Hindlimb hypokinesia was induced in rats by the Morey method to characterize the response of the soleus muscle. Rats suspended for 1-4 wk exhibited continuous and significant declines in soleus mass, function, and contractile duration. Soleus speeding was in part explained by an alteration in fiber type. The normal incidence of 70-90% type I fibers in the soleus muscle was reduced after 4 wk of suspension to 50% or less in 9 of 11 rats. A significant decline in type I myosin isozyme content occurred without a change in that of type II. Other observed histochemical changes were characteristic of denervation. Consistent with soleus atrophy, there was a significant increase in lysosomal (acid) protease activity. One week of recovery after a 2-wk suspension was characterized by a return to values not significantly different from control for muscle wet weights, peak contraction force, one-half relaxation time, and type I myosin. Persistent differences from control were observed in maximal rate of tension development, contraction time, and denervation-like changes.

A B S T R A C T Bolus injections of gastrin or pentagastrin (PG) cause a marked elevation in lower esophageal sphincter pressure (LESP), and it has been suggested that serum gastrin concentration is the main physiological and pathophysiological regulator of LESP. We evaluated this hypothesis by measuring LESP and gastric acid secretion simultaneously in normal subjects during continuous infusion of PG (0.004-12 /Lg/ kg per h), since continuous infusion of a hormone probably simulates physiological hormone release better than bolus injection. In groups of 8-13 subjects there was no statistically significant increase in average LESP with any of seven PG infusion rates. However, a bolus of PG superimposed on the continuous infusion of PG resulted in a 20-mm Hg increase in LESP. Examination of results in individual subjects suggested that PG by infusion might be stimulating LESP in some subjects and inhibiting it in others. Therefore, individual dose-response studies were performed in two normal subjects. These revealed that 0.9 /Ag/kg per h PG by infusion elevated LESP by 10-12 mm Hg. This dose of PG also elicited maximal rates of gastric acid secretion. In one of the subjects an infusion of PG calculated to give one-half maximal acid secretion (Dw) elevated LESP by 8 mm Hg; in the other the PG-D6o for acid secretion had no effect on sphincter pressure. Infusion of smaller amounts of PG had no effect on LESP, even though gastric acid secretion was stimulated submaximally.Preliminary results of this study were reported in abstract form in Gastroenterology. 1973. 64

Cholografin and Renografin 76 were studied to determine their effects on platelet function. In vitro platelet aggregation was significantly inhibited by at least 3.4 micron/ml Cholografin and 19.5 micron/ml Renografin 76. Patients who received Cholografin for intravenous cholangiography, and Renografin 76 for non-cardiac angiography, had low levels of plasma contrast agent, and hemostasis was clinically unimpaired. Patients who received Renografin 76 for cardiac angiography had inhibition of platelet aggregation at high levels of plasma contrast agent; there was no correlation with prolonged bleeding times, or with bleeding complications. High levels of plasma contrast agent may inhibit platelet aggregation in vitro and in vivo, although this may not be associated with clinically significant bleeding.

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