Biomedical subjects

A S Greene

Publications and source records attributed to A S Greene.

At least 19 recordsLinked to original sources

PubMed1992

Effect of microvascular rarefaction on tissue oxygen delivery in hypertension.

A mathematical model of oxygen transport in tissue was used to analyze the effects of microvessel rarefaction and nonhomogeneous oxygen consumption on tissue oxygen distribution. The model was based on the diffusion equation with a nonhomogeneous consumption term. Solutions were computed for several configurations of vessel and oxygen sink distributions on a finite domain using the finite element method. A microcirculatory unit consisting of a tissue slice of 100-microns depth and 40-microns width was chosen. Symmetry boundary conditions were applied so that the entire tissue consisted of a series of such microvascular units placed side by side. The boundary condition at the surface of the unit was chosen to simulate a tissue suffusion experiment in which the suffusion oxygen was varied from 0 to 37 mmHg. Results of the model, which were compared with direct measurements with oxygen microelectrodes, indicate that vascular oxygen delivery strongly dominates the tissue oxygen field for suffusion PO2 values of less than 20 mmHg, whereas above this level tissue oxygen is dominated by the suffusion PO2. Reduction of vessel density within the tissue was found to have the largest effect on tissue oxygen levels at low suffusion oxygen. Finally, under some configurations of oxygen sources (vessels) and sinks (mitochondria), extremely low PO2 levels may exist within the area of high consumption, which could limit the metabolic activity of the tissue.

Animals↗

PubMed1992

Venous myogenic tone: studies in human and canine vessels.

Active and passive mechanical properties of human saphenous and canine femoral and saphenous vein segments were measured in vitro to assess the degree of pressure-dependent venous myogenic tone (% change in diameter, physiological saline solution vs. Ca(2+)-free solution) in these vessels. Stepwise elevation of intraluminal pressure from 2 to 20 mmHg caused an active myogenic response, which was calcium dependent. Side branches of human saphenous veins (OD at 20 mmHg: 1.92 +/- 0.15 mm control; 2.41 +/- 0.18 mm relaxed) displayed a larger degree of myogenic tone (approximately 25%) compared with dog saphenous (OD: 2.84 +/- 0.16 mm control; 2.89 +/- 0.16 mm relaxed) and femoral (OD: 3.56 +/- 0.32 control; 3.66 +/- 0.31 mm relaxed) veins (2-3%). This alteration in myogenic tone results in over 120% change in lumen capacity for the human saphenous vein, whereas for the dog saphenous and femoral veins, the change in lumen capacity is less than 10%. The vessels showed a constriction to norepinephrine as well as a reversible dilation to Ca(2+)-free perfusion. These results support the hypothesis that an active myogenic response may play an important role in the regulation of vascular capacity in the human saphenous vein, which is subject to substantial pressure variations due to changing orthostatic loads.

Animals↗

PubMed1992

Salt intake and angiotensin II alter microvessel density in the cremaster muscle of normal rats.

This study investigated the effect of salt intake and angiotensin II (ANG II) levels on microvessel density (MVD). Rats with indwelling arterial and venous catheters were placed on either a high-salt (HS; 4%) or a low-salt diet (LS; 0.4%) for 2 or 4 wk, and blood pressure, heart rate, and plasma renin activity were measured. Plasma ANG II was fixed at normal levels in half of the rats on HS by continuous intravenous infusion of ANG II (5 ng.kg-1.min-1). Samples of cremaster muscle were examined histologically to determine MVD. No difference in MVD was observed between HS and LS groups after 2 wk. After 4 wk on HS, MVD was reduced (22.4%, P less than 0.05) compared with the LS group. In rats fed HS, ANG II infusion induced a significant dose-dependent increase in MVD from 85.11 +/- 3.34 to 98.94 +/- 4.62 (ANG II, 5 ng.kg-1.min-1) and to 107.60 +/- 7.00 (ANG II, 10 ng.kg-1.min-1) (P less than 0.05), with no change in blood pressure. Maintenance of ANG II levels for 4 wk blocked the rarefaction due to salt. These results suggest that the decrease in MVD due to salt could be the result of a dietary-induced fall in plasma ANG II levels.

Angiotensin II↗

PubMed1991

Structural alterations of microvascular smooth muscle cells in reduced renal mass hypertension.

Loss of microvessels (anatomic rarefaction) occurs in chronic reduced renal mass (RRM) hypertension and is mediated via structural degeneration of vascular smooth muscle (VSM) and endothelial cells. The purpose of the present study was to determine if structural changes occur in VSM cells of the microvessels that remain in the tissue of rats with chronic RRM hypertension. Samples of cremaster muscles were taken from normotensive control rats and rats with acute (3-7 days) and chronic (14-28 days) RRM hypertension (75% reduction in kidney mass with 4% NaCl loading). The samples were fixed in situ and processed for light and electron microscopy. Ultrastructural morphology of VSM cells in terminal arterioles of control animals was normal. Although VSM morphology in many microvessels of RRM hypertensive rats was also normal, some vessels exhibited structural changes that were not present in arterioles of the normotensive animals. The most striking change was the appearance of more extensive dense bodies anchoring the contractile filaments around the outer membrane of the cells. Extreme vasoconstriction was observed in some arterioles of RRM rats as long as 2 weeks after salt loading. Focal areas of VSM cell proliferation were evident. Many of the changes occurring in RRM were detected as early as 1 week after the onset of hypertension. These observations suggest that renal mass reduction-salt loading hypertension is associated with early structural and functional changes in the VSM cells.

Animals↗

PubMed1990

Role of blood volume expansion in Dahl rat model of hypertension.

Continuous measurement and servo control (SC) of total body weight of unrestrained rats were used to investigate the role of volume expansion in the development of hypertension in Dahl salt-resistant (SR) and Dahl salt-sensitive (SS) rats. A change in sodium intake from 1 to 20 meq/day was associated with an increase in total body weight of 7.2% in both SS and SR rats over 96 h. Plasma sodium (pNa) increased from 145.0 to 147.4 meq/l in both SS (n = 10) and SR (n = 10) rats. Only in the SS rats was the volume expansion associated with an increase in arterial pressure of 27 +/- 3 mmHg. Prevention of the volume expansion by SC blocked the rise in arterial pressure in the SS rats (n = 10) but increased pNa from 143.5 to 152.4 meq/l. Hematocrit fell from 36.6 to 27.5% in both non-SC groups but decreased less in SC groups (35.7 to 32.0%). Plasma volume expansion from 17.6 +/- 0.6 to 25.2 +/- 0.8 ml in non-SC rats was greatly blunted by SC. In non-SC rats, SS (n = 10) and SR (n = 9) rats an increase in salt intake was associated with a rise in cardiac output from 413 +/- 6 to 507 +/- 12 ml.min-1.kg-1 in both groups. These results indicate that fluid retention is required to trigger the rise of pressure in Dahl SS rats.

Animals↗

PubMed1990

Regional autoregulatory responses during infusion of vasoconstrictor agents in conscious dogs.

We investigated pressure-dependent autoregulatory responses in mesenteric, iliac, and renal vascular beds of conscious dogs during intravenous infusion of angiotensin II, phenylephrine, or arginine vasopressin at rates which increased arterial pressure by 20-40 mmHg. The arteries supplying these beds were instrumented with an electromagnetic flow probe, a nonoccluding catheter, and an electromagnetic flow probe, a nonoccluding catheter, and an occluder cuff connected with a servo-amplifier, which enabled us to return perfusion pressure to control levels during infusion of the vasoconstrictor agents. We attempted to differentiate between the increase in vascular resistance due to the direct effect of the vasoconstrictor agent and the increase induced by an autoregulatory response induced by elevations of aortic perfusion pressure. We measured a strong degree of autoregulation in the renal vascular bed with a fractional compensation value close to 1. Moderate autoregulation occurred in the mesenteric vascular bed, where the compensation was 0.4-0.5 with angiotensin II and phenylephrine and between 0.74 and 0.94 with vasopressin. No autoregulatory capacity could be demonstrated in the hindlimb. The findings indicate that, under conditions of increased systemic blood pressure, both the renal and the mesenteric vascular beds contribute to the increase in total peripheral resistance by pressure-dependent vasoconstrictor responses.

Angiotensin II↗

PubMed1990

Microvessel changes in hypertension measured by Griffonia simplicifolia I lectin.

Commonly used methods for assessing reductions in microvascular density (rarefaction) in hypertension detect only perfused microvessels. In the present study, samples of cremaster and spinotrapezius muscles were taken from rats with chronic (4-week) reduced renal mass hypertension and normotensive sham-operated control rats, as well as from 12-week-old spontaneously hypertensive rats and their normotensive Wistar-Kyoto control strain. Mean arterial pressure was 149 +/- 8 mm Hg in the rats with reduced renal mass hypertension, 114 +/- 7 mm Hg in sham-operated rats, 177 +/- 9 mm Hg in spontaneously hypertensive rats, and 95 +/- 4 mm Hg in Wistar-Kyoto rats. Muscle samples were incubated with rhodamine-labeled Griffonia simplicifolia I lectin, which identifies both perfused and nonperfused microvessels. Microvascular density was assessed by counting intersections with a 20-microns grid. Microvessel density was significantly reduced in cremaster muscles of both spontaneously hypertensive and reduced renal mass hypertensive rats, and in the spinotrapezius muscle of spontaneously hypertensive rats, compared with their respective normotensive controls. Further studies in the reduced renal mass rats on low salt diets indicated that lectin binding was also decreased as salt intake was increased, independent of blood pressure. This change was not due to an alteration in lectin-binding affinity. These studies indicate that lectin binding can be a useful tool for assessing microvessel density that does not depend on the perfusion state of the vessels and that rarefaction due to hypertension is not evenly distributed in all vascular beds. These results also provide evidence that dietary salt intake alone can influence microvessel density, as measured by the lectin technique.

Animals↗

PubMed1990

Structural changes during microvascular rarefaction in chronic hypertension.

Previous physiological studies have suggested that loss of microvessels (anatomic rarefaction) occurs in the skeletal muscle microcirculation of rats with chronic hypertension. However, little is known of the exact structural changes that occur during the process of anatomic rarefaction. The purpose of this study was to examine the muscle at the ultrastructural level to search for evidence of microvessel degeneration that would correlate with the concept of anatomic rarefaction in chronic hypertension. Cremaster muscles were removed from normal rats and from rats with chronic reduced renal mass hypertension, which was produced by a 75% reduction in kidney mass followed by salt loading (4% NaCl chow with water ad libitum) for 4 weeks. The muscles were fixed and prepared for histological examination by light and electron microscopy. Atrophy and degeneration of both endothelial cells and vascular smooth muscle cells were observed in many arterioles of the hypertensive rats. Some arterioles of hypertensive rats were degenerated to such an extent that the original identity of the cells could not be determined. The hypertensive rats also exhibited degeneration of capillaries and extravasation and uptake of red blood cells into lymphatic vessels. In contrast, age-matched control rats exhibited normal histology. The results of this study support previous physiological evidence for anatomic rarefaction in the cremaster muscle of chronically hypertensive rats.

Animals↗

PubMed1989

Microvascular rarefaction and tissue vascular resistance in hypertension.

The purpose of this study was to quantitatively estimate the relative contribution of arteriolar rarefaction (disappearance of microvessels) and arteriolar constriction to the increases in total peripheral resistance and changes in the patterns of flow distribution observed in hypertension. A mathematical model of the hamster cheek pouch intraluminal microcirculation was constructed based on data from the literature and observations from our own laboratory. Separate rarefaction and constriction of third-order (3A) and fourth-order (4A) arterioles were performed on the model, and the results were quantified based on the changes of the computed vascular resistance. The degree of increase in resistance depended both on the number and the order of vessels rarefied or constricted and also on the position of those vessels in the network. The maximum increases in resistance obtained in the model runs were 21% for rarefaction and 75% for constriction. Rarefaction, but not constriction, produced large increases in the degree of heterogeneity of blood flow in the various vessel orders. These results demonstrate that vessel rarefaction significantly influences tissue blood flow resistance to a degree comparable with vessel constriction; however, unlike constriction, microvascular rarefaction markedly altered blood flow distribution in our model of the hamster cheek pouch vascular bed. These findings conform with the hypothesis that a significant component of the increase in total peripheral resistance in hypertension may be due to vessel rarefaction.

Algorithms↗

PubMed1989

Whole body autoregulation in conscious areflexic rats during hypoxia and hyperoxia.

We have previously shown whole body autoregulation during normoxia in conscious areflexic rats in response to an acute increase and decrease in blood volume. In this study we used this technique to determine the effect of hypoxia and hyperoxia on whole body autoregulation. Rats with an arterial catheter for blood pressure measurement and an electromagnetic flow probe for cardiac output measurement were placed in a chamber with a controlled oxygen environment. Neurohumoral blockade was achieved with chlorisondamine (10 mg/kg), methscopolamine (0.5 mg/kg), captopril (1 mg/kg), and [d(CH2)5Tyr(Me)]arginine vasopressin (10 micrograms/kg). Hemodynamic variables were restored to normal with a constant norepinephrine infusion. Group 1 (n = 7) underwent a 6-min infusion of donor blood (0.9 ml) during hypoxia (Po2 = 52 +/- 3 mmHg) and hyperoxia (Po2 = 296 +/- 12 mmHg). Group 2 (n = 8) was subjected to a 6-min withdrawal of blood (0.9 ml) during hypoxia (72 +/- 2 mmHg) and hyperoxia Po2 = 258 +/- 8 mmHg). The slope of the pressure-flow relationship was used as an index of autoregulation so that a slope of 0 indicated complete autoregulation and a slope of 1 represented no autoregulation. The pressure-flow slopes with volume expansion were 0.54 during hypoxia and 0.15 during hyperoxia, while the slopes with volume contraction were 0.29 during hypoxia and 0.54 during hyperoxia. Thus, when arterial pressure was raised above normal, the autoregulatory capacity was greater during hyperoxia than with hypoxia. Conversely, when arterial pressure was lowered below normal, the autoregulatory capacity was greater during hypoxia than with hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Concerning reflex summation.

A simple, linear, noninteractive model of the reflex control of blood pressure was developed to demonstrate that simple linear addition of the responses of the baroreceptor reflexes can produce observations that appear to have resulted from a redundant control system. Our analysis indicated that common experimental paradigms such as hemorrhage with sequential reflex ablation, which are often used to evaluate reflex interactions, can be simply interpreted. Complex nonlinear interactions need not be postulated to explain data that appear to indicate a redundant control system.

Aorta, Thoracic↗

PubMed1988

Carotid sinus baroreceptor control of splanchnic resistance and capacity.

The contribution of the splanchnic vascular bed in the carotid sinus baroreceptor reflex control of vascular resistance and capacity was studied in nine pentobarbital-anesthetized dogs. The splanchnic circulation was vascularly isolated in an unopened abdomen and perfused at constant flow and venous pressure. Decreasing carotid sinus pressure from 200 to 50 mmHg resulted in a 72% increase in splanchnic vascular resistance and a decrease in splanchnic blood volume of 4.7 ml/kg. Changes in splanchnic inflow from 0 to 70 ml.min-1.kg-1 resulted in linear changes in splanchnic arterial pressure. Increasing carotid sinus pressure significantly decreased the slope (P less than 0.005) and intercept (P less than 0.025) of the splanchnic pressure-flow relationship. It is concluded that in the dog, the splanchnic vascular bed contributes a major portion of blood volume mobilized by the carotid sinus reflex.

Animals↗

PubMed1988

Autoregulation of the systemic circulation in conscious rats.

Autoregulation of blood flow in various organ systems is a well-documented phenomenon. However, the net effect of these regional autoregulatory responses on the systemic circulation has not been studied in conscious rats despite the now extensive use of rats in cardiovascular research. The ability of the systemic circulation to autoregulate cardiac output has been proposed to play an important role in the development of increased vascular resistance in volume-dependent forms of hypertension. To better understand these events, we characterized responses to acute increases and decreases in blood volume in conscious areflexic rats that were chronically instrumented with arterial and venous catheters and an electromagnetic flow probe around the ascending aorta. Neurohumoral blockade was achieved with chlorisondamine (10 mg/kg), methscopolamine (0.5 mg/kg), captopril (1.0 mg/kg), and d(CH2)5Tyr(Me)arginine vasopressin (10 micrograms/kg). Mean arterial pressure was restored to normal levels with a constant i.v. norepinephrine infusion, which resulted in normal values of cardiac output, total peripheral resistance, and blood gases. Blood volume expansion (0.9 ml i.v. blood infusion for 6 minutes) increased cardiac output 9 +/- 1% and mean arterial pressure 30 +/- 3% and caused a 22 +/- 2% increase in total peripheral resistance (n = 7). Blood volume contraction (6-minute withdrawal of 0.9 ml of blood) decreased cardiac output 12 +/- 1% and mean arterial pressure 26 +/- 4%, which resulted in a 16 +/- 4% decrease in total peripheral resistance (n = 8). The slopes of the pressure-flow relationships during volume expansion were 0.24 and 0.41 during volume contraction, as compared with a nonautoregulating system (slope = 1) and a completely autoregulating system (slope = 0).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Aortic arch reflex control of total systemic vascular capacity.

The ability of the aortic arch baroreceptors to change vascular capacity was measured and, in the same animal, compared with carotid sinus reflex changes in capacity. Seven dogs were anesthetized with pentobarbital sodium and perfused with constant flow. Changes in external reservoir volume reflected reciprocal changes in total systemic vascular capacity and changes in arterial pressure parallel changes in total peripheral resistance. The aortic arch and carotid sinus baroreceptor areas were isolated, and the pressures were controlled separately. With carotid sinus pressure held constant at 125 mmHg, aortic arch pressure was increased and decreased between 225 and 50 mmHg, and the changes in reservoir volume and systemic arterial pressure were measured. Results from increasing and decreasing aortic arch or carotid sinus pressure were not significantly different and were averaged. The mean change in reservoir volume was 1.9 +/- 0.2 ml/kg and the change in mean arterial pressure was 18.7 +/- 3.7 mmHg. The changes in reservoir volume and arterial pressure caused by the aortic arch reflex were not influenced by the level of carotid sinus pressure. Carotid sinus pressure changes between 200 and 50 mmHg at a constant aortic arch pressure caused reservoir volume and arterial pressure to change by 7.2 +/- 0.9 ml/kg and 45.1 +/- 4.1 mmHg, respectively. The level of aortic arch pressure did not modify these responses.

Animals↗

PubMed1986

Measurement of peripheral blood flow by thermodilution techniques.

Recent advances in the diagnosis and treatment of cardiovascular pathology, including balloon angioplasty of atherosclerotic lesions in peripheral vascular disease, have led to an increased need for in vivo quantitation of blood flow. This study has three purposes: (1) to validate thermodilution techniques as a viable method for measuring low blood flow rates, (2) to calibrate accurately thermodilution catheters at these low flows, and (3) to develop an animal model that can be used to quantitate and compare many different flow measuring techniques. Modified commercially available 6F thermodilution catheters were used with a standard cardiac output computer to measure flows between 200 and 700 ml/minute. Eight anesthetized dogs were surgically interfaced with a variable flow, pressure, and compliance carotid-carotid/jugular bypass perfusion system. Three milliliters of normal saline at room temperature were injected through the catheters intra-arterially to measure different flows below, at, and above physiologic pressures and compliances. Results of this study indicate that with proper calibration, thermodilution techniques of measuring arterial and venous flows between 200 and 700 ml/minute are simple, accurate, and reliable. Using the designed system to generate known flows in vivo at various physiologic conditions allowed easy calibration of catheters and should facilitate calibration and comparison of other measurement techniques.

Animals↗

PubMed1986

Interaction of right and left carotid sinus baroreflexes in the dog.

Carotid sinus reflex interactions were studied in 10 dogs anesthetized with pentobarbital sodium. The right and left carotid sinus regions were isolated and perfused at controlled pressures. Pressure in the right and left carotid sinuses were independently varied, and the resulting steady-state reflex changes in arterial pressure, heart rate, respiratory frequency, tidal volume, and total ventilation were measured. Reflex changes when carotid sinus pressure was changed on one side were strongly influenced by pressure in the contralateral carotid sinus (P less than 0.05). Right carotid sinus gain was found to be 0.628 +/- 0.058 at a left carotid sinus pressure of 50 mmHg and 0.148 +/- 0.027 when left carotid sinus pressure was 200 mmHg. Similar results were found for left carotid sinus gain. Suppression was also found for heart rate, respiratory rate, tidal volume, and total ventilation. The hypothesis that rapid resetting of one carotid sinus baroreflex might influence responses from the other side was also tested. Although ipsilateral resetting was consistently observed, no contralateral component of the resetting was detected. An additional inhibitory summation between the right and left carotid sinuses was found such that simultaneous excitation of both receptors resulted in a smaller reflex response than did the sum of individual responses. Sympathetic denervation of the carotid sinus region had no effect.

Animals↗

PubMed1986

Changes in canine cardiac function and venous return curves by the carotid baroreflex.

Venous return curves and cardiac function relationships were simultaneously determined in 10 pentobarbital-anesthetized dogs at three different isolated carotid sinus pressures. Changing carotid sinus pressure (CSP) between 50 and 200 mmHg produced large changes in the zero flow intercept of the venous return curves from 15.37 +/- 0.97 to 11.94 +/- 1.36 mmHg (P less than 0.001) but no change in slope. These changes in the intercept of the venous return curve were due to alterations in systemic vascular capacity caused by the carotid sinus baroreceptor reflex. Changes in the cardiac function curve with baroreceptor pressure were masked by concomitant changes in arterial pressure afterload; however, when arterial pressure was controlled, there was a significant change in the slope of the cardiac function curve from 60.32 +/- 26.9 to 37.06 +/- 13.31 ml X min-1 X kg-1 X mmHg-1 as CSP was changed from 50 to 200 mmHg. We conclude that changes in vascular capacity are the primary mechanism responsible for changes in cardiac output during activation of the carotid sinus baroreflex.

Animals↗

PubMed1984

Interaction of canine carotid sinus and aortic arch baroreflexes in the control of total peripheral resistance.

Interaction of carotid sinus and aortic arch reflex control of total peripheral resistance was studied in eight dogs anesthetized with sodium pentobarbital and placed on constant flow cardiac bypass. Carotid sinus and aortic arch baroreceptor areas were isolated and separately perfused at controlled pressures. Combinations of carotid sinus and aortic arch pressures were delivered at random in steps of 25 mm Hg over the 50-225 mm Hg pressure range, and systemic arterial pressure was measured. Changes in arterial pressure reflected changes in total peripheral resistance. A multiple linear regression showed that both carotid sinus and aortic arch pressures exhibited a sigmoidal relationship with arterial pressure. Independent of carotid and aortic baroreceptor pressures, arterial pressure was found to be a periodic function of time (period = 2 hours) in all dogs. The average carotid sinus reflex open loop gain was found to be 0.231 +/- 0.092, while average aortic arch open loop gain was 0.141 +/- 0.088. The gain of either the carotid sinus or aortic arch reflex was not influenced by the absolute pressure level of the other receptor area. In a separate series of experiments performed in the same dogs, we tested the hypothesis that a nonlinear temporal summation of the reflex control of total peripheral resistance might exist when the inputs to carotid and aortic baroreceptors are changed simultaneously. With both inputs held at the region of maximum gain, 25 mm Hg step changes were imposed first on carotid sinus pressure, then on aortic arch pressure, and then on both simultaneously. A temporal inhibition of the two reflexes showed that simultaneous excitation of both receptors resulted in a smaller reflex response than the sum of individual responses.

Animals↗