The aim of this work was to investigate physiological responses to torque reaction forces produced by hand-held power tools used to tighten threaded fasteners. Such tools are used repetitively by workers in many industries and are often associated with upper limb musculoskeletal complaints. The tools considered for stimulation in this study had straight handles and required from 100 to 400 ms to tighten fasteners to a peak torque of 1.0 to 2.5 Nm and from 50 to 150 ms for the torque to decay to zero. A tool stimulator was constructed to apply a programmed torque profile to a handle similar to that of a straight in-line power screwdriver. Wrist flexor and extensor surface EMGs and handle position were recorded as subjects held handles subjected to controlled torque loads that tended to flex the wrist. It was found that: (1) very high EMG values occurred even though torques were of short duration (50 to 600 ms) and the peak torques were low (7-28% of maximum strength); (2) high EMGs in anticipation of torque are directly related to torque build-up rate and peak torque; (3) high peak flexor and extensor EMGs during and following torque onset are related to torque build-up rate and peak torque; (4) minimum time of peak EMGs of 72-87 ms following the onset of torques with 50 ms build-up suggests the contribution of an extensor muscle stretch reflex component; delayed peak for longer build-ups suggests a central control of muscle force in response to torque; (5) angular excursions of handles increase with decreasing torque build-up time and increasing torque magnitude causes increasing eccentric work; (6) the results show that the slow torque build-up times (450 ms) correspond to minimum peak EMGs; and (7) accumulated EMGs increase with increasing torque and torque build-up times. Further studies are needed to evaluate fatigue and musculoskeletal injuries associated with prolonged periods of tool use.

A laboratory study was conducted to determine the effects of back disability status on endurance time and perceived discomfort during trunk flexion. Eighty participants (40 with chronic or recurrent low back pain (CRLBP), 40 pain-free) were tested. The trunk was flexed to 15 degrees, 30 degrees, 45 degrees and 60 degrees under three conditions: 1) continuous static flexion; 2) cyclical flexion with 20% rest; and 3) cyclical flexion with 40% rest. Each condition was performed for up to 600 s or until the participant reached his/her pain tolerance limit. Dependent variables included time to distracting discomfort (TDD), total endurance time (TET) and perceived discomfort. For continuous exertions, CRLBP participants had lower TDD (p < 0.001), lower TET (p < 0.001) and greater discomfort (p < 0.001) compared to pain-free controls. In both groups, TDD and TET decreased and perceived discomfort increased as the flexion angle increased. For intermittent exertions, CRLBP participants reported greater discomfort than pain-free participants (p < 0.001). Increasing rest from 20 to 40% reduced discomfort in CRLBP participants, but produced no consistent benefit in pain-free participants. To accommodate persons with CRLBP, consideration should be given to reducing both the magnitude (angle) and duration of trunk flexion required by their jobs.

In order to examine the relationship between local adenosine concentrations before, during, and after ischemia and the extent of ischemic myocardial damage, measurements of interstitial fluid (ISF) nucleosides were made using microdialysis probes implanted in the ischemic region of isoflurane anesthetized Micropigs undergoing 60' coronary artery occlusion (CAO) and 3 h of reperfusion (REP). Nucleoside concentrations in the dialysate collected from the microdialysis probes were used as an index of ISF levels. Dialysate nucleoside concentrations (ADO, inosine and hypoxanthine), myocardial infarct size, and myocardial blood flow (MBF) were determined in control animals (n = 6), animals preconditioned with a single 10' cycle of CAO and REP (PC, n = 6), and those treated with the adenosine deaminase inhibitor pentostatin (n = 6, 0.2 mg/Kg i.v. 30' prior to CAO). The brief PC occlusion resulted in a transient but significant increase in dialysate ADO (6.7 +/- 1.8 microM vs. 0.67 +/- 0.1 microM at baseline). Pentostatin administration had no significant effect on either dialysate nucleosides or MBF at baseline. During the 60' CAO, dialysate ADO increased in control animals. In PC animals, however, dialysate ADO during CAO was lower than control. Pretreatment with pentostatin resulted in a six-fold augmentation in dialysate ADO during the 60 min CAO when compared to the control values (110.62 +/- 30.2 microM vs. 16.31 +/- 2.1 microM at 60 min of ischemia). Pentostatin also resulted in a significant reduction in the accumulation of inosine and hypoxanthine, indicating inhibition of adenosine deaminase activity. There were no significant differences in MBF between groups at any time point. Following 3 h REP, infarct size was 35.4 +/- 5.5%, 8.1 +/- 1.5% and 8.3 +/- 1.8% of the region at risk in control, PC, and pentostatin groups, respectively. These data suggest that marked increase in ISF ADO during CAO, may be as effective in reducing INF as a modest increase in ISF ADO prior to prolonged CAO.

Pentostatin (2-deoxycoformycin) is a potent inhibitor of adenosine deaminase and has been demonstrated to augment endogenous adenosine levels during regional and global myocardial ischemia. Based on the rationale that increasing endogenous adenosine during ischemia may be cardioprotective, the objective of this study was to determine if adenosine deaminase inhibition with pentostatin could improve postischemic contractile dysfunction (stunning) in open-chest anesthetized dogs. All animals underwent 15 min of coronary occlusion followed by 3 h of reperfusion preceded by an intravenous bolus of either 0.2 mg/kg of pentostatin (n = 8) or saline (n = 7). Sonomicrometers were placed in the ischemic area and were used to measure systolic wall thickening before, during, and after occlusion of the left anterior descending artery. Myocardial blood flow was measured with tracer labeled microspheres at baseline, 10 min of occlusion and at 1 h of reperfusion. Both groups were equally dyskinetic during occlusion (-21 +/- 5% of baseline thickening in the controls and -28 +/- 8% in the pentostatin group). The pentostatin group, however, demonstrated better contractile function at all time points during reperfusion, which was significantly different from the control group at 3 h of reperfusion. The improvement in regional function in the pentostatin group was not due to significant disparities in hemodynamic variables, size of the region at risk, or in collateral blood flow. These results indicate that pentostatin can ameliorate the severity of myocardial stunning, an effect we propose is due to increasing endogenous levels of adenosine during the ischemic interval. Although significant improvement was detected with pentostatin, the improvement was modest compared to controls, suggesting that the utility of inhibiting adenosine deaminase to modify regional mechanical stunning is limited.

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