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From knee extension moments measured with a dynamometer, the quadriceps muscle force, the patellar ligament force and the reaction force in the patellofemoral joint at various knee angles (0–90°) were estimated. The information needed to calculate the combined effect of both patellofemoral and tibiofemoral joint on the mechanical advantage of the muscle was obtained from lateral-view radiographs of autopsy knees.The results show that the smallest quadriceps force (2,000 N) is exerted at maximal extension, and the largest force (8,000 N) at about 75° of flexion. The patellar ligament force reaches a maximum (5,000 N) at 60°. The reaction force in the patellofemoral joint is the smallest (1,000 N) at extension and is of the same values as the muscle force in a range from 75 to 90°. Especially at large flexion angles, the value of the estimated forces is considerably larger (by 100%) than reported in the literature. This difference is attributed to the influence of the patellofemoral joint on the mechanical advantage of the muscle, which has not been taken into account in other studies.

To determine whether duodenogastric reflux into the thoracic stomach could be caused by the transmission of negative intrapleural pressure fluctuations into the gastric lumen, a physical model is described and an equation calculated Pm + Pa - Pmb - (Sv.Pmb.Vmb/Pm) = Ppl - Sv.Vmb where Pm is intragastric pressure, Pa is atmospheric pressure, Pmb is end-expiratory gastric base pressure, Vmb is corresponding gastric volume, Sv is stiffness of gastric wall, and Ppl is intrapleural pressure. The validity of the model is demonstrated in six anesthetized mongrel dogs (18-31 kg) in which a thoracic stomach was constructed. The transmission of the intrapleural pressure fluctuations across the gastric wall proved to be greatly influenced by the gastric stiffness. The latter parameter varied from 0.05 to 1.97 cmH2O/ml, corresponding with a pressure transmission of 100 and 60%, respectively. Because high degrees of gastric stiffness are only present for large gastric volumes or when gastric peristalsis is present, it is concluded that, in general, the intrapleural pressure fluctuations are transmitted into the thoracic stomach. For this reason, respiratory efforts may play an important role in inducing duodenogastric reflux into the thoracic stomach.

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