To elucidate the role of loading sequence in afterload-dependent slowed relaxation in hearts in situ, the time constants (Texp from best exponential fitting method and TL from semilogarithmic method) of isovolumetric left ventricular (LV) pressure decay were studied in nine anesthetized open-chest dogs under the pharmacological blockade of autonomic nerve activity. An afterload change was imposed by clamping the ascending or descending aorta to make the peak LV pressure early or late in systole. During afterload interventions, in contractions with the peak LV pressure in late systole Texp and TL were significantly (P less than 0.05) larger than in those with the peak LV pressure in early systole in any comparable peak LV pressure range. Moreover, both time constants were directly correlated (P less than 0.01) with the time of peak LV pressure irrespective of peak LV pressure and clamp mode of aorta. In another protocol, marked differences both in Texp and TL were also observed between each of 25 pairs of contractions with different loading sequence but with comparable peak LV pressure and LV dimension (segment length). Thus afterload-dependent slowed relaxation in hearts in situ could not be attributed to an increased total load but to the altered loading sequence associated with an increase in afterload.

Influence of fibril length (porosity) upon synthetic vascular graft healing has not been investigated in detail. The purpose of this study was to determine the dependence of neoendothelial healing, cellular response, and biocompatibility on the fibril length of expanded polytetrafluoroethylene (ePTFE) grafts with an internal diameter of 1.5 mm. ePTFE grafts of different fibril length, 20, 40, 60, and 90 microns, were implanted into the abdominal aorta of rats (n = 5 for each group). After 5 weeks, the implants were harvested and examined for neointimal and pseudointimal coverage by light microscopy and SEM. The hydroxyproline content of the implants was measured, and the distribution of collagen types was examined. The neointimal and pseudointimal coverage was related to the fibril length, and the neoendothelial healing was better on 60-microns and 90-microns grafts than on 20-microns and 40-microns grafts. The amount of hydroxyproline was also related to the fibril length, however, no significant difference could be observed between 60-microns and 90-microns grafts. Collagen types I and III were almost identically located in the middle portion of the implants. Our results demonstrate that the fibril length of ePTFE grafts affected neoendothelial healing and its affinity to collagen.

No abstract

No abstract

SUMMARY We studied the dynamic changes in mitral flow patterns and in mitral valve motion before and after producing acute, reversible aortic insufficiency (Al) in nine open-chest dogs. Phasic mitral flow, the mitral valve echocardiogram, the intracardiac phonocardiogram and other hemodynamic variables were measured. During moderate Al (mean regurgitant fraction 52 ± 5%) (± SD), the antegrade filling volume decreased from 31 ± 7 to 24 ± 6 ml (p < 0.01), but the peak protodiastolic mitral flow rate increased from 139 ± 37 to 157 ± 42 ml/sec (p < 0.01), reflecting the shift of a larger fraction of total mitral filling volume to early diastole. In six dogs, atrial pacing was used to examine the hemodynamic effects of tachycardia. Increasing the heart rate from 90 to 120 beats/min increased cardiac output from 2.64 ± 0.56 to 3.3 ± 0.831/min (p < 0.05) and decreased left atrial pressure from 24 ± 8 to 17 ± 7 mm Hg (p < 0.05).Increasing heart rate to 150 beats/min compromised mitral filling, reduced cardiac output and increased left atrial pressure. Moderate tachycardia improves cardiac performance in Al by reducing regurgitant volume, without significantly reducing transmitral filling volume. The mitral valve echocardiogram showed only a small decrease in cusp opening amplitude during Al. A low-pitched left ventricular inflow tract murmur was recorded in protodiastole and corresponded in time to the rapidly increasing mitral flow. We conclude that the major determinant of the turbulence responsible for the creation of the Austin Flint murmur is the antegrade mitral flow stream and its mixing with the retrograde aortic flow.THE PATHOPHYSIOLOGY, clinical recognition and management of aortic insufficiency (Al) have been studied extensively in recent years. Clinical expressions of chronic and acute aortic regurgitation have been well defined,' and data regarding the natural history of the disease2' 3 and the proper selection of patients for medical vs surgical treatment is rapidly accumulating.f7 However, little is known about the dynamics of atrioventricular diastolic flow transport and, hence, about the significance of alterations in diastolic left ventricular (LV) filling in Al. To compensate for the immediate decrease in effective flow, Al may rapidly activate other physiologic mechanisms in addition to the Starling mechanism. Tachycardia is of particular benefit to patients with chronic or acute Al,8 although the mechanism by which increased heart rate (HR) specifically favors the hemodynamics of A! is not clear.9-12We undertook the present study to investigate the dynamic changes that occur on the left side of the heart with the onset of acute Al. Using our established technique of simultaneous phasic mitral flow and echocardiographic measurements, we placed particular emphasis on LV filling and mitral valve motion during the different phases of diastole. We concentrated on two aspects of mitral flow: the mechanism by which moderate increases in HR affect mitral and aortic flow to improve LV pump function, and th...