Para-aminohippurate (PAH) and para-aminobenzoate (PAB) are estimated in plasma and urine from wethers after a subcutaneous injection of PAB. The rate of synthesis of PAH from injected PL4B is taken as a measure of liver function and the rate of urinary excretion of the synthesized PAH as a measure of kidney function. It is shown that extrahepatic synthesis of PAH from PAB is unlikely to interfere with these tests of function. Some values for normal animals are given.
SummaryCreatinuria was found in normal rams, wethers, and ewes on ordinary diets. This finding emphasizes the need for caution> in interpreting urine creatine concentration or creatine to creatinine ratios used as diagnostic aids in muscular dys· trophy in sheep. No change in creatine output per 24 hr was observed when the ewes were fasted for 6 days. Values are given for the ratio creatine clearance to creatinine clearance in rams, wethers, and ewes and for creatine clearance in ewes.
A chronic model of acute myocardial infarction was developed to study the mechanisms involved in adverse postinfarction ventricular remodeling. In an acute myocardial infarction (AMI), the left circumflex coronary artery of New Zealand White rabbits (n = 9) was occluded by ligature for 1 h, followed by reperfusion. A specific care protocol was applied before, during, and after the intervention, and the results were compared with those of a sham operated group (n = 7). After 5 weeks, programmed stimulation and high-resolution mapping were performed on isolated and perfused hearts using the Langendorff technique. The infarct size determined by 2,3,5-triphenyltetrazolium chloride inside of the area at risk (thioflavin-S) was then determined. The area at risk was similar in both groups (54.33% (experimental infarct group) vs. 58.59% (sham group), ns). The infarct size was 73.16% as a percentage of the risk area. The experimental infarct group had a higher inducibility of ventricular arrhythmias (100% vs. 43% in the sham group, p = 0.009). A reproducible chronic experimental model of myocardial infarction is presented in which the extent and characteristics of the lesions enable the study of the vulnerability to develop ventricular arrhythmias because of the remodeling process that occurs during cardiac tissue repair.
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