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Biomedical subjects

K A Gaar

Publications and source records attributed to K A Gaar.

15 recordsLinked to original sources
PubMed1991

Oxygen transport: interrelationship between arterial pressure regulation and blood flow autoregulation.

An oxygen transport model was used to study the effects of blood flow autoregulation and arterial pressure regulation on tissue oxygen delivery. At low to moderate levels of oxygen consumption, autoregulatory increases in blood flow act in conjunction with increased tissue diffusing capacity to maintain oxygen delivery as oxygen demand becomes increased. However, an increase in the arterial pressure becomes necessary to augment oxygen delivery at higher levels of oxygen usage. At exercise levels approaching the "maximum aerobic oxygen consumption' rate, arterial pressure regulation appears to be as important as autoregulation for maintaining delivery of oxygen to the tissues. The total negative feedback gain for autoregulatory control of tissue oxygenation varies with the rate of tissue oxygen uptake and is almost 2.0 at the maximum aerobic oxygen consumption rate. Furthermore, the feedback gain is only slightly affected by changes in the mean arterial pressure that occur normally during strenuous exercise, which is indicative of the complementary relationship between these two important control mechanisms.

Biological Transport, Active↗
PubMed1991

Model to facilitate studying oxygen and carbon dioxide transport.

A simple model has been constructed for microcomputer (PC) simulations involving basic cardiopulmonary principles of oxygen transport. Students can change parameters such as metabolic rate, blood hemoglobin concentration, barometric pressure, air composition, etc., and study parameter effects on blood gas concentrations and partial pressures. An important feature of the model program is that there are no negative feedback controls to maintain homeostasis. However, after a perturbation has been introduced, adjustments can be made to appropriate variables to correct for abnormal effects. For example, ventilation rate and blood hemoglobin concentration might be adjusted to compensate for low atmospheric oxygen. Because these do not change automatically in the model program, learning is enhanced when the student has to make the appropriate adjustments needed to correct disturbances in the blood gases that follow a perturbation.

Biological Transport↗
PubMed1988

Erythrocytosis: a key to understanding the hemodynamic changes in hypertension.

Theories that would propose to explain the increased vascular resistance that accompanies hypertension include the presence circulating vasoconstrictor substances (angiotensin II, vasopressin, epinephrine, etc.), a centrally mediated generalized increase in sympathetic tone, increased vascular smooth muscle tone due to increased calcium ion permeability, and perhaps others. While each of these may be valid in some circumstances there exists yet another mechanism, indirect and potent, that could account for much of the change in peripheral vascular resistance that accompanies hypertension. This is the erythrocytosis mechanism that is mainly controlled by the kidneys. This treatise concerns the manner in which the kidneys supposedly react to disturbances in oxygen transport coincident with the development of hypertension and the effect that this might have in modifying peripheral resistance to blood flow.

Blood Volume↗
PubMed1987

Oxygen transport: an analysis of short-term blood flow autoregulation.

A model for studying oxygen transport was used to examine the acute blood flow autoregulation phenomenon and its effectiveness for maintaining tissue oxygenation under different physiological conditions. The effectiveness of tissue oxygenation was judged by the level of venous blood oxygen tension, PVo2. Three sets of conditions were studied with, and again without, autoregulation present. First, arterial blood oxygen tension, Pao2, was lowered in steps while changes in PVo2 and blood flow were recorded. Second, blood hemoglobin concentration was lowered in steps while Pao2 remained normal. Finally, the rate of oxygen consumption was increased, simulating the increase in metabolism that occurs during strenuous exercise. Although the basic negative feedback gain had been set at the same level in each case, in comparing the results of the different simulations it became apparent that there were notable differences in each of the autoregulatory responses. These observations indicated that the overall effectiveness and the total feedback response of autoregulation could be highly variable, depending on the conditions.

Animals↗
PubMed1987

Cardiac output: is there a sex difference?

An analysis is presented which challenges the supposition that men, in general, have higher resting cardiac outputs than women. The basis of the challenge relies on the fact that the blood oxygen carrying capacity of women is generally below that of men, which should be an offsetting factor. To test this hypothesis, data was obtained from standard tables of normal physiological indices. Using this data, simple calculations were made which did indeed tend to support the belief that a true sex difference exists. However, other calculations were made using a different method which tended to refute this supposition.

Basal Metabolism↗
PubMed1986

Renal disease and hypertension: the erythrocytosis factor.

For some unknown reason, the blood hematocrit will become elevated 50 percent or more in some cases of renal disease where hypertension is a factor. In the absence of other identifiable causes of erythrocytosis, this is believed to result from the formation of erythropoietin stimulating factor (ESF) by the kidney in response to some intrarenal hypoxic stimulus. In this study it could be demonstrated with the help of computer simulations, that the hypertension was caused by excess fluid being retained by the kidneys, whereas, the elevated hematocrit could only be attributed to primary increase in the resistance to blood flow. This suggests that the high hematocrit levels that have been reported probably could not have occurred, except for powerful excess vasoconstrictor activity affecting the whole circulation.

Blood Pressure↗
PubMed1978

Estimation of the filtration coefficient of pulmonary exchange vessels.

Filtration characteristics of the exchange vessels in isolated dog lung were studied by calculating the volume conductance (LP,C) with use of different components of the weight-gain curve following changes in capillary pressure. In one series of lungs, capillary pressure was elevated to levels that produced alveolar edema (29.4 +/- 5.3 (mean +/- SD) mmHg), and total alveolar capillary membrane conductances (LP,T) were calculated using different components of the accumulated weight-gain measurements. These conductance values are similar to those found in the literature for studies in which alveolar edema developed and LP,T was calculated using wet-to-dry weight ratios as a measure of filtered volume. In another series of lungs, capillary pressure was altered by only 5.8 +/- 2.5 mmHg, and LP,C was calculated by estimating the initial filtration rate by an extrapolation method LP,C calculated by use of the extrapolation method (0.71 X 10(-11) cm3/dyn-s) was larger than the LP,T reported in the literature, because LP,T is an estimate of the conductance of the alveolar plus the capillary membrane. Also, for the most calculations of LP,T, tissue forces have changed which causes an overestimation of the filtration driving pressure and thus an underestimate of the capillary volume conductance. After estimating both LP,C and LP,T, the maximum volume conductance of the alveolar membrane (LP,a) was calculated to be 0.13 X 10(-11) cm3/dyn-s.

Animals↗