Erythrocyte-containing capillaries were counted in dog gracilis muscles freeze-clamped at rest and after twitch contraction at 4/s. In each of 21 muscles, 6--8 blocks were examined at -70 degrees C without fixation or staining; 15 fields were counted per block. Frequency analysis of capillaries per field based on the negative binomial distribution indicated that capillary density at rest was controlled by arterioles. Active vasomotion of these arterioles was "switched off" within 5 s after onset of exercise. Capillary density was then determined passively by stochastic rheologic factors acting at the individual capillaries. Thus exercise changes the site and the mechanism of capillary control. Recruitment occurred first where capillary density was lowest, and was complete in 15 s; this greatly decreased the heterogeneity of capillary spacing. Mean capillary density increased 1.5- to 3-fold, whereas flow increased almost 7-fold. Calculated mean velocity and mean transit time of erythrocytes in capillaries were 1.1 mm/s and 920 ms at rest and 4.2 mm/s and 215 ms after 3 min of exercise.
Capillary control was quantified in dog gracilis muscles from in situ. About 550 capillaries/mm2, one-third the total number present, were perfused with erythrocytes simultaneously at rest; two-thirds the total could be perfused during maximal vasodilation. The functional capillary reserve was about 600/mm2. Capillary distribution at rest reflects a passive, random process at individual capillaries and an active process that coordinates perfusion of small groups of capillaries. The latter creates long diffusion distances. These are unaltered by denervation, or flow per se, but are abolished by adenosine. Twitch contraction at 4/min recruited about 400 capillaries/mm2 without any change in flow. Capillaries opened selectively where diffusion distances were longest. The same changes occurred within 5 s during work at 4/s, even if flow was held constant. If flow could increase, about 200 additional capillaries/mm2 were slowly recruited, without change in capillary distribution. Conclusions are that 1) hemodynamics and active vasomotion contribute equally to capillary density at rest; 2) active papillary control in exercise is ungraded and solely responsible for eliminating metabolically significant diffusion paths; 3) flow and capillary density can be controlled independently by proximal and terminal arterioles, respectively.
The biplot is a graphical display of multivariate data. A number of examples from biomedical research illustrate its use. Biplots allow for inspection of data preliminary to formal analysis, and can follow an analysis by the graphical inspection of residuals. The simplicity and intuitive appeal of these displays is stressed. An appendix indicates their method of construction and the software for producing them.
We assessed the role of physiologic measurements of heart function in predicting mortality after myocardial infarction. Most of the 866 patients enrolled in our multicenter study underwent 24-hour Holter monitoring and determination of the resting radionuclide ventricular ejection fraction before discharge. Univariate analyses showed a progressive increase in cardiac mortality during one year as the ejection fraction fell below 0.40 and as the number of ventricular ectopic depolarizations exceeded one per hour. Only four risk factors among eight prespecified variables were independent predictors of mortality: an ejection fraction below 0.40, ventricular ectopy of 10 or more depolarizations per hour, advanced New York Heart Association functional class before infarction, and rales heard in the upper two thirds of the lung fields while the patient was in the coronary-care unit. Various combinations of these four factors identified five risk subgroups with two-year mortality rates ranging from 3 per cent (no factors) to 60 per cent (all four factors).
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