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Biomedical subjects

R D Manning

Publications and source records attributed to R D Manning.

At least 37 records · Page 2Linked to original sources
PubMed1992

Mechanism of decreased cardiac output during ANP infusion in conscious anephric dogs.

Atrial natriuretic peptide (ANP) may decrease cardiac output (CO) by lowering circulating blood volume (BV) or by altering the vasculature in a manner that would decrease venous return. The purpose of this study was to determine the role of decreased BV in mediating the decrease in CO during acute infusion of ANP. BV was measured by dilution of 51Cr-labeled red blood cells in seven trained conscious splenectomized dogs studied after unilateral (UNX) and total (TNX) nephrectomy. BV, hematocrit (Hct), CO, mean arterial pressure (MAP), and total peripheral resistance (TPR) were determined during a 90-min control period and 270 min of infusion of ANP (20 ng.kg-1.min-1 iv). In UNX dogs, ANP decreased BV from 60.9 +/- 1.4 to 58.6 +/- 1.4 ml/kg and increased Hct from 39.3 +/- 1.8% to 41.1 +/- 1.8% (P less than 0.05). MAP was not changed and CO fell to a low that was 86 +/- 2% of control (P less than 0.05) 240 min after starting ANP. TPR increased significantly during ANP infusion. All variables returned to control after ANP was stopped. In the same dogs studied 24 h after TNX, MAP averaged 111 +/- 5 mmHg during control and did not change during ANP infusion. CO fell to a low of 82 +/- 3% of control (P less than 0.05) after 120 min of infusion and remained reduced until after the ANP was stopped.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Chronic transvascular fluid flux and lymph flow during volume-loading hypertension.

The chronic roles of the transcapillary fluid flux and lymph flow in the distribution of extracellular fluid volume during volume-loading hypertension were investigated in five conscious dogs. Similarly, the distribution of plasma proteins across the microvasculature was evaluated. During the early phases of volume-loading hypertension the fluid balance was positive, which caused the extracellular fluid volume and the plasma volume to increase 25 and 15%, respectively. The thoracic duct lymph flow more than doubled, but the increase in transcapillary fluid flux was even greater. Therefore the interstitial fluid volume increased 30%. This fluid shift from the vasculature into the interstitium probably prevented an even greater rise in arterial pressure. In addition, the transcapillary protein flux more than doubled, but the accompanying increase in lymph protein transport prevented any change in plasma protein mass. During the latter part of the saline-infusion period, the lymph flow declined toward its control, which caused a net transfer of fluid into the interstitium. In conclusion, the transcapillary fluid flux and lymph flow play significant roles in extracellular fluid volume distribution.

Albumins↗
PubMed1990

Effects of hypoproteinemia on blood volume and arterial pressure of volume-loaded dogs.

Studies were performed in 14 conscious, anephric dogs to clarify the role of blood volume in the genesis of hypertension. The dogs were splenectomized and had plasma protein concentration (PPC) reduced to 2.7 g/dl by daily plasmapheresis for 9 days. This hypoproteinemia resulted in a 20% decrease in both blood volume and mean arterial pressure. On the 10th day the dogs were nephrectomized. On the 11th day after a 3-h control period with plasmapheresis, lactated Ringer equivalent to 10 or 20% of body weight was intravenously infused. By 25 h postinfusion blood volume had not increased, and the dogs were still hypotensive. At 25 h plasma protein mass was returned to normal by intravenous infusion of autologous plasma, the average blood volume of the three low PPC groups increased approximately 50%, and the arterial pressure increased greater than 60%. The decrease in PPC shifted the regression of blood volume on sodium space down the blood volume axis. In conclusion, the dependence of arterial pressure on blood volume was demonstrated by the decrease in both blood volume and arterial pressure after PPC reduction, the constancy of blood volume and pressure during Ringer infusion, and the increase in both volume and pressure after plasma infusion.

Animals↗
PubMed1990

Chronic lymph flow and transcapillary fluid flux during angiotensin II hypertension.

The roles of the transvascular fluid flux and lymph flow in the distribution of extracellular fluid volume during angiotensin II (ANG II) hypertension were evaluated in 11 conscious dogs. Similarly, the factors regulating the distribution of plasma protein across the microvasculature were assessed. By the second day of ANG II infusion, the thoracic duct lymph flow had increased 58% above control, transcapillary fluid flux had increased 45%, and plasma volume, sulfate space, and interstitial fluid volume remained close to control. In addition, the thoracic duct lymph protein transport had increased 34%, and the accompanying increase in transcapillary protein flux prevented any change in plasma protein mass. Also, at this time, the lymph flow and protein transport from subcutaneous tissue in the hind limb were not increased, and the permeability-surface area product of this region decreased 40%. The origin of the increased thoracic duct lymph flow on day 2 probably was from the splanchnic bed. In conclusion, the increased lymph flow during ANG II hypertension compensated for the increase in transcapillary fluid flux, thus preventing edema formation.

Angiotensin II↗
PubMed1988

Computer models for designing hypertension experiments and studying concepts.

This paper demonstrates how computer models along with animal experiments have been used to work out the conceptual bases of hypertensive mechanisms, especially the following: (1) The renal-fluid volume pressure control mechanism has a feed-back gain for pressure control of infinity. Therefore, the chronic level to which the arterial pressure is controlled can be changed only by altering this pressure control mechanism. (2) An increase in total peripheral resistance is not sufficient by itself to cause hypertension. The only resistances in the circulatory system that, when increased, will cause hypertension are those along a restricted axis from the root of the aorta to Bowman's capsule in the kidneys. (3) Autoregulation in the peripheral vascular beds does not increase the arterial pressure in hypertension. However, autoregulation can convert high cardiac output hypertension into high peripheral resistance hypertension. (4) In a computer simulation that cannot yet be performed in animals, a simulated hypertension caused by a combination of increased renal afferent and efferent arteriolar resistances has characteristics that match almost exactly those of essential hypertension.

Animals↗
PubMed1987

Effects of hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume.

The effects of long-term hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume were studied in eight conscious dogs over a 34-day period. Plasma protein concentration (PPC) was decreased by daily plasmapheresis, and the effects of decreasing and increasing sodium intake were measured. By the 12th day of plasmapheresis, during which sodium intake was 30 meq/day, PPC had decreased to 2.5 g/dl from a control value of 7.2 g/dl, mean arterial pressure had decreased to 78% of control, glomerular filtration rate (GFR) was 75.2% of control, and urinary sodium excretion was decreased. By day 18 of plasmapheresis, estimated renal plasma flow (ERPF) was decreased to 60% of control due to the decreased arterial pressure and an increase in renal vascular resistance. Also, plasma renin activity and plasma aldosterone concentration were both increased, and the relationship between mean arterial pressure and urinary sodium excretion was distinctly shifted to the left along the arterial pressure axis. In contradistinction to acute experiments, chronic hypoproteinemia results in decreases in GFR, ERPF, and urinary sodium excretion and has marked effects on both fluid volume and arterial pressure regulation.

Aldosterone↗
PubMed1987

Renal hemodynamic, fluid volume, and arterial pressure changes during hyperproteinemia.

The chronic effects of hyperproteinemia on renal hemodynamics, fluid volume, and arterial pressure were determined in six conscious dogs over a 32-day period. Plasma protein concentration was increased by intravenous infusion of approximately 300 ml/day of previously collected autologous plasma, and the responses to changes in sodium intake were studied. By the end of a 9-day period of hyperproteinemia and normal sodium intake, plasma protein concentration had increased 2.2 g/dl, plasma colloid osmotic pressure had increased 7-8 mmHg, mean arterial pressure had increased 12 mmHg, glomerular filtration rate (GFR) had increased 15%, estimated renal plasma flow (ERPF) had increased 51% primarily due to renal vasodilatation, and filtration fraction had decreased 23%. Also, sodium balance was negative, water balance was positive, sodium iothalamate space had increased, plasma sodium concentration had decreased, and the relationship between mean arterial pressure and urinary sodium excretion was shifted to the right along the arterial pressure axis. In conclusion, long-term increases of plasma protein concentration result in a marked increase in ERPF as well as significant increases in GFR, extracellular fluid volume, and arterial pressure.

Aldosterone↗
PubMed1986

Current concepts and perspectives of renal volume regulation in relationship to hypertension.

The renal-body fluid mechanism for arterial pressure control is almost certainly the most primitive of all the pressure-regulating mechanisms in animals. Through the stages of evolution, the system has been greatly improved. Nervous controls provide rapid pressure-control mechanisms that function almost instantaneously, many hours or days before the renal-body fluid mechanism can act fully. The renin-angiotensin-aldosterone system plays another important role: this system ensures that very large changes in salt intake, from as little as one-tenth normal up to as high as 10 times normal, have very little effect on the regulated level of the arterial pressure. Finally, the long-term autoregulatory mechanism helps to dissociate the long-term control of cardiac output from long-term control of arterial pressure; it also makes it possible for extremely slight increases in body fluid volume to cause chronic volume-loading hypertension.

Aldosterone↗
PubMed1984

The pathogenic role of the kidney.

The discussions of this article suggest that the pressure natriuresis mechanism of the kidneys is the most important of all long-term regulators of arterial pressure. This is especially so because of the infinite-gain feature of this mechanism, a feature that is explained here. However, experiments have shown that it is not the accumulation of sodium per se in the body that causes hypertension. Instead, it is the increase in extracellular fluid volume that usually accompanies sodium accumulation that increases the arterial pressure. If the increase in fluid volume is prevented, hypertension will not occur despite marked sodium retention. Long-term autoregulation in hypertension plays a very important role for two major reasons: (a) it greatly increases the total peripheral resistance when the cardiac output increases only a small amount, and (b) when it promotes arteriolar constriction, capillary pressure is reduced, which in turns allows a very large proportion of the extracellular fluid to remain in the blood rather than to leak into the interstitium. Marked loss of renal mass usually does not cause hypertension because, as long as there is a proper balance between glomerular filtration capability and tubular reabsorption capability, as little as 10% of the normal kidney mass theoretically can excrete the normal daily load of salt without a significant rise in arterial pressure. However, whenever the ratio of glomerular filtration capability to tubular reabsorption capability falls below normal, salt and water are retained until enough hypertension develops to overcome the deficit in glomerular filtration.

Adaptation, Physiological↗
PubMed1984

Long-term changes in plasma protein concentration have marked effects on arterial pressure and renal function.

During a number of pathological states, plasma protein concentration (PPC) changes dramatically; however, the chronic relationship between PPC, mean arterial pressure (MAP), and renal function have never been quantified. Therefore, PPC was decreased by plasmapheresis or increased by intravenous infusion of autologous plasma in a series of three experiments on 17 unanaesthetized dogs. During experiments 1 and 2, PPC was reduced to 2.5 g/dl over 12 days; blood volume decreased to 63.9% of control; mean arterial pressure decreased 25 mmHg; and glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) both decreased markedly. During experiment 3, PPC was increased by more than 2 g/dl; MAP and GFR increased moderately; and ERPF increased 40-50%. Decreased PPC was associated with a marked shift to the left of the MAP-natriuresis relationship while increased PPC caused a moderate shift to the right. In conclusion, chronic alterations in PPC result in striking changes in both MAP and renal function.

Animals↗
PubMed1983

Effects of hypoproteinemia on fluid volumes and arterial pressure.

The effects of both moderate and large decreases in plasma protein concentration on arterial pressure and fluid volumes were studied in 23 conscious dogs. In experiment 1, plasma protein concentration decreased 33% during a 5-day plasmapheresis period. During this time sodium space increased 11%, mean arterial pressure decreased slightly, and neither blood volume nor plasma volume decreased. Experiment 2 was performed to see if blockade of the alpha-sympathetic and angiotensin systems could prevent the blood volume homeostasis during moderate hypoproteinemia. Sodium space increased; however, blood volume was unchanged. During experiment 3 plasma protein concentration decreased 68% over a 12-day plasmapheresis period. By the last day of plasmapheresis, plasma protein concentration was 2.4 g/100 ml, mean arterial pressure had decreased 26 mmHg, sodium space had increased 12%, plasma renin activity had increased 11-fold, and blood volume and plasma volume were 63.9 +/- 4.0 and 66.9 +/- 2.5% of control, respectively. We conclude that the maintenance of a normal blood volume during moderate hypoproteinemia does not require active participation of the renin-angiotensin and alpha-sympathetic systems and large decreases in plasma protein concentration are accompanied by marked hypovolemia, hypotension, and hyperreninemia.

Animals↗
PubMed1980

Dynamics of fluid distribution between the blood and interstitium during overhydration.

The dynamics fluid volume distribution between the blood and interstitium was studied in 24 anephric conscious dogs by making serial measurements of blood volume, sodium space, and plasma proteins during several different states of hydration. After recovery from splenectomy and unilateral nephrectomy, the remaining kidney was removed, and intravenous infusion of lactated Ringer solution equivalent to 5%, 10%, or 20% of the body weight followed the next day. Blood volume and sodium space were elevated in each infusion group for the entire 25-h postinfusion period of measurements, while total amount of circulating proteins increased in the 10% group and decreased in the 20% group, which blunted the increase in blood volume in this group. During the first 5 h after infusion, the increase in blood volume was proportional to the increase in sodium space up to a sodium space of 50% above control. By 24 h postinfusion the relationship between blood volume (BV%) and sodium space (SS%) as percent control was linear over the entire range of sodium spaces (BV% = 68.0 + 0.32 SS%, r = 0.99).

Animals↗