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Biomedical subjects

R L Hester

Publications and source records attributed to R L Hester.

36 records · Page 2Linked to original sources
PubMed1993

Endothelium-derived relaxing factor responses in Doca-salt hypertensive rats.

This study examined the contribution of endothelium-derived relaxing factor (EDRF) to the susceptibility of uninephrectomized rats to deoxycorticosterone acetate (DOCA)-salt hypertension. N omega-nitro-L-arginine, a probe for EDRF, produced smaller increases (P < 0.001) in mean arterial pressures in anesthetized hypertensive DOCA-salt rats than in sham rats. Acute L-arginine administration (300 mg/kg body wt i.v.) failed to reduce pressure in anesthetized DOCA-salt rats. Chronic oral and intraperitoneal L-arginine did not lower pressure in conscious DOCA-salt rats with established hypertension, nor did it prevent hypertension when begun in prehypertensive DOCA-salt rats. Preconstricted aortic rings from DOCA-salt rats had attenuated relaxation to acetylcholine compared with sham rats. Rings L-arginine-treated DOCA-salt rats had responses similar to DOCA-salt rats. Relaxation to nitroprusside was not different between any rat group. Thus EDRF is attenuated in DOCA-salt hypertension. However, unlike several other hypertensive models, the blunted EDRF response cannot be overcome by provision of L-arginine. These data suggest synthesis or release of EDRF may be noncompetitively inhibited in DOCA-salt hypertension.

Acetylcholine↗
PubMed1993

Role of pressure natriuresis in long-term control of renal electrolyte excretion.

If pressure natriuresis is to play an important role in arterial pressure control, renal perfusion pressure must have a long-term effect on urinary sodium excretion. The aim of this study was to quantitate the importance of renal perfusion pressure per se in controlling renal hemodynamics and electrolyte excretion chronically. Female mongrel dogs (n = 6) were instrumented with bilateral renal artery catheters for measurement of renal perfusion pressure and occluders on both renal arteries for servo-control of renal perfusion pressure at different levels; the urinary bladder was split for determination of renal clearances and electrolyte excretion from each kidney separately. Because both kidneys were exposed to the same neurohumoral influences, any changes in renal function could be attributed to differences in renal perfusion pressure between the two kidneys. After 5 days of control, renal perfusion pressure to one kidney was reduced from 86.7 +/- 0.2 to 74.2 +/- 0.6 mm Hg for 12 days, and pressure in the contralateral kidney increased to 91.5 +/- 0.4 mm Hg. Sodium excretion decreased from 41 +/- 2 to 25 +/- 1 mmol/d in the servo-controlled kidney and increased from 41 +/- 1 to 55 +/- 1 mmol/d in the contralateral kidney during 12 days of servo-control. Urine volume, chloride excretion, and potassium excretion exhibited similar patterns during servo-control. In addition, autoregulation of effective renal plasma flow and glomerular filtration rate was relatively well maintained; however, in the low-pressure kidney, glomerular filtration rate was slightly but significantly lower (approximately 8%) than in the contralateral kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

The determination of hemodialysis blood recirculation using blood urea nitrogen measurements.

The determination of blood recirculation using blood urea nitrogen (BUN) measurements in hemodialysis patients is a standard technique. The accuracy and reproducibility of these calculations have never been determined. Two pairs of recirculation studies (study A and study B) were performed in 13 patients during a single dialysis treatment. Blood samples were analyzed for BUN and recirculation was calculated. The first recirculation study (study A) was performed within 1 hour of the initiation of dialysis, with a duplicate test of recirculation performed within 15 minutes. In study B, the dialyzer blood lines were reversed in an attempt to enhance blood recirculation. After 15 minutes, duplicate tests of recirculation were again performed. Calculated recirculations before the line reversal (study A) ranged from -3.3% to 11.9% in the first test and -2.9% to 12.2% in the second test. In study A, there was no correlation (P > 0.05, r = 0.09) between the first and second calculated recirculations. In study B, an increase in recirculation was observed. Calculated recirculations ranged from 16.3% to 53.5% for the first test and 5.4% to 58.1% for the second test. A significant relationship was observed in the calculated recirculation in study B (P < 0.05, r = 0.81). The results from the present study show that the use of BUN measurements may not provide a consistent indicator of access recirculation in a patient with a low recirculation. This lack of consistency should be considered when determining further clinical treatment.

Adult↗
PubMed1992

Hemodynamic changes in rats after opening an arteriovenous fistula.

Time course of multiple hemodynamic changes in rats after opening an AV fistula was assessed. The fistula was made in male Sprague-Dawley rats by anastomosing the aorta and vena cava below the renal arteries. At 1 h (1H), 1 day (1D), 1 wk (1W) and 5 wk (5W) in sham controls or after opening an AV fistula, we measured cardiac output (CO) and tissue flows by using radioactive microspheres. The flow of microspheres to the lungs was used as a measure of shunt flow. In the fistula animals this lung flow (fistula flow) was 50-77% of the CO compared with 1-3% in the control animals. Cardiac index in the fistula animals increased by 40, 107, 129, and 307% compared with the respective control animals in the consecutive time groups. Systemic flow, tissue flows, and mean arterial blood pressure (MAP) in the fistula animals in the 1H and 1W groups were significantly decreased below control values, but each of these variables returned to control levels after 5W. Hematocrit (Hct) significantly decreased, whereas right atrial pressure (RAP) gradually increased over the experimental period. These two observations suggest retention of fluid. Plasma renin activity increased in the 1H animals but returned to control in the 1D animals. Atrial natriuretic peptide (ANP) gradually increased throughout the 5 wk from 86 +/- 22 (1H) to 709 +/- 217 pg/ml (5W). The increase in ANP correlated with the increase in RAP. Calculated total peripheral resistance in fistula animals was significantly decreased throughout the experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Hemodynamic studies in DOCA-salt hypertensive rats after opening of an arteriovenous fistula.

We determined the cardiovascular responses in normal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats with reduced total peripheral resistance due to an arteriovenous (a-v) fistula. Animals were divided into four groups: control, fistula, DOCA-salt, and DOCA-salt fistula. The fistula was made by anastomosing the aorta and vena cava below the renal arteries. Four weeks after the creation of the fistula both DOCA-salt and DOCA-salt fistula animals received DOCA and salt for 6-8 wk. At the end of 10-12 wk we measured mean arterial pressure, cardiac output, tissue flows, and right atrial pressure. Flow measurements using radioactive microspheres were made in anesthetized animals. Cardiac index (CI) was 202% higher in the fistula group than in the control animals and 165% higher in the DOCA-salt fistula than in the DOCA-salt animals. There was no difference in cardiac output between the control and DOCA-salt animals. The increase in cardiac output was due to the fistula flow as evidenced by a significant increase in the number of microspheres in the lung. Mean arterial pressure was 115 +/- 4 mmHg (control) and 108 +/- 5 mmHg (fistula) in non-DOCA rats but increased in both DOCA groups, 159 +/- 3 mmHg (DOCA-salt) and 145 +/- 5 mmHg (DOCA-salt fistula). Right atrial pressure was increased above control in both fistula animals but was normal in DOCA-salt animals. Total peripheral resistance (TPR) was higher than control in DOCA-salt animals, but TPR in both the fistula and DOCA-salt fistula animals was lower than control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Development of hypertension in animals with reduced total peripheral resistance.

The object of the present study was to determine whether deoxycorticosterone acetate (DOCA)-salt hypertension can be produced in rats in the presence of low total peripheral resistance (TPR) induced by long-term administration of minoxidil, a vasodilator. The rats were divided into four groups: sham-control, DOCA-salt, minoxidil, and DOCA-salt with minoxidil. The rats in both DOCA groups had DOCA pellets implanted subcutaneously and were given saline to drink. The rats in both minoxidil groups were given minoxidil (3 mg/day) in the drinking water throughout the experiment. Final measurements, including mean arterial blood pressure, cardiac index, and renal blood flow were made after 4-6 weeks. Flow measurements were made using radioactive microspheres. Cardiac index (ml.min-1.100 g-1) in sham-control rats averaged 18 +/- 2 and was higher in the other groups: 23 +/- 4 (DOCA-salt), 25 +/- 2 (minoxidil), and 30 +/- 2 (DOCA-salt plus minoxidil). Mean arterial pressure (mm Hg) was increased in both DOCA-salt rats (160 +/- 8) and DOCA-salt plus minoxidil rats (153 +/- 5) as compared with sham-control (116 +/- 2) and minoxidil (113 +/- 3) rats. There was no significant difference in TPR between the sham-control and DOCA-salt rats, but TPR in minoxidil and DOCA-salt plus minoxidil rats was 30% and 28% lower than that in untreated sham-control and DOCA-salt hypertensive rats, respectively. In contrast, renal vascular resistance was significantly increased in both DOCA-salt groups as compared with non-DOCA-salt groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Hormonal and circulatory responses to chronically controlled increments in right atrial pressure.

To study the time-dependent changes in the secretion of atrial natriuretic peptide (ANP) in response to chronic stimulation by controlled increments in atrial pressure, we developed methodology for precise control of right atrial pressure (RAP) in dogs by employing an externally adjustable occluder around the pulmonary artery and a servo-control system. During 7 days of servo-control of RAP at 6.3 +/- 0.1 mmHg above control levels (1.3 +/- 0.1 mmHg), the 24-h coefficient of variation in RAP was 1/45 the variation that occurred under control conditions. After 30 min of increased RAP, mean arterial pressure (MAP) was reduced from 101 +/- 4 to 84 +/- 3 mmHg in association with increments in plasma renin activity (PRA) from 0.6 +/- 0.1 to 2.5 +/- 0.9 ng angiotensin I (ANG I).ml-1.h-1 and in the plasma concentrations of ANP, arginine vasopressin (AVP), and epinephrine from 93 +/- 18 to 484 +/- 61 pg/ml, from 0.5 +/- 0.1 to 9.2 +/- 2.4 pg/ml, and from 82 +/- 27 to 585 +/- 133 pg/ml, respectively. In comparison, on day 7 of servo-control of RAP, sodium balance was achieved and MAP remained depressed (82 +/- 4 mmHg) along with sustained increments in both plasma ANP concentration (482 +/- 67 pg/ml) and PRA (1.7 +/- 0.6 ng ANG I.ml-1.h-1); on the other hand, the plasma concentrations of AVP and epinephrine returned to control levels. This quantitative study indicates that ANP secretion does not chronically adapt to stimulation by increased atrial pressure and suggests that the plasma levels of ANP achieved in heart failure markedly increase renal excretory capability and allow fluid balance to be achieved at a substantial fall in renal perfusion pressure.

Angiotensin I↗
PubMed1990

Venular-arteriolar diffusion of adenosine in hamster cremaster microcirculation.

During increases in blood flow, both the terminal and the proximal arterioles dilate. The mechanism behind the dilation of the proximal arterioles is not known but may be the result of the diffusion of a vasoactive metabolite from adjacent venules. To determine whether an increase in venous adenosine (ADO) concentration could affect an adjacent arteriole, venules were perfused using a micropipette containing 10(-7)-10(-4) M ADO. During the venular perfusion, arteriolar diameter and red blood cell velocity were measured at a site 0.5 to 6 mm from the micropipette tip. The adjacent arteriole of the venular arteriolar pair dilated 29 +/- 3% with a 5-s 10(-4) M ADO perfusion, 32 +/- 4% with a 10-s 10(-4) M ADO perfusion, and 85 +/- 22% with a 60-s 10(-4) M ADO perfusion. One and 2-min perfusions with 10(-5) M ADO resulted in a 36 +/- 6% and 33 +/- 4% increase in diameter of the paired arteriole, respectively. The red blood cell velocity responses were variable, yet, on average, calculated blood flow increased in each group of experiments. Venular perfusions with saline resulted in a 2% change in arteriolar diameter. To rule out nondiffusional effects, venular perfusions were performed when the arteriole was not paired with the venule but crossed the venule. Venular perfusion with 10(-6) and 10(-7) M ADO resulted in a significant increase in diameter of the crossing arteriole of 19 +/- 3% and 6 +/- 2%, respectively. Therefore, the diffusion of a vasoactive metabolite from a venule to an arteriole may provide a mechanism by which the tissue can send a signal to cause a dilation of the more proximal arterioles.

Abdomen↗
PubMed1988

Red cell velocity during functional hyperemia: implications for rheology and oxygen transport.

Muscle blood flow increases during work. Any associated change in blood velocity that occurs during functional hyperemia can have profound effects on wall shear rate and arteriolar hemoglobin saturations. We measured arteriolar red cell velocity and cross-sectional area during muscle contraction to determine the physiological significance of any of these changes in calculations of wall shear rate and the in situ spectrophotometric measurement of hemoglobin oxygen saturation. Calculated cremaster muscle blood flow increased 64-236% during twitch and tetanic stimulation, respectively, which was due entirely to an increase in cross-sectional area, with muscle work producing little change in either the red cell velocity or the calculated wall shear rate. Small changes ranging from a 3% increase to a 4% decrease in hemoglobin saturation were evident in second- and third-order arterioles, which apparently reflects offsetting effects of the increase in metabolic rate and the increase in arteriolar blood volume. A simple model explaining the microcirculatory adjustments made during muscle work requires dilation of both feed arteries and arterioles if red cell velocity is to remain constant during hyperemia.

Animals↗
PubMed1986

Spindle activity in the waking electroencephalogram: report of a case with hemispheric glioblastoma.

In this paper, we reported a patient with a hemispheric glioblastoma extending into the lateral thalamus and the posterior limb of the internal capsule. The waking electroencephalogram showed spindle activity on the side ipsilateral to the tumor. Based on the topography of the tumor in our patient, we speculate that a disruption of the synaptic pathways within the thalamus-cortex-thalamus circuit was primarily involved in the pathogenesis of abnormal spindling.

Aged↗
PubMed1986

Mechanisms of sodium balance in hypertension: role of pressure natriuresis.

This paper summarizes the role of the renal pressure natriuresis and diuresis mechanisms in maintaining sodium and water balance in hypertension. In all forms of chronic hypertension studied to date, the renal pressure natriuresis and diuresis mechanisms are abnormal, since increased arterial pressure is required to maintain normal excretion of sodium and water, and therefore fluid balance. When renal perfusion pressure is prevented from increasing in various forms of experimental hypertension, caused by infusion of mineralocorticoids, angiotensin II, vasopressin, or norepinephrine and adrenocorticotrophic hormone (ACTH), sodium and water retention continues until ascites, pulmonary oedema and circulatory collapse occur within a few days. Thus, chronic hypertension appears to be an essential homeostatic response that permits sodium and water balance to be maintained despite various abnormalities which tend to decrease renal excretory capability. The intrarenal mechanisms by which increased renal perfusion pressure maintains sodium and water balance in hypertension have not been fully elucidated, but appear to involve small changes in glomerular filtration rate (GFR) and reductions in fractional sodium reabsorption, due either to the direct hydraulic effects of pressure or to various indirect effects, such as changes in angiotensin II formation.

Adrenocorticotropic Hormone↗
PubMed1985

Interactions between adenosine and angiotensin II in controlling glomerular filtration.

This study examined interactions between adenosine (Ado) and angiotensin II (ANG II) in controlling renal blood flow (RBF) and glomerular filtration rate (GFR). In six normal dogs, intrarenal Ado infusion (1.0 mumol/min) transiently decreased RBF, but during sustained Ado infusion RBF increased to 122 +/- 7% of control, although GFR remained at 75 +/- 6% of control. Blockade of ANG II formation with the converting enzyme inhibitor SQ 14225 (n = 6) almost abolished the transient decrease in RBF but did not prevent the sustained fall in GFR caused by Ado. When circulating ANG II was held constant by intravenous infusion of SQ 14225 and 20 ng . kg-1 . min-1 of ANG II (n = 6), Ado transiently decreased RBF but the return of RBF was much slower than in normal dogs and RBF did not increase above control. Maintenance of constant circulating ANG II did not prevent Ado-mediated decreases in GFR. These observations suggest that Ado-mediated reductions in GFR do not depend entirely on ANG II and may be due to dilation of efferent arterioles by Ado. However, the transient renal vasoconstriction caused by Ado depends on ANG II, and data from this study suggest that part of the waning constrictor response to Ado is due to suppression of renin secretion and endogenous ANG II formation. In circumstances where high ANG II levels are maintained (i.e., ischemic renal failure), Ado may be capable of causing sustained renal vasoconstriction.

Adenosine↗
PubMed1984

Mechanisms of escape from sodium retention during angiotensin II hypertension.

This study examined the role of increased renal arterial pressure (RAP) in renal escape from the chronic Na-retaining effects of angiotensin II (ANG II). When RAP was allowed to increase during ANG II infusion (5 ng X kg-1 X min-1), urinary Na excretion (UNaV) decreased transiently on the first day but there was no significant change in Na iothalamate space or cumulative Na balance when ANG II infusion was continued for 6 days. Mean arterial pressure (MAP) rose from 100 +/- 3 to 132 +/- 2 mmHg after 3 days and remained near that level for the next 5 days of ANG II infusion. When RAP was prevented from rising with a servo-controlled aortic occluder, UNaV remained below control even after 6 days of ANG II infusion, cumulative Na balance increased by 210 +/- 37 meq, and Na iothalamate space rose by 1,158 +/- 244 ml. MAP did not plateau when RAP was servo-controlled during ANG II infusion but continued to rise and after 6 days averaged 157 +/- 3 mmHg. In three of the eight dogs in which RAP was servo-controlled during ANG II infusion, Na and water retention became so severe that MAP increased to 165-180 mmHg and pulmonary edema developed within 4-6 days. These data suggest that a rise in RAP is essential in allowing the kidneys to escape from the chronic Na-retaining actions of ANG II and in attaining Na balance and a stable level of MAP without severe volume expansion.

Aldosterone↗
PubMed1983

Acute and chronic servo-control of renal perfusion pressure.

We describe a servo-control system for acute and chronic regulation of renal perfusion pressure or pressures in other parts of the circulation. The system employs a Dacron-reinforced inflatable silastic occluder of sufficient strength and durability to produce large pressure gradients for long periods of time (at least 10 days) in the abdominal aortas of large dogs. The occluder is inflated with an inexpensive, bidirectional DC motor syringe pump that is controlled by a comparator feedback circuit connected to the output of a driver amplifier of a Grass polygraph or any other suitable recorder. The system has a rapid response time for precise control and has been used to maintain a constant renal perfusion pressure in experiments lasting as long as 10 days. The system has diverse applications in studies of acute or chronic regulation of renal hemodynamics as well as the hemodynamics of other organ systems. The main advantages of this system, besides its durability and precision of control, are that it is very inexpensive (total cost including the syringe pump is less than $150), easy to construct, and can be used in chronic studies for servo-controlling renal perfusion pressure or pressures in other parts of the circulation.

Animals↗
PubMed1982

Reactive and exercise hyperemia during high levels of adenosine infusion.

In these experiments we tested the quantitative importance of adenosine as a mediator in the regulation of muscle with blood containing adenosine at concentrations more than 1,000 times the normal resting adenosine level (1, 7) so that the effect of any endogenously released adenosine would be miniscule in comparison with the effect of this perfused adenosine. Therefore, any major blood flow responses that should occur while the muscle remained continuously under the influence of the perfused adenosine could hardly be ascribed to endogenous adenosine. At the onset of the perfusion with the adenosine the blood flow increased approximately sevenfold. However, over 1-3 h of continued perfusion, the blood flow returned to or near to control despite the extreme amounts of adenosine. Then, while the muscle was still exposed to the adenosine, both reactive hyperemia and exercise hyperemia were elicited for varying time periods and varying degrees for a total of 96 separate measurements in 12 preparations. In all instances the increases in blood flow during hyperemia were almost exactly identical to those recorded prior to adenosine perfusion. Because it would have been almost impossible for the small amounts of endogenous adenosine to cause the large hyperemia responses in the face of the extreme amounts of perfused adenosine, it is concluded that both the reactive and exercise hyperemia responses are probably caused either entirely or almost entirely by factors other than adenosine.

Adenosine↗
PubMedDate not supplied

Non-invasive determination of recirculation in the patient on dialysis.

Recirculation of blood flow occurs when the fistula flow rate is inadequate to support the desired dialyzer blood flow. The percentage recirculation is normally calculated using the blood urea nitrogen of blood samples from the two dialyzer blood lines and a peripheral blood sample. However, this method is time consuming, costly, and may not always give accurate measurements. A technique was developed to measure recirculation using the injection of saline into the venous dialysis line. For this technique, an optical detector is placed across the arterial dialysis tubing, and the light intensity, which is proportional to the hematocrit, is continually measured using a computerized data collection system. After a baseline data collection period, 10 ml of saline is injected into the venous dialysis line using the sampling port. The saline that appears in the arterial dialysis line as a result of recirculation will cause a dilution of the blood and an increase in light intensity. In vitro testing showed an excellent correlation between the area under the dilution curve and percentage recirculation. This technique will provide a quick, inexpensive, and reliable measurement of recirculation.

Arteriovenous Shunt, Surgical↗