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R W Barbee

Publications and source records attributed to R W Barbee.

36 records · Page 2Linked to original sources
PubMed1992

Microsphere and dilution techniques for the determination of blood flows and volumes in conscious mice.

Although the mouse is the most commonly used transgenic species, little is known regarding cardiovascular and fluid homeostasis in this animal. Therefore, the reference microsphere and dilution techniques were adapted for the measurement of cardiac output (CO), regional blood flows, and intravascular fluid volumes in the conscious mouse. Previously acclimatized C3H mice were studied 4-5 h after surgery and recovery from anesthesia. Approximately 40,000 85Sr-labeled microspheres were injected into the left ventricle while a reference sample was withdrawn at one of two rates from the femoral artery. 51Cr and 125I were used for the determination of blood volume (BV), plasma volume (PV), and Fcells ratio (whole body hematocrit/large vessel hematocrit). CO and BV in the conscious mouse were 16 +/- 1.4 ml/min and 2.3 +/- 0.1 ml, respectively. Anesthesia lowered heart rate, blood pressure, PV, and altered the distribution of CO. Two successive injections of 15,000-20,000 microspheres were tolerated in the mouse without an increase in total peripheral resistance. The results indicate that the microsphere and indicator dilution techniques can be applied to study cardiovascular and fluid homeostasis in the mouse.

Animals↗
PubMed1992

Effect of endothelin on plasma volume and albumin escape.

Previous studies have demonstrated that endothelin-1 (ET-1) is a potent vasoconstrictor that decreases cardiac output and increases hematocrit. The present study was designed to determine if the rise in hematocrit and decrease in cardiac output are in part due to shifts of plasma from the vascular space to the interstitial space. Red blood cell volume and plasma volume were determined by using chromium-51-labeled erythrocytes and iodine-125-labeled albumin, respectively, in anesthetized, nephrectomized, splenectomized rats. The present study demonstrates that ET-1 increases mean arterial pressure and hematocrit. This effect is associated with an increase in total-body albumin escape, which is reflected by a marked reduction in whole-body plasma volume. ET-1 enhanced albumin escape primarily in the liver, lung, and heart at low doses. At high doses, albumin escape increased primarily in the liver, heart, and gastrointestinal tract but not the lung. The present study demonstrates that ET-1 increases hematocrit independent of splenic contraction or renal losses by enhancing loss of plasma volume to the interstitial space without affecting red blood cell volume. Because of the profound pressor effects of ET-1, it is likely that the plasma loss results from increased capillary hydrostatic pressure.

Animals↗
PubMed1991

Chronic vs. acute hemodynamic effects of atrial natriuretic factor in conscious rats.

The present study was designed to examine acute (2 h) and chronic (5 day) effects of pathophysiological elevations of plasma atrial natriuretic factor (ANF) in conscious normotensive rats. Acute infusion of ANF (100 ng.kg-1.min-1; n = 15) resulted in a decrease in mean arterial pressure (MAP) of 5 +/- 3 mmHg, which was associated with a 23 +/- 4% decrease in cardiac output (CO) and a 27 +/- 6% increase in total peripheral resistance (TPR). Hematocrit increased from 41.9 +/- 0.7 to 46.0 +/- 0.6%, which is suggestive of vascular volume contraction. Chronic infusion of ANF (n = 9) produced a significant fall in MAP from a control value of 114 +/- 2 to 100 +/- 3 and 99 +/- 2 mmHg on days 1 and 5, respectively. CO decreased significantly (27 +/- 2%) and TPR increased (21 +/- 5%) on day 1; neither variable was significantly different from control on day 5. Plasma immunoreactive ANF levels were significantly elevated during acute (791 +/- 76 pg/ml) and chronic (626 +/- 202 pg/ml) ANF infusion compared with control values of approximately 100 pg/ml. The results indicate that elevations in plasma ANF within the pathophysiological range can significantly alter systemic hemodynamics, initially mediated by a decrease in CO. Autoregulatory phenomena may counteract these hemodynamic effects, returning CO to control levels and reducing TPR when the elevations in plasma ANF are chronically sustained.

Animals↗
PubMed1990

Cardio-renal effects of endothelin-3 in the rat.

Endothelin-3 (ET-3), a recently described vasoconstricting peptide was infused in Inactin anesthetized rats at 0, 40, 170 or 340 ng/kg/min for 45 minutes (n = 8 in each group). ET-3 infusion increased mean arterial pressure at all infusion rates by increasing total peripheral resistance. Cardiac output (delta CO) was significantly decreased at the two highest ET-3 infusion doses. The decrease in cardiac output was associated with a decrease in central venous pressure and stroke volume and an increase in hematocrit. ET-3 infusion at 40 ng/kg/min increased sodium excretion (delta UNaV) by 0.14 +/- 0.08 microEq/min (p less than 0.05 compared to vehicle infusion) without affecting the glomerular filtration rate (GFR). At higher infusion rates ET-3 markedly decreased the GFR, urine flow and urinary potassium excretion. ET-3 infusion significantly increased circulating levels of ANF. The present study demonstrates that ET-3 increases blood pressure by increasing total peripheral resistance but decreases cardiac output. Further, ET-3 has natriuretic effects at low doses but markedly attenuates renal function at high doses.

Animals↗
PubMed1990

Atrial natriuretic factor blocks the pressor action of endothelin.

The present study was designed to determine the pharmacologic effects of rat atrial natriuretic factor (r-ANF; 250 ng/kg/min), endothelin-3 (ET-3; 340 ng/kg/min), and combined r-ANF and ET-3 infusion on cardiac hemodynamics and renal function in anesthetized rats. The change in mean arterial pressure (delta MAP) was 13 +/- 2 mm Hg during ET-3 infusion alone. Delta MAP was -9 +/- 2 mm Hg during r-ANF infusion alone. Combined infusion of ET-3 and r-ANF resulted in a change in MAP of -7 +/- 3 mm Hg. The decrease in MAP during combined infusion of ET-3 and r-ANF occurred due to a decrease in cardiac output. Infusion of r-ANF did not block the cardiac output. Infusion of r-ANF did not block the ET-3-induced increase in total peripheral resistance (TPR). Infusion of r-ANF alone resulted in an 11-fold increase in urinary sodium excretion. ET-3 infusion completely blocked the ANF-induced natriuresis in part by markedly decreasing the glomerular filtration rate (GFR). ET-3 or r-ANF infusion alone resulted in two- or eightfold increases, respectively, in circulating r-ANF levels compared to vehicle alone. However, combined infusion of r-ANF and ET-3 resulted in a dramatic 27-fold increase in circulating r-ANF when compared to levels obtained during vehicle infusion alone. The present study demonstrates that at pharmacologic levels, r-ANF blocks the pressor action of ET-3 by decreasing cardiac output rather than TPR. Furthermore, ET-3 blocks the natriuretic action of r-ANF, partly by decreasing GFR.

Anesthesia↗
PubMed1990

Atrial appendectomy reduces ANF but not sodium excretion in acute vasopressin hypertension.

The present study was designed to determine whether atrial appendectomy would decrease the sodium excretion associated with pressor doses of arginine vasopressin (AVP) infusion in rats by decreasing circulating levels of atrial natriuretic factor (ANF). Ten to 21 days after either sham (n = 9) or bilateral atrial appendectomy (n = 13) AVP (19 ng.kg-1.min-1) was infused for 90 min in anesthetized Sprague-Dawley rats. Atrial appendectomy decreased circulating ANF levels from 469 +/- 70 pg/ml in sham-operated animals to 259 +/- 50 pg/ml (P less than 0.05) in atrial-appendectomized animals after 90 min of AVP infusion. Despite a reduction in circulating levels of ANF, sodium excretion, potassium excretion, and urine flow increased and were not affected by bilateral atrial appendectomy. Glomerular filtration rate and mean arterial pressure significantly increased in both groups of rats. The present study supports non-ANF factors such as increases in renal perfusion pressure and/or glomerular filtration rate as potential mechanisms in AVP-induced natriuresis.

Acute Disease↗
PubMed1990

Sympathectomy fails to reveal prominent vasodilation by atrial natriuretic factor.

Reflex activation of the sympathetic nervous system may conceal direct vasodilatory actions of atrial natriuretic factor and mediate atrial natriuretic factor-induced increases in total peripheral resistance. We determined whether peripheral sympathectomy would enhance the hypotensive actions of atrial natriuretic factor and convert the increase in total peripheral resistance to peripheral vasodilation. Sympathectomized rats studied included 1) conscious rats treated with 6-hydroxydopamine alone (partially sympathectomized) and 2) conscious anephric rats sympathectomized with adrenal demedullation and 6-hydroxydopamine (totally sympathectomized), with vascular tone returned to levels of sham-operated (control) rats with norepinephrine infusion. Sympathectomized rats and appropriate control rats received rat atrial natriuretic factor infusion (0.5 microgram/kg/min) or vehicle for 1 hour. Atrial natriuretic factor infusion lowered mean arterial pressure and increased hematocrit in control rats but not in partially sympathectomized rats. Changes in cardiac output and total peripheral resistance were not significantly different between control and partially sympathectomized rats. In totally sympathectomized rats, atrial natriuretic factor lowered mean arterial pressure more than in control rats; changes in cardiac output were nearly identical in both groups, but there were no changes in total peripheral resistance from control levels in the totally sympathectomized group. Changes in plasma volume and central venous pressure were similar in totally sympathectomized rats and control rats. These findings suggest that reflex sympathetic activity largely mediated atrial natriuretic factor-induced increases in total peripheral resistance but failed to reveal an atrial natriuretic factor-mediated sustained vasodilation in the absence of sympathetic reflexes. Furthermore, atrial natriuretic factor decreased cardiac output, central venous pressure, and plasma volume independent of the sympathetic nervous system.

Adrenal Medulla↗
PubMed1990

High-dose atrial natriuretic factor enhances albumin escape from the systemic but not the pulmonary circulation.

Atrial natriuretic factor (ANF) causes plasma fluid to shift out of the circulation and enhances the escape of radiolabeled albumin. Examination of the mechanisms by which ANF alters microcirculatory fluid and protein transfer will likely require studies in localized vascular regions. This study was aimed at determining the specific organs in which ANF increases the escape of albumin. Anesthetized, splenectomized rats that had both kidneys removed were infused with vehicle alone or rat ANF-(99-126) at 0.025, 0.05, 0.1, or 0.5 micrograms.min-1.kg-1 for 2 hours (n = 8 per group). Total red cell and plasma volumes were measured with chromium-51-labeled erythrocytes and iodine-125-labeled albumin, respectively. At the end of 2 hours, the rats were frozen in liquid nitrogen, and organ blood volumes and tissue 125I-albumin were determined. ANF decreased plasma volume at infusion rates of 0.1 and 0.5 micrograms.min-1.kg-1. ANF increased the rate at which 125I-albumin escaped from the overall circulation at infusion rates of 0.1 and 0.5 micrograms.min-1.kg-1. At an ANF infusion rate of 0.1 micrograms.min-1.kg-1, the albumin escape rate increased in the gastrointestinal tract, skeletal muscle, heart, and lungs. At an infusion rate of 0.5 micrograms.min-1.kg-1, the albumin escape rate increased in the gastrointestinal tract, muscle, and skin, but not the lungs. These findings suggest that at pathophysiological levels, ANF shifts protein out of the circulation in peripheral vascular beds and the lungs and may contribute to pulmonary edema in states such as congestive heart failure. At pharmacological levels, ANF may be protective of the lungs by preventing increased pulmonary albumin escape.

Animals↗
PubMed1989

Exercise training attenuates the myocardial dysfunction induced by endotoxin.

The purpose of this study was to determine whether exercise training protected against endotoxin-induced myocardial dysfunction. After a 12-wk treadmill training period, carotid catheters were implanted 24 h before saline or endotoxin administration into four groups of animals: trained saline-injected (TS), trained endotoxin-injected (TE), sedentary saline-injected (SS), and sedentary endotoxin-injected (SE). Heart rate and mean arterial pressure were monitored 4 h after in vivo endotoxin or saline injection. Mean arterial pressure decreased an average of 32 +/- 3 mmHg 1 h after endotoxin administration but was normal (109 +/- 6 mmHg) 2 h later. Plasma catecholamines, in vitro myocardial performance, and isolated myocyte adenosine 3',5'-cyclic monophosphate (cAMP) production in response to isoproterenol were assessed 4 h after endotoxin injection. Plasma catecholamine levels were 5- to 15-fold higher in SE compared with the other groups. These data suggest that myocardial protection may be related to the lowered catecholamine levels elicited in TE compared with SE in response to endotoxin administration. The product of cardiac output and peak systolic pressure, an index of cardiac work, was 24-32% greater in TS compared with SS. Cardiac work was decreased 32% in TE compared with a 45% decrease in SE. cAMP was reduced in myocytes from SE in response to isoproterenol (-28%) and to forskolin (-44%) but not in myocytes from TE, compared with TS and SS. The difference in cAMP accumulation suggests that training maintains the integrity of the beta-adrenergic receptor adenylate cyclase system, which can be depressed by in vivo endotoxin administration.

Animals↗
PubMed1988

T3 treatment does not prevent myocardial dysfunction in chronically diabetic rats.

The isolated working heart preparation was used to investigate the effect of continuous triiodothyronine (T3) administration on cardiac function and metabolism of rats rendered diabetic for a period of 4 wk with streptozocin (STZ). T3 controlled-release pellets were implanted 1 wk after STZ (70 mg/kg) injection. Rats injected with citrate buffer without STZ received T3 pellets 1 and/or 2 wk later. A comparable number of rats received placebo pellets. Untreated diabetic rats exhibited a decrease in spontaneous heart rate and myocardial cytochrome c concentrations concurrent with depressed plasma T3 values compared with untreated controls. T3 treatment did not improve in vitro cardiac performance (assessed as cardiac output times peak systolic pressure per gram dry heart weight) in hearts from diabetic rats perfused with glucose alone. Addition of octanoate reversed this depression and improved cardiac function to a greater extent in treated than in untreated diabetic animals. However, these differences between treated and untreated diabetic animals disappeared when heart rate was controlled by cardiac pacing. Furthermore, T3 treatment of controls and diabetics did not alter the oxidation of octanoate or the cardiac responsiveness to isoproterenol. These results suggest that experimental diabetic cardiomyopathy is partly attributable to a substrate deficiency and is not due entirely to hypothyroidism.

Animals↗
PubMed1988

Increased ANF secretion after volume expansion is preserved in rats with heart failure.

To examine whether the failing heart has reached a maximal capacity to increase plasma atrial natriuretic factor (ANF) concentration, the change in plasma immunoreactive ANF level due to acute blood volume expansion was determined in conscious rats with chronic heart failure. Varying degrees of myocardial infarction and thus heart failure were induced by coronary artery ligation 3 wk before study. Compared with controls, infarcted rats had decreases in mean arterial pressure (-10 mmHg, P less than 0.01), cardiac index (-27%, P less than 0.001), renal blood flow (-35%, P less than 0.01), and peak left ventricle-developed pressure after aortic occlusion (an index of pressure generating ability; -15%, P less than 0.01), and increases in central venous pressure (+1.7 mmHg, P less than 0.01), left ventricular end-diastolic pressure (+10 mmHg, P less than 0.001), total peripheral resistance (+28%, P less than 0.01), and plasma ANF level (752 +/- 109 vs. 244 +/- 33 pg/ml, P less than 0.001). Plasma ANF was correlated with infarct size, cardiac filling pressures, and left ventricle pressure-generating ability. At 5 min after 25% blood volume expansion, plasma ANF in rats with heart failure increased by 2,281 +/- 345 pg/ml; the magnitude of the changes in circulating ANF and hemodynamic measurements was similar in controls. The results suggest that plasma ANF level can be used as a reliable index of the severity of heart failure, and that the capacity to increase plasma ANF concentration after acute volume expansion is preserved in rats with heart failure. There was no evidence of a relative deficiency of circulating ANF in this model of heart failure.

Animals↗
PubMed1987

Enhanced myocardial depression in diabetic rats during E. coli sepsis.

The aim of this study was to determine whether diabetes enhanced the sensitivity of the myocardium to the deleterious effects of in vivo-administered Escherichia coli. Diabetes was induced in two groups of animals. One group received 70 mg/kg streptozotocin (iv) and exhibited a severe diabetes with elevated fasting and fed blood glucose concentrations and a markedly abnormal response to an oral glucose load. The second group received 45 mg/kg streptozotocin, was mildly diabetic (termed "latent" diabetes), and was characterized by normal fasting blood glucose but slightly elevated fed blood glucose and an abnormal response to a glucose load. A third group of rats received vehicle and served as time-matched control animals. Four weeks after induction of diabetes, all animals were catheterized under ether anesthesia and some received intraperitoneal injections of live E. coli. In vitro myocardial performance was assessed using the isolated, perfused working heart preparation. Ventricular function curves were generated by changing left atrial filling pressure and measuring changes in heart rate, cardiac output, and aortic peak systolic pressure. Cardiac performance in the severe diabetic group was depressed at the highest preload but was unchanged at lower preloads. Function in the latent diabetic group was not different from control. Sepsis induced a slight decrease in cardiac performance in the control group and resulted in larger reductions in the latent and severe diabetic groups. A depression in aortic flow was the major consequence of sepsis in the latent diabetic group, whereas decreased coronary flow was the primary change in the severe diabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Atrial natriuretic factor decreases whole-body capillary absorption in rats.

Previous studies suggested that exogenous atrial natriuretic factor (ANF) altered extracellular fluid partition between plasma and interstitium. The effect of ANF and a similarly effective diuretic dose of furosemide on whole-body transcapillary fluid movement was studied in anesthetized rats by measuring changes in urine and plasma volumes, while accounting for the volume of fluid administered. After 75 min of infusion, urine volume was 9.9 +/- 1.0 ml/kg in rats receiving ANF (0.5 micrograms X min-1 X kg-1), and plasma volume decreased by 3.7 ml/kg (P less than 0.01) compared with rats receiving vehicle only. In the furosemide rats, urine volume was 12.3 +/- 1.9 ml/kg, yet plasma volume was not significantly different from that in the vehicle rats. These results suggested that unlike furosemide, which allowed sufficient capillary absorption to maintain plasma volume constant despite the large diuresis, ANF attenuated whole-body net capillary absorption. The effect of ANF on capillary absorption was quantitated in anephric rats by measuring the increase in plasma volume after intravenous administration of hyperoncotic albumin. After accounting for the volume administered, whole-body net capillary absorption was less (P less than 0.05) in the rats receiving ANF (4.8 +/- 0.4 ml/kg) than in those receiving vehicle (5.9 +/- 0.2 ml/kg). Plasma protein concentration was greater in other anephric rats receiving a similar ANF infusion than in those receiving vehicle. These findings suggest that ANF decreased capillary absorption because of increased average capillary hydrostatic pressure and not because of altered capillary permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1987

The contribution of atrial natriuretic factor to acute volume natriuresis in rats.

To explore the role of atrial natriuretic factor (ANF) in acute volume-expansion natriuresis, right atrial pressure (RAP), mean arterial pressure (MAP), rate of urinary sodium excretion (UNaV), and plasma immunoreactive ANF (IR-ANF) were measured in anesthetized, open-chest rats. All groups received 33% blood volume expansion with whole blood in 15 min. RAP was not allowed to increase in one group by using a caval snare. MAP was controlled in a second group with the use of an aortic snare. A third group (RAP-controlled ANF) with control of RAP received rat ANF (99-126) at doses designed to mimic the IR-ANF measured in the MAP-controlled rats. IR-ANF was similar 5 min after blood infusion in rats exhibiting increased RAP (490 +/- 111 pg/ml) and in those without increased RAP but receiving ANF infusion (447 +/- 44 pg/ml); this was also true at 45 min after blood infusion (232 +/- 44 vs. 263 +/- 27 pg/ml). IR-ANF in rats with constant RAP (without ANF infusion) remained low throughout the experiment (61 +/- 10 and 74 +/- 10 pg/ml). UNaV increased only in the MAP-controlled and ANF-infused groups, but peak responses occurred 15-30 min after the onset of volume expansion in the former, and 60-75 min in the latter. Thus, factors other than ANF mostly accounted for the immediate natriuresis after volume expansion, whereas ANF predominated after a delayed period. The results suggest that increased plasma ANF accounted for at least 34% of the observed natriuretic response to acute volume expansion in anesthetized rats.

Animals↗
PubMed1984

Net O2, CO2, lactate, and acid exchange by muscle during progressive working contractions.

The net O2 uptake (VO2), CO2 output (VCO2), lactate output (L), and non-CO2 acid output (HA) by the gastrocnemius-plantaris muscle group of the dog were measured during progressively loaded isotonic tetanic contractions. Shortening during the 1/s contractions was maintained constant as load was increased by raising the stimulus voltage applied to the motor nerve. Contractions at each load continued for 5 min with two arterial and four venous blood samples obtained during the last minute at each load. Work rate (W) during the contractions was calculated from the load and the shortening. The VO2 increased linearly with time and W. The VCO2 generally followed VO2 with a modest lag during the first two work periods. L increased with time, W, and VO2. Maximal L was lower than that seen during repetitive maximal twitch contractions. HA also increased with time, W, and VO2 and was much larger than L at the higher work rates. It is concluded that L and HA are independent variables during progressive working contractions, as they were during repetitive twitch contractions. Both L and HA patterns may be explained as summations of the respective exchanges of L and HA with time by sequentially recruited groups of muscle fibers.

Acid-Base Equilibrium↗
PubMed1981

O2 uptake and work by in situ muscle performing contractions with constant shortening.

The oxygen uptake by the gastrocnemius-plantaris muscle group of the dog was measured during brief submaximal isotonic-tetanic contractions. Shortening in the contractions was kept constant while the load was altered by adjusting the stimulation voltage applied to the motor nerve. Incompletely fused tetanic contractions were produced by 200 msec trains of impulses at a frequency of 20/sec. The trains were delivered once a second. The rate of oxygen uptake (VO2) was linearly related to the external work rate (W). The relationship between VO2, microliter/g min, vs W, gM/g min, is described by the equation VO2 = 18.0 + 3.36 W. The average maximal gross efficiency was 12.5%. The major determinant of VO2 during contractions appeared to be the number of muscle fibers which were activated during the contractions.

Animals↗
PubMedDate not supplied

Microvascular effects of atrial natriuretic peptide in rat cremaster.

Experiments utilized the open cremaster preparation to test the hypothesis that atrial natriuretic peptide (ANP)-induced volume changes result from microvascular resistance alterations. Atrial natriuretic peptide (25, 100, and 500 ng/kg/min, IV) or vehicle was infused into anesthetized rats. At the two highest ANP infusion rates, mean arterial pressure was significantly reduced from 104 +/- 3 (control) to 87 +/- 2 and 77 +/- 2 mmHg, respectively. Hematocrit was 41.0 +/- 0.8 and 45.6 +/- 0.9% (p < 0.05) at the end of vehicle and ANP infusions, respectively. Despite these effects of ANP, there were no significant arteriolar or venular diameter alterations. Thirty microM nitroprusside significantly dilated all vessel segments except large venules. These observations suggest that resistance alterations in the skeletal muscle microvasculature are not the cause of ANP-induced fluid movement.

Animals↗