Aims: The present experimental study raised the question whether corticosteroid therapy inßuences the sensitivity of the femoral head circulation to ischemia induced by hip joint tamponade. Methods: 31 Landrace pigs were treated in 4 groups. 12 animals received a 14 day methylprednisolone intramuscular application before hip joint tamponade. 11 pigs underwent hip joint tamponade without previous medication. Control groups comprised 4 animals not undergoing hip joint tamponade. Blood ßow measurement was undertaken in predeþned regions by radioactive microsphere technique. Results: Epiphyseal blood ßow decreased signiþcantly during hip joint tamponade. Reperfusion occurred to a level not signiþcantly differing from that before ischemia, whereas epiphyses remained ischemic in 2 pigs. In the steroid treated animals, the basic blood ßow appeared 2–3 times lower than that of the non medicated pigs. Also in the steroid group 2 epiphyseal remained ischemic. The metaphyseal corticalis in the steroid treated animals revealed signiþcant hyperperfusion. Conclusions: Ischemia by hip joint tamponade in a porcine model was produced quantitatively for the þrst time. The majority of femoral head epiphyses was reperfused on steady state blood ßow level. Nonreperfusion of 2 epiphyses in each group indicated that 6 hours of ischemia might be just below the minimum stress in order to produce necrosis of the femoral head. High dose steroid medication reduced the steady state blood ßow level of the femoral head 2–3 times but did not inhibit or disturb reperfusion.

Aims: The present experiment addressed the question whether lipopolysaccharides (LPS), hip joint tamponade or their combination modulate hip perfusion. Methods: 16 immature Danish Landrace pigs of both genders were treated in 3 groups. 4 animals received LPS from escherichia coli intravenously 4 hours previous to hip joint tamponade. 8 pigs underwent the hip operation without previous medication. 4 animals without treatment served as control group. Blood ßow measurement was done by the Radioactive Tracer Microspheres technique. Results: Femoral head epiphyseal blood ßow decreased signiþcantly during hip joint tamponade. Reperfusion occurred to a level not signiþcantly differing from that before ischemia, whereas epiphyses remained ischemic in 2 pigs. The hip joint capsule showed signiþcant hyperperfusion during and after joint tamponade. No signiþcant difference was revealed comparing the LPS-treated and non-treated groups of pigs in all hip regions (p = 0.79, U-test). In addition, in the LPS-group, none of the femoral head epiphyses remained ischemic. Conclusions: LPS and hip joint tamponade, which have separately been discussed as pathomechanic factors of Non Traumatic Femoral Head Necrosis, have been combined in a bifactorial porcine model. Systemic lipopolysacchrides as bacterial endotoxin have no acute effect on regional hip perfusion which would make a consequent osteonecrosis probable. 6hourly hip joint tamponade alone evoked non reperfusion in 2 out of 8 pigs and a prolongation of the 6 hours ischemia might evoke more cases of non reperfusion.

Aims: The pathomechanism of avascular necrosis of the femoral head (AVN) is still debated. Hip joint synovitis and effusion may impair blood ßow to the femoral head. The critical ischemia time is around 6 hours, but repeated ischemic episodes may impair reperfusion and elicit AVN. The aims of this study were to investigate the value of dynamic MRI in femoral head after ischemia and during reperfusion. Methods: In 15 domestic pigs, 3–4 months old, femoral head ischemia was achieved by raising the joint pressure to 250 mmHg by dextran infusion through a hole in the acetabular wall. MRI was performed (Philips gyroscan S15, 1.5 T, Gd-DTPA enhancement, dynamic imaging interval 39 sec.) before ischemia, after 6 hours of ischemia, and again after 4 hours of reperfusion. Results: Signal intensity versus time (SI/t) plots were constructed from 347 MR studies. By regression analysis of SI/t curves an index (enhancement/decrease) was developed as criterion for arterial or venous circulatory disturbance. Index values < 1.1 signiþed arterial impairment, > 100 venous disturbance. Values between 1.1 and 100 were considered normal. The positive predictive value for disturbed osseous blood ßow was 96%. Conclusions: Early detection of intraosseous circulatory disturbance was possible with a mathematical model for dynamic MRI results. The method is reproducible and may be employed in the early diagnosis of AVN and during treatment for monitoration of revascularisation.

Aims: Increased intraarticular hip joint pressure has been considered a pathomechanism in femoral head necrosis. The aim of this study was to investigate histopathological femoral head changes in an immature big animal model of arterial hip joint tamponade. Methods: Out of a total of 15 domestic pigs, 11 animals were randomly chosen to undergo 6h unilateral hip joint tamponade at an intraarticular pressure of 250mmHg while 4 animals underwent a unilateral sham operation serving as controls. 4h after the end of hip joint tamponade, the animals were killed with potassium chloride, the femoral heads were excised, and þxed in Schafferñs solution for undecalciþed Goldnerñs, alcianblue-PAS, Krutsay, methyl green pyronine, toluidin blue O, and standard Giemsa staining. Results: A great number of congested sinus and vessels of the terminal vascular system showed inclusions of blood cells dominantly in the tamponaded hip side. Congestion also be documented by dilated sinus with deformed blood cells. Bone remodeling of normal osteoblast and osteoclastic lacuna activity was noted in all trabeculae. None of the known signs of osteonecrosis were found. Conclusions: Our acute histological study in immature pigs shows the early microcirculatory disturbances which may precede femoral head necrosis. Future research is needed to investigate histologic changes after a longer time interval following hip joint tamponade, and into the duration of the joint tamponade.