Discussion Arising from Session on Cardiac Filling

DR. HALES: I don't think I will have a great deal to say now, but I hope that you will agree that my co-proponent showed that blood volume maintenance is a very important factor in heat stress. The question then is what is sensed as volume changes. Dr. Kirsch talked about the importance of the venous pressure gradient from the skin or systemic vasculatures into the central venous pool and the gradient being maintained by a lowering of central venous pressure, at least partially. Now if that is the case, then the low-pressure baroreceptors are not the central key to the whole issue. If the lowpressure baroreceptors are important, then how is the decrease in filling pressure brought about? One might ask why the key experiments have not been done and what should be done. I think that the main contributions to this area have come from two groups-those in Seattle around Rowell's laboratory, and those here around Nadel's laboratory. Both groups have worked with human subjects and therefore are restricted in their abilities to manipulate central venous pressure experimentally. So I have thought of several key experiments that are quite feasible and need to be done in lower animals. First of all, it would be important to try to lower skin blood flow during heat stress by lowering the central venous pressure in conscious, chronically prepared animals. This is quite a feasible proposition by having a chronically implanted pneumatic cuff around the inferior vena cava. Second, it would be important to see if it is possible to defer the reduction in skin blood flow by maintaining central venous pressure through expanding the blood volume of the conscious animal or perhaps by removing the receptor input. I feel this is quite feasible by means of a chronically implanted catheter in the pericardial sac and infusion of local anesthetic at various stages of heat stress. With that food for thought, I will leave it for the time being. Thanks. DR. KIRSCH: We have really had a hard time understanding each other because so many different models are used to make a point. For instance, Dr. Senay suggested that long-term exercise experiments need to be done to show both what is changed and how these variables change. I think this is true because, in such experiments, the hydration level of the volunteers changes and probably so does the distribution of fluid between the vascular and extravascular compartments. This is a missing link, and there are methods available to explore this problem. Cardiovascular physiologists, or as you would call them plumbers, examine first the mechanics of the system. Before describing a reflex, we try to explain everything by simple mechanical models. I think we should really know about the basic mechanics of the system, and later start looking for explanations by these reflex maneuvers. The other thing I cannot understand is that Dr. Hales saw a defense of central venous pressure. A defense of central venous pressure would mean keeping the central venous pressure almost unchanged. Where then does the information come from if you keep central venous pressure constant? We have never seen an absolute defense of the central venous pressure; it always goes up and down in a certain range. This variabilty is important because it provides the system with needed information. For the future, I think we should examine the models we use and attempt to unify our models. Second, our methodology is limited. Today there is isotope methodology to