The objects of these experiments were to determine to what extent oleic acid, removed from plasma by forearm muscles, was oxidized immediately, and to search for evidence of an intramuscular lipid pool which may be composed of triglycerides synthesized from plasma free fatty acids and which may supply substantial portions of lipid substrates for oxidation by muscle. To these ends [1-w"C]oleic acid was infused at constant rate into the brachial artery of seven healthy young men at rest in the postabsorptive state. Results were: (1) muscle respiratory quotient (0.76) implied that about 80% of the oxygen consumed was for the oxidation of lipid. (2) Muscle free fatty acid uptake, had it been oxidized directly, could account for more than 100% of observed oxygen uptake.(3) There was a lag of at least 30 min before 'COn appeared in forearm venous blood. (4) "CO2 release from forearm muscle tended to reach an apparent plateau after 3 h of infusion of ["C]oleic acid. (5) During the time of plateau "CO2 release, oleic acid extracted from plasma could account for only 20% of oxygen consumption; most of the oleic acid taken up was not oxidized directly. (6) "CO2 release persisted at a high level during the 1-3 h follow-up period after the infusion ended. (7) Neither the delay in initial appearance of "CO2 nor its continued release after cessation of infusion was due to delay and distribution in a forearm COa pool, since intra-arterial infusion of Dr. Dagenais was a fellow of the Canadian Heart Foundation.Dr. NaH"CO3 in two additional subjects demonstrated much more rapid distribution of 'CO2 in the forearm. Results show that most, if not all, free fatty acids taken up by resting muscle are not oxidized directly, but probably enter an intramuscular pool which has a slow turnover during resting metabolism and is the immediate source of oxidized lipid substrate.
A B S T R A C T A reduction in the release of substrate amino acids from skeletal muscle largely explains the decrease in gluconeogenesis characterizing prolonged starvation. Brief starvation is associated with an increase in gluconeogenesis, suggesting increased release of amino acids from muscle. In the present studies, accelerated amino acid release from skeletal muscle induced by brief starvation was sought to account for the accompanying augmentation of gluconeogenesis. To do this amino acid balance across forearm muscles was quantified in 15 postabsorptive (overnight fasted) subjects and in 7 subjects fasted for 60 h.Fasting significantly reduced basal insulin (11.3-7.5 /AU/ml) and increased glucagon (116-134 pg/ml).Muscle release of the principal glycogenic amino acids increased. Alanine release increased 59.4%. The increase in release for all amino acids averaged 69.4% and was statistically significant for threonine, serine, glycine, alanine, a-aminobutyrate, methionine, tyrosine, and lysine. Thus, with brief starvation, muscle release of glycogenic amino acids increases strikingly. This contrasts with the reduction in amino acid release characterizing prolonged starvation. The adaptation of peripheral tissue metabolism to brief starvation is best explained by the decrease in insulin.
Cardiac involvement in polymyositis was investigated in 20 autopsied cases. Clinically, 13 of 18 patients had abnormal electrocardiograms, and 9 of the 20 patients had previous evidence of congestive heart failure. Histologically documented myocarditis was detected in 6 patients (4 with congestive heart failure and 2 without), 4 of whom also had small vessel disease of the myocardium. Patients with polymyositis may have a cardiopathy in the absence of overt myocardial inflammatory disease.
In the standard precordial echocardiographic imaging planes, there is frequent dropout of atrial septal echoes in the region of the fossa ovalis that can be minimized by use of the subcostal imaging approach. The diagnostic sensitivity of this approach was reviewed in 154 patients (mean age 31 years, range 2 months to 74 years) with documented atrial septal defect in whom a satisfactory image of the atrial septum could be obtained. Subcostal two-dimensional echocardiography successfully visualized 93 (89%) of the 105 ostium secundum atrial septal defects, all 32 (100%) ostium primum defects and 7 (44%) of the 16 sinus venosus defects. A defect was not visualized (false negative response) in 12 patients (11%) with an ostium secundum defect and in 9 patients (56%) with a sinus venosus defect. In three of the former and five of the latter, a two-dimensional echocardiographic contrast examination established the presence of the interatrial shunt. Twenty-four patients (16%) with clinical findings of uncomplicated atrial septal defect confirmed by two-dimensional echocardiography underwent surgical repair of the defect without preoperative cardiac catheterization. There were no perioperative complications. Two-dimensional echocardiographic examination of the atrial septum utilizing the subcostal approach is the preferred method for the confident, noninvasive diagnosis and categorization of atrial septal defects. Two-dimensional echocardiographic contrast and Doppler examinations complement the technique and enhance diagnostic accuracy.
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