Mechanical Properties of the Tendinous Equine Interosseus Muscle are Affected by in Vivo Transducer Implantation

Liquid metal strain gauges (LMSGs) were implanted in the tendinous interosseous muscle, also called suspensory ligament (SL), in the forelimbs of 6 ponies in order to quantify in vivo strains and forces. Kinematics and ground reaction forces were recorded simultaneously with LMSG signals at the walk and the trot prior to implantation, and 3 and 4 days thereafter. The ponies were euthanised and tensile and failure tests were performed on the instrumented tendons and on the tendons of the contra lateral limb, which were instrumented post mortem. The origo–insertional (OI) strain of the SL was computed from pre- and post-operative kinematics, using a 2D geometrical model. The LMSG-recorded peak strain of the SL was 5.4±0.9% at the walk and 9.1±1.3% at the trot. Failure occurred at 15.4±2.1% (mean±S.D.). The LMSG strain was higher than the simultaneously recorded OI strain 0.5±0.7% strain at the walk and 2.2±1.1% strain at the trot. Post-operative OI strains were only slightly higher than pre-operative values. Failure strains of in vivo instrumented SLs were 2.0±1.2% strain higher, and failure forces were slightly lower, than those of the contra lateral SLs that were instrumented post mortem. SL strains appeared to be considerably higher than those found in earlier acute experiments. Differences between in vivo LMSG and OI strains, supported by lower failure strains comparing in vivo and post mortem instrumented SLs, revealed that local changes in tendon mechanical properties occurred within 3 to 4 days after transducer implantation. Therefore, measurements of normal physiological tendon strains should be performed as soon as possible after transducer implantation

Mechanical Properties of the Tendinous Equine Interosseus Muscle are Affected by in Vivo Transducer Implantation

Liquid metal strain gauges (LMSGs) were implanted in the tendinous interosseous muscle, also called suspensory ligament (SL), in the forelimbs of 6 ponies in order to quantify in vivo strains and forces. Kinematics and ground reaction forces were recorded simultaneously with LMSG signals at the walk and the trot prior to implantation, and 3 and 4 days thereafter. The ponies were euthanised and tensile and failure tests were performed on the instrumented tendons and on the tendons of the contra lateral limb, which were instrumented post mortem. The origo–insertional (OI) strain of the SL was computed from pre- and post-operative kinematics, using a 2D geometrical model. The LMSG-recorded peak strain of the SL was 5.4±0.9% at the walk and 9.1±1.3% at the trot. Failure occurred at 15.4±2.1% (mean±S.D.). The LMSG strain was higher than the simultaneously recorded OI strain 0.5±0.7% strain at the walk and 2.2±1.1% strain at the trot. Post-operative OI strains were only slightly higher than pre-operative values. Failure strains of in vivo instrumented SLs were 2.0±1.2% strain higher, and failure forces were slightly lower, than those of the contra lateral SLs that were instrumented post mortem. SL strains appeared to be considerably higher than those found in earlier acute experiments. Differences between in vivo LMSG and OI strains, supported by lower failure strains comparing in vivo and post mortem instrumented SLs, revealed that local changes in tendon mechanical properties occurred within 3 to 4 days after transducer implantation. Therefore, measurements of normal physiological tendon strains should be performed as soon as possible after transducer implantation

Influence of different head-neck positions on vertical ground reaction forces, linear and time parameters in the unridden horse walking and trotting on a treadmill

Reasons for performing study: It is believed that the head-neck position (HNP) has specific effects on the loading pattern of the equine locomotor system, but very few quantitative data are available. Objective: To quantify the effects of 6 different HNPs on forelimb-hindlimb loading and underlying temporal changes. Methods: Vertical ground reaction forces of each limb and interlimb coordination were measured in 7 high level dressage horses walking and trotting on an instrumented treadmill in 6 predetermined HNPs: HNP1 - unrestrained; HNP2 - elevated neck, bridge of the nose in front of the vertical; HNP3 - elevated neck, bridge of the nose behind the vertical; HNP4 - low and flexed neck; HNP5 - head and neck in extreme high position; and HNP6 - forward downward extension of head and neck. HNP1 served as a velocity-matched control. Results: At the walk, the percentage of vertical stride impulse carried by the forehand (Izfore ) as well as stride length and overreach distance were decreased in HNP2, HNP3, HNP4 and HNP5 when compared to HNP1. At the trot, Izfore was decreased in HNP2, HNP3, HNP4 and HNP5. Peak forces in the forelimbs increased in HNP5 and decreased in HNP6. Stance duration in the forelimbs was decreased in HNP2 and HNP5. Suspension duration was increased in HNP2, HNP3 and HNP5. Overreach distance was shorter in HNP4 and longer in HNP6. Conclusions: In comparison to HNP1 and HNP6, HNPs with elevation of the neck with either flexion or extension at the poll as well as a low and flexed head and neck lead to a weight shift from the forehand to the hindquarters. HNP5 had the biggest effect on limb timing and load distribution. At the trot, shortening of forelimb stance duration in HNP5 increased peak vertical forces although Izfore decreased. Potential relevance: Presented results contribute to the understanding of the value of certain HNPs in horse training

Cardioprotection by Ischemic and Nonischemic Myocardial Stress and Ischemia in Remote Organs Implications for the Concept of Ischemic Preconditioning

Ischemic preconditioning studies employ one or more brief total coronary artery occlusions separated by complete reperfusion to limit infarct size during a subsequent prolonged coronary artery occlusion. We now present evidence that in anesthetized pigs a partial coronary artery occlusion without intervening reperfusion between the partial and prolonged total occlusions can also precondition the myocardium provided that the reduction in coronary blood flow is sufficiently severe. Thus infarct size was reduced after a 60 min total coronary artery occlusion when the total occlusion was preceded by a partial coronary occlusion that reduced coronary blood flow by 70% but not when the flow reduction was only 30%. In this two-stage coronary occlusion model the degree of protection appears greater in the epicardial than in the endocardial half. In view of evidence that brief occlusions of a coronary artery also protect myocardium outside its perfusion territory, we subsequently investigated whether ischemia in remote organs can protect myocardium. Because of reports that development of infarct size may be temperature dependent, we also investigated whether the cardioprotection by remote organ ischemia was temperature dependent. In anesthetized rats a 15 min coronary artery occlusion was more effective in reducing infarct size produced by a subsequent 60 min total coronary artery occlusion when the experiments were performed at a body core temperature of 30-31 degrees C than at 36-37 degrees C, while infarct size of animals which were subjected to only the 60 min total coronary artery occlusion was the same for the two body core temperatures. In rats with a body core temperature of 36-37 degrees C a 15 min mesenteric artery occlusion, but not a 15 min renal artery occlusion, reduced infarct size produced by a subsequent 60 min coronary artery occlusion. When the experiments were performed at 30-31 degrees C both the mesenteric and renal artery occlusions were protective. These observations indicate the local myocardial ischemia is not required to protect the myocardium during a prolonged coronary occlusion. We further investigated whether myocardium could also be protected by a cardiac stimulus which does not produce ischemia at all. For this purpose we electrically paced the left ventricle of anesthetized pigs to produce heart rates of 200 bpm (which did not lead to ischemia as assessed by a number of functional and biochemical variables) and found that 30 min of ventricular pacing reduced myocardial infarct size produced by a subsequent 60 min coronary artery occlusion. The protection by ventricular pacing involved activation of K+ATP channels as pretreatment with glibenclamide abolished the protection by ventricular pacing. We conclude that a number of distinctly different stimuli can protect the myocardium suggesting that ischemic myocardial preconditioning could be just one feature of a more general protection phenomenon