ABSTRACT— In patients with chronic liver disease, the reliability of various criteria generally used to diagnose impaired glucose tolerance and diabetes was evaluated. Twenty‐one patients with chronic persistent hepatitis, 68 patients with chronic active hepatitis and 57 patients with liver cirrhosis were studied. All subjects underwent an oral glucose tolerance test (75 g). Impaired glucose tolerance and diabetes were diagnosed according to the criteria established by: the National Diabetes Study Group; Fajans and Conn; the European Diabetes Study Group; Deutsche Diabetes Gesellschaft; Kobberling & Creutzfeld criteria 1 and 2; Wilkerson; and the University Group Diabetes Program. The results obtained are in partial agreement with other reported data, showing a high prevalence of both impaired glucose tolerance and diabetes in chronic liver disease, with a positive correlation to the severity of hepatic involvement. However, our results show that the agreement among the criteria most frequently used for diagnosing impaired glucose tolerance and diabetes is still far from satisfactory.

In order to try and evaluate through what prevailing mechanism verapamil (V) can induce an improvement in left ventricular (LV) diastolic early filling in mild to moderate essential hypertension, 43 properly classified essential hypertensives, aged 41-74 years (mean age 58.1 ± 10.3), and 20 age-matched normotensives were studied. All subjects underwent both echocardiographic evaluation and ^99mTc radionuclide angiocardiography in basal conditions between 8.00 a.m. and noon, after an overnight rest. In essential hypertensives gated equilibrium angiocardiography was repeated 3 and 30 min after i.v. V (0.1-mg/kg bolus, followed by 0.005 mg/kg/min for the period of radionuclide data acquisition). Simultaneously, supine arterial pressure was measured with a cuff manometer. In 36 essential hypertensives a phono-echo evaluation was obtained, both at 3 and 30 min after V, deriving a LV isovolumetric relaxation index (IRTI). Among diastolic early filling indices, we particularly considered the ratio of peak filling rate (PFR) to peak ejection rate (PER) in order to take into account the interaction of systolic performance with LV relaxation and diastolic early filling. Three minutes after V the increase in PFR (from 2.47 ± 0.5 to 3.04 ± 0.8 EDV/s, p < 0.001) and the upwards tendency of PFR/PER were coupled with the enhancement in ejection fraction (from 61.1 ± 13.3 to 63.9 ± 13.8%, p < 0.001) and heart rate (from 70.3 ± 12.6 to 77.7 ± 12.2 b/min, p < 0.001) and with the reduction in mean arterial pressure (from 122 ± 16 to 107 ± 14 mm Hg, p < 0.001), systemic arterial resistance index (from 3,234 ± 968 to 2,432 ± 678 dyn s cm^-5 m², p < 0.001) and end-systolic volume index (from 32.9 ± 17.1 to 31.5 ± 18.3 ml/m2, p < 0.02). On the contrary, 30 min after V, when systolic indices, heart rate, mean arterial pressure and systemic arterial resistance index had returned towards baseline values, PFR/PER showed a persistent improvement when compared with basal values (0.71 ± 0.12 vs. 0.63 ± 0.08, p < 0.005). No changes were observed in LV volumes and IRTI, either at 3 or 30 min. Moreover, also the pulmonary blood volume ratio was unchanged. A weak negative correlation was found between Δ% of IRTI and Δ% of PFR/PER 30 min after drug administration (r = 0.58, p < 0.05). Finally, essential hypertensives with increased LV LV Filling after i.v. Verapamil in Essential Hypertension mass and LV concentric hypertrophy showed a greater improvement in PFR/PER (from 0.66 ± 0.1 to 0.76 ± 0.2 and from 0.67 ± 0.1 to 0.77 ± 0.1, p < 0.005 for both). Our data indicate that the improvement in LV diastolic early filling in mild to moderate essential hypertension can be ascribed not only to the hemodynamic effect of the drug, but also to a primary influence on the functional abnormalities of the myocardial cells.

425trasylol and leupeptin on trypsin-like proteolytic enzymes such as kallikrein, CIr, tissue activator, pancreatin, plasmin and thrombin were studied. The derivatives of phenyl ester of these acids showed potent inhibitory effect on the trypsin-like enzymes. The effect of these esters on inflammation induced by croton oil and on experimental pancreatitis in animals will be reported. CI esterase activity and the conversion of CI to CI esterase were competitively inhibited by aromatic esters of guanidinocaproic acid. However, p-aminophenyl-phenylpropionate, chymotrypsin inhibitor, had no effect on CI esterase activity. Such synthetic inhibitors as described above reversibly inhibited trypsin, while derivatives of p-guanidinobenzoic acid inhibited trypsin irreversibly (E. Shaw; 1969).

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