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Patch-clamp recording techniques have permitted measurement of the fast Na+ current (INa) [Na+]., and the current was completely blocked by 100 ,uM tetrodotoxin, findings typical of the fast cardiac Na+ current. The tetrodotoxin dose-response curve was best fitted by an equation describing binding to high-and low-affinity sites. INa was activated at a voltage threshold of -70 to -60 mV, and peak inward current was obtained at =-30 mV (holding potential, -140 mV). The inactivation time course was voltage dependent and was fitted best by the sum of two exponentials. The relation between voltage and steady-state availability (h.,) was sigmoidal with the half-inactivation at -95.8±0.9 mV and a slope factor of 5.3+0.1 mV (n=46), and we did not observe a significant difference with disease and age.

The purpose of this study was to examine whether morphologic abnormalities in human respiratory muscles are related to increased airway obstruction. 43 patients who were undergoing thoracotomy for suspected neoplasm had biopsies taken from one or more of the following muscles: external intercostal (EXT), internal intercostal (INT), diaphragm (DIA), latissimus dorsi (LAT), and quadriceps femoris (LEG). Mean FEV₁/FVC was 65% of predicted (range 43–90%). 21 of the 43 patients had a malignancy. Atrophy of type I fibers was found in 27% of respiratory and 11 % of nonrespiratory muscles. Type II fiber atrophy was more common, being found in 58% of all muscles studied. The degree of type II fiber atrophy correlated significantly with the amount of weight loss, but not with age or the presence of malignancy. A unique and significant relationship was found between type II fiber atrophy in the INT (an expiratory muscle) and all measured indices of airway obstruction. This relationship did not exist in the DIA, EXT, or LAT, ordinarily considered muscles of inspiration. The percentage of type I and type II fibers bore no relationship to indices of airway obstruction. Depletion of muscle metabolites was common to all muscles and could not be related to airway obstruction or fiber atrophy. These data suggest that fiber atrophy and metabolite depletion occur commonly in both respiratory and nonrespiratory muscles in patients with stable obstructive lung disease. These changes probably reflect a generalized disease process and may predispose to muscle fatigue. Whether or not airway obstruction produces fiber atrophy in expiratory muscles requires further investigation.

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This study demonstrates that, in the clinically relevant, intact animal model, good myocardial protection is independent of cardioplegia calcium concentration in nonhypoxic (noninjured) hearts; hypoxic (stressed) hearts are extremely sensitive to the cardioplegic calcium concentration; and normocalcemic cardioplegia is detrimental to neonatal myocardium subjected to a preoperative hypoxic stress.

1. Retrograde cardioplegia provides poor right ventricular myocardial perfusion as assessed by contrast echocardiography and coronary ostial drainage. (2) This poor perfusion is inadequate to meet myocardial demands as demonstrated by the high right ventricular oxygen extraction after a prolonged retrograde infusion. (3) Therefore surgeons must not rely solely on retrograde cardioplegia for right ventricular myocardial protection. This concept is especially important if continuous warm blood cardioplegia is used, because myocardial requirements are then higher.

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