In both ground sections and demineralized frozen sections of the rat tibial cortex, osteoid but not mature bone matrix stained for proteinpolysaccharides with the Alcian Blue and toluidine blue techniques. The loss of proteinpolysaccharide staining occurred precisely at the mineralizing front, which was identified by in vivo lead or procion markers, not only in normal animals but also in animals in which osteoid width was either increasing or decreasing. In vitro, both proteases and saccharidases abolished proteinpolysaccharide staining of osteoid. Critical electrolyte concentration and other procedures indicated that the major acid polysaccharide component in osteoid is chondroitin sulfate. Consistent with these findings, electron microprobe analyses revealed that sulfur concentration was high in osteoid but dropped abruptly as calcium concentration increased at the mineralizing front. The precise synchronization between loss of proteinpolysaccharides and onset of mineralization under various experimental conditions provides strong indirect evidence that the loss of these macromolecules is somehow involved in initiation of mineralization in bone.
In a three-way crossover study, 23 patients with hepatic cirrhosis, ascites, and dependent edema received 40 mg/day of furosemide alone and combined with triamterene 50 mg/day and triamterine 100 mg/day. Baseline potassium excretion did not increase when furosemide was given alone, but potassium excretion fell when 50 mg or 100 mg of triamterene was also given. Both doses of triamterene augmented the natriuretic effect of furosemide.
In 13 patients admitted to a coronary care unit, antiarrhythmic efficacy and safety of quinidine gluconate in a nonmatrix formulation were compared to placebo and quinidine sulfate. Both quinidine preparations were effective in reducing the number and severity of ventricular and supraventricular extrasystoles when compared to placebo. Except for a few cases in which quinidine gluconate was significantly more effective, both quinidine preparations appear to have similar clinical antiarrhythmic efficacy and duration of action. A 24-hour Holter ECG monitoring device and electrocardioscanner were utilized in this research. No major unexpected adverse effects were observed.
A patient is presented in whom repeated attacks of ventricular tachycardia occurred. His last and fatal attack revealed an alternation or coupling of the cycle lengths of the ventricular beats. A large left ventricular wall aneurysm was found, which probably accounted for the unusual arrhythmias.
A technique for the study of patients with angina pectoris has been described, in which systolic time interval (STI) measurements are obtained at intervals after the onset of stress-induced angina. The technique is uniquely suited to the evaluation of anti-anginal drugs. Sublingual isosorbide dinitrate (SISD) was randomly alternated with a placebo (P) tablet in a double-blind study of 20 patients with stable angina pectoris. After SISD, compared to placebo, a highly significant shortening of Q-S2 and LVET occurred (p less than 0.001) which lasted throughout the entire 120 minute study period. The hemodynamic basis for these differences was felt to be improved myocardial contractility secondary to a reduction in systemic vascular resistance and reduced venous return induced by the SISD. A significant prolongation of PEP occurred at 60 minutes post-SISD (p less than 0.01). This was attributed to an increase in the gradient between LVEDP and aortic diastolic pressure resulting from reduced venous return after SISD. The PEP/LVET ratio was significantly increased up to 60 minutes after SISD (P less than 0.05). Heart rate was uniformly higher post-SISD, compared to post-placebo values; the differences were highly significant up to 60 minutes (P less than 0.001) and remained significant at 120 minutes (p less than 0.05). The time to angina was significantly longer (immediately post SISD, p less than 0.05; 30 min, p less than 0.001; 60 mins, p less than 0.05; 120 mins, p less than 0.05); and the work load greater, for 120 minutes following SISD: the increase in the latter was highly significant for 30 minutes after SISD (p less than 0.001) and remained significant up to 120 minutes (60 mins, p less than 0.05; 120 mins, p less than 0.05). These observations were attributed to an improvement in myocardial function due to the sublingual isosorbide dinitrate. A high degree of correlation was found to exist between heart rate and the STI. This correlation was negative for the QS2 interval (-0.996) and LVET (-0.993) and positive for PEP (+0.817) and the PEP/LVET ratio (+0.950).
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