially for posterolateral lesions. Classic treatment of displaced or symptomatic chronic lesions is excision, usually with a distal fibular osteotomy and turndown procedure. Subsequent removal of the syndesmosis screw is required. The surgical dissection of the distal fibula is extensive and devascularizing. An alternate technique for debriding posterolateral talar dome lesions through a medial transmalleolar approach is described. Exposure of the lateral talar dome is sufficient to allow debridement and curettage of the lesion. Anatomic rigid fixation of the medial malleolus allows for rapid healing of the osteotomy site and immediate ankle rehabilitation. For those ankle lesions that are not accessible to arthroscopy or an anterolateral arthrotomy, this approach is preferable to the distal fibular osteotomy and turndown.

Pharmacologic modulation of experimental postischemic hepatic function.

The present study evaluated and compared the effects of SRI 63-441, a potent platelet activating factor antagonist, superoxide dismutase (SOD), an oxygen free radical scavenger, and ibuprofen, a cyclooxygenase inhibitor on hepatic function after 90 minutes of warm ischemia. After warm ischemia, livers were harvested and underwent 90 minutes of warm, oxygenated, sanguinous perfusion on an isolated liver perfusion apparatus. Pretreatment of donor animals with 20 mg/kg intravenous (I.V.) SRI 63-441 5 minutes before induction of total hepatic ischemia resulted in significantly increased bile production, a significant decrease in transaminase release, and a higher tissue adenosine triphosphate (ATP) content when compared with ischemic nontreated controls. SOD resulted in improved bile production and decreased transaminase liberation only when present in the perfusate at the time of in vitro reperfusion. Ibuprofen did not improve postischemic hepatic function in this model. Electron microscopy revealed patchy hepatocellular vacuolization with an intact sinusoidal endothelium in all ischemic livers. However, the degree of damage was less severe in the livers from those rats pretreated with 20 mg/kg SRI 63-441. This study demonstrates that SRI 63-441 pretreatment significantly reduces hepatic warm ischemic injury, and in the present model, appears superior to two other agents that have been advanced in the treatment of ischemic injury. The use of such agents singly or in combinations have important implications as regards gaining a better understanding of the basic mechanisms in organ ischemia, and moreover, for therapeutic applications in organ ischemia and preservation.

Response of cultured hepatocytes to a hepatomitogen after initiation by conditioned medium or other factors.

Injection of a substantially purified hepatomitogen into recipient rats that had 40% of their liver removed resulted in a significant stimulation of hepatic DNA synthesis as determined by the labeling index and the mitotic index. Normal or sham-operated rats did not respond to the injection of the mitogen. The extraction and partial purification of this hepatomitogen have previously been reported (A. Francavilla et al., Cancer Res., 47:5600-5605, 1987). Addition of the factor to an epithelial-like liver-derived cell line in culture (clone 9) or to a hepatoma cell line (HTC-SR) resulted in a dose-dependent stimulation of DNA synthesis. Hepatocytes in primary culture, on the other hand, were not stimulated by the addition of the factor. However, when the mitogen was added to hepatocytes in primary culture, together with conditioned medium, obtained from the responsive cell lines, a significant stimulation of DNA synthesis could be demonstrated in hepatocytes in culture. The stimulation was dose dependent with respect to the mitogen, was abolished by 10 mM hydroxyurea, and was independent of epidermal growth factor. The conditioned medium could be replaced by a protein factor extracted from the two cell lines as previously reported (P. Ove et al., J. Cell. Physiol., 131: 165-174, 1987). It appears that a cofactor is provided by the conditioned medium or by the cell extract, enabling the hepatomitogen to act on hepatocytes in primary culture.

Improved hepatic function in the 24-hour preserved rat liver with UW-lactobionate solution and SRI 63-441.

The present study compares rat liver preservation for 9, 12, and 24 h in the standard Eurocollins solution with preservation for the same time periods in the new UW-lactobionate solution. Pharmacologic manipulation with a potent platelet-activating factor antagonist, SRI 63-441, was also evaluated. After cold storage in each of the test solutions, the livers underwent 90 min of warm, oxygenated, sanguinous perfusion. A significant increase in liver weight was noted in Eurocollins-stored versus UW-lactobionate-stored livers. After 90 min of perfusion, livers preserved in UW-lactobionate produced significantly more bile and liberated significantly less glucose and transaminases when compared with Eurocollins-stored livers. Significant augmentation of bile production was observed when donor animals were pretreated with SRI 63-441 and the livers were then stored in UW-lactobionate for 24 h. Eurocollins-stored livers demonstrated increased hepatocyte vacuolization and endothelial disruption when compared with UW-lactobionate-stored livers after 12 and 24 h of preservation. This study demonstrates the superiority of UW-lactobionate solution in liver preservation and suggests that SRI 63-441 may be beneficial in the further reduction of cold ischemic injury.