Myo-[3H]-inositol accumulation in cultured bovine lens epithelial cells (BLECs) occurred by both high- and low affinity, Nat-dependent transport sites. High ambient glucose significantly inhibited myo-[ 3 H]-inositol uptake; the co-administration of sorbinil, an aldose reductase inhibitor, prevented the inhibitory effect on the low affinity transport site. A glucose-sensitive process for myo-[3 H]-inositol uptake on the high-affinity transport site was uncovered by Lineweaver-Burk analysis. Dixon plot analysis confirmed that the effect of glucose was due to competitive inhibition of the high-affinity myo-inositol transport site while the effect of sorbitol was due to competitive inhibition of the low-affinity myo-inositol transport site.

Cardiovascular and hormonal responses to +700 head-up tilt (HUT: orthostatic challenge) were compared between six endurance exercise trained (ET) and six untrained (UT) subjects prior to and immediately following 4 hours of -60 head-down rest (HDR). The ET subjects showed a significant (P < 0.05) decrease in orthostatic tolerance time (pre syncopal symptoms) during post-HDR HUT, while no difference was observed between ET and UT groups in pre-HDR HUT. The volume regulatory hormonal responses were similar between ET and UT groups whether during HUT or HDR. The pre-syncopal subjects had a greater increase in plasma arginine vasopressin and less increase in plasma renin activity and plasma aldosterone during HUT than was observed in non syncopal subjects. These data suggest that HDR deconditioning was more effective in the ET subjects.

Sudden Infant Death (SIDS) has been associated with medium-chain acyl-CoA dehydrogenase (MCAD) deficiency, an inborn error of fatty acid oxidation. Blood and tissue samples from a large cohort of SIDS victims were analyzed for the presence of dodecanoic acid (C₁₂) by gas chromatography. A subgroup of these cases had a significantly higher blood concentration than age-matched controls, suggesting MCAD deficiency. An animal study using Sprague-Dawley rats was done to mimic the effects of MCAD deficiency. Significantly increased blood concentrations of dodecanoic acid were observed. Decreased values in heart and liver were puzzling findings. The data indicate that dodecanoic acid is a blood marker for MCAD deficiency.

The effect of hypoxemia on coronary autoregulation was investigated in nine anesthetized, open-chest dogs. The anterior descending coronary artery (LAD) was cannulated and perfused with normoxic arterial blood and with moderately hypoxic blood (0₂ content = 10 + 1 ml 0₂ /dl). LAD blood flow was measured as perfusion pressure was varied from 140 to 40 mmHg. At perfusion pressures at and above 40 mmHg, hypoxemia significantly increased LAD flow. During normoxia, the autoregulatory closed-loop gain (Gc) was significantly greater than zero at perfusion pressures from 60 to 120 mmHg. During hypoxemia, Gc was greater than zero only at perfusion pressures from 80 to 100 mmHg. During hypoxemia, LAD blood flow increased sufficiently to maintain oxygen delivery and consumption constant, but the range and potency of autoregulation was attenuated.

An efficient two step procedure has been developed using CI GC/MS for analyzing amphetamines and related compounds. The first step allows the analysis of underivatized amphetamines with the necessary sensitivity and specificity to give spectral identification, including differentiation between methamphetamine and phentermine. The second step involves preparing a chiral derivative of the extract to identify d and 1-isomeric composition.