Meniscal injuries: A critical review.

Although once perceived as an unimportant vestigial structure, the menisci of the knee are now known to be a common source of knee pain and disability. The medial meniscus is more vulnerable to injury to due to its intimate attachment to the medial collateral ligament. The moveable lateral meniscus is less prone to tear except when the ACL is injured. The medial and lateral menisci are usually injured as a result of sudden knee flexion with a component of knee internal or external rotation. However, older patients may present without a specific mechanism of injury as their meniscal injuries are often due to degenerative processes. Most meniscal injuries can be diagnosed with a thorough physical examination utilizing the McMurray, Apley, and ``bounce home'' maneuvers. Joint line tenderness and the presence of a knee effusion aid in the diagnosis. Magnetic Resonance Imaging (MRI) has become the test of choice in confirming injury. MRI also defines the type, location, and severity of meniscal injury. Some meniscal injuries, particularly peripheral, well-vascularized tears, may be more prone to healing with nonsurgical management. Typical initial management includes reduction of swelling and pain. Rehabilitation stresses tri-planar functional retraining. The final phases of rehabilitation incorporate a functional progression to sports or work specific activities. Arthroscopic knee surgery has become a prevalent treatment method for bucket handle tears and non-vascularized meniscal injuries. Meniscal repair is currently preferred over partial menisectomy to avoid premature osteoarthritis. In sum, clinicians can return patients with meniscal pain to a high level of function with appropriate recognition of injury and functional rehabilitation.

Beneficial effects of a specific leukotriene receptor antagonist in splanchnic artery occlusion shock.

The purpose of this study was to examine the effects of a new potent peptidoleukotriene receptor antagonist, SK&F 104353, in splanchnic artery occlusion shock. SK&F 104353 was administered as a 1 mg/kg initial bolus followed by an infusion of 3 mg/kg per h for the entire 2 h post-reperfusion observation period. In a group of conscious rats, this dose of SK&F 104353 shifted the LTD4 dose response curve rightward 10-fold, indicating effective antagonism of peptidoleukotriene responses in the rat. Anesthetized rats subjected to splanchnic artery occlusion shock survived an average of only 98 +/- 8 min whereas all animals receiving SK&F 104353 survived the 2 h reperfusion period (P less than 0.02 from vehicle). Therefore, the survival rate of the splanchnic artery occlusion shock group of rats receiving SK&F 104353 was improved to 100% compared with 50% survival for the vehicle-treated splanchnic artery occlusion shock group (P less than 0.025). In the splanchnic artery occlusion shock + SK&F 104353 group the increase in the plasma activities of the lysosomal hydrolase, cathepsin D, and the cardiotoxic peptide, myocardial depressant factor, were significantly attenuated in comparison to the splanchnic artery occlusion shock + vehicle group (P less than 0.025). These data indicate that the peptidoleukotriene receptor antagonist, SK&F 104353 is beneficial in splanchnic artery occlusion shock, and furthermore suggests that it may be a therapeutically useful agent in bowel ischemic shock.

Cardiovascular effects of acute hypercholesterolemia in rabbits. Reversal with lovastatin treatment.

Hypercholesterolemia was induced in New Zealand white rabbits by feeding them a 0.5% cholesterol-enriched rabbit chow for 2 wk. Half of the cholesterol-fed rabbits were given lovastatin, a potent inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate limiting enzyme in cholesterol biosynthesis, and the other half were given its vehicle (i.e., DMSO). At the end of 2 wk, the rabbits underwent experimental myocardial ischemia or a sham ischemia procedure. Ischemic animals fed the cholesterol-enriched diet for 2 wk experienced much greater cardiac damage than ischemic rabbits fed the control diet, despite the absence of any atherosclerosis. Lovastatin was shown to protect the ischemic rabbit myocardium by three different indices of ischemic damage: (a) maintenance of creatine kinase (CK) activity in the ischemic myocardium; (b) reduced loss of free amino-nitrogen containing compounds from the ischemic myocardium; and (c) blunting the rise of plasma CK activity. These effects were not due to differences in myocardial oxygen demand between the groups. Arteries isolated from animals fed the cholesterol-enriched diet developed defects in endothelium-dependent relaxation in both large vessels as well as coronary resistance vessels. Acute hypercholesterolemia increases the severity of myocardial ischemia while at the same time impairing endothelium-dependent relaxation. These deleterious changes can be significantly attenuated by treatment with lovastatin.

Detection of platelet-activating factor during traumatic shock.

The purpose of this study was to determine if platelet-activating factor (PAF) is formed in the peritoneal fluid of rats following traumatic shock. Anesthetized rats subjected to Noble-Collip drum trauma developed a lethal shock state characterized by a mean survival time of 80 +/- 16 min and a final mean arterial blood pressure of 54 +/- 7 mm Hg compared with 117 +/- 14 mm Hg in sham-shock control rats. Peritoneal fluid from traumatized and PAF-infused rats analyzed by high performance liquid chromatography (HPLC) contained a phospholipid which had a similar retention time as authentic PAF, but was absent in sham shock rats. Furthermore, aliquots of this chromatographic peak aggregated washed rabbit platelets, and the aggregation was blocked by a specific PAF receptor antagonist, CV-6209. Moreover, extraction of peritoneal fluid from traumatized rats aggregated washed rabbit platelets and this activity increased nearly four-fold in traumatized rats compared to sham shock rats. These findings are consistent with the formation of PAF in traumatic shock, and along with previous data of PAF antagonists ameliorating traumatic shock, support a role of platelet-activating factor in the pathogenesis of traumatic shock.