scholarly journals FLUID UPTAKE AND THE MAINTENANCE OF BLOOD VOLUME IN OCTOPUS

1993 ◽  
Vol 175 (1) ◽  
pp. 211-218
Author(s):  
M. J. Wells ◽  
J. Wells
Keyword(s):  
Blood Pressure ◽  
Digestive Gland ◽  
Blood Volume ◽  
Urine Volume ◽  
Peripheral Resistance ◽  
Pulse Amplitude ◽  
Volume Of Fluid ◽  
Octopus Vulgaris ◽  
Fluid Uptake ◽  
Urine Production

The replacement of fluid following withdrawal of up to 40 % of the blood from Octopus vulgaris can be tracked over a period of days by measuring the dilution of haemocyanin, which is not simultaneously replaced. Haemocyanin concentration was measured from the copper content or the oxygen-carrying capacity of further small blood samples. Fluid lost was replaced within 1–2 h, provided that the digestive gland ducts were left intact. If these were ligated, the haemocyanin concentration remained the same as before withdrawal of the initial large blood sample and the animals died within a few hours. Evidence presented elsewhere has indicated that the site of the fluid uptake is the digestive gland appendages. Urine production would be continued or increased during the restoration of blood volume. When urine volume is added to the volume of fluid replaced, it appears that this fluid transport system must be capable of moving at least its own volume of fluid from the gut into the blood every 5 min. An immediate consequence of blood withdrawal is a fall in blood pressure and pulse amplitude, followed within minutes by a transient rise to high blood pressures, apparently as a result of an increase in peripheral resistance as circulation to the arms is restricted, conserving the blood for vital central organs. Following these transient swings, the diastolic blood pressure returns to normal values despite blood loss; pulse amplitude returns as blood volume is replaced. Duct-ligated animals continue to show a reduced pulse.

Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Blood Volume ◽  
Total Peripheral Resistance ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

scholarly journals Postural hypocapnic hyperventilation is associated with enhanced peripheral vasoconstriction in postural tachycardia syndrome with normal supine blood flow

2006 ◽  
Vol 291 (2) ◽  
pp. H904-H913 ◽  
Author(s):  
Julian M. Stewart ◽  
Marvin S. Medow ◽  
Neil S. Cherniack ◽  
Benjamin H. Natelson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Blood Volume ◽  
Peripheral Resistance ◽  
Impedance Plethysmography ◽  
Postural Tachycardia Syndrome ◽  
Peripheral Vasoconstriction ◽  
Postural Tachycardia ◽  
End Tidal

Previous investigations have demonstrated a subset of postural tachycardia syndrome (POTS) patients characterized by normal peripheral resistance and blood volume while supine but thoracic hypovolemia and splanchnic blood pooling while upright secondary to splanchnic hyperemia. Such “normal-flow” POTS patients often demonstrate hypocapnia during orthostatic stress. We studied 20 POTS patients (14–23 yr of age) and compared them with 10 comparably aged healthy volunteers. We measured changes in heart rate, blood pressure, heart rate and blood pressure variability, arm and leg strain-gauge occlusion plethysmography, respiratory impedance plethysmography calibrated against pneumotachography, end-tidal partial pressure of carbon dioxide (PetCO2), and impedance plethysmographic indexes of blood volume and blood flow within the thoracic, splanchnic, pelvic (upper leg), and lower leg regional circulations while supine and during upright tilt to 70°. Ten POTS patients demonstrated significant hyperventilation and hypocapnia (POTSHC) while 10 were normocapnic with minimal increase in postural ventilation, comparable to control. While relative splanchnic hypervolemia and hyperemia occurred in both POTS groups compared with controls, marked enhancement in peripheral vasoconstriction occurred only in POTSHC and was related to thoracic blood flow. Variability indexes suggested enhanced sympathetic activation in POTSHC compared with other subjects. The data suggest enhanced cardiac and peripheral sympathetic excitation in POTSHC.

scholarly journals THE PHYSIOLOGICAL RESPONSE OF THE CIRCULATORY SYSTEM TO EXPERIMENTAL ALTERATIONS

1925 ◽  
Vol 42 (5) ◽  
pp. 661-679 ◽  
Author(s):  
Emile Holman ◽  
Claude S. Beck
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Peripheral Resistance ◽  
Circulatory System ◽  
Blood Stream ◽  
Volume Flow ◽  
Volume Control ◽  
Total Blood ◽  
Full Compensation ◽  
The Right

An abnormal communication, experimentally produced between the right and left ventricles, causes a deflection of part of the blood stream into the shorter pulmonary circuit. Proceeding pari passu with the increase in volume flow of blood through this shorter circuit, there occurs a gradual enlargement of the heart limited to that part of the circulatory system through which the deflected blood passes; namely, the left ventricle, the right ventricle, the pulmonary artery, and the left auricle. There is also a demonstrable hypertrophy of the right and left ventricles, which presumably is the result of the increased effort necessary to propel forward an increased volume flow of blood, since it cannot be attributed to an increased peripheral resistance. Immediately after the production of the defect, the right auricle and aorta become smaller than usual, conforming in size to the decreased volume flow of blood through them. As full compensation for the deflected flow occurs by an increase in total blood volume, they return to their normal size. If full compensation has not occurred they remain smaller than normal (Dog X 11). The changes incident to the establishment of an opening in the septum are entirely dependent upon the size of the defect, and hence, upon the extent of the volume of blood deflected into the shorter circuit. Commensurate with the volume of blood deflected, there is a fall in general blood pressure. If the animal survives the immediate fall in blood pressure, certain compensatory adjustments occur which reestablish a more normal blood pressure: (a) an immediate increase in pulse rate; (b) a gradual increase in total blood mass. The increase in blood volume is directly commensurate with the size of the defect. The pulse returns to a normal rate when complete compensation through an increase in blood volume has been attained. It is suggested that the enlargement of the heart seen clinically in so called "idiopathic hypertrophy," "essential hypertension," and also in certain cases of cardiorenal disease, may be due to an increase in total blood mass following some interference with the mechanism for its control. The seat of this impairment in blood volume control may be: (a) in a chemical alteration in the blood; (b) in a diseased function of the kidneys which may be responsible for a decreased elimination, or for a change in the chemical composition of the blood; or (c) in an abnormal stimulation of the organs producing the cellular elements of the blood.

IMMEDIATE EFFECTS OF RAPID HEMORRHAGE ON HEMODYNAMICS IN THE DOG

1956 ◽  
Vol 34 (5) ◽  
pp. 827-834
Author(s):  
Russell A. Waud ◽  
Douglas R. Waud
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Index ◽  
Specific Gravity ◽  
Blood Cell ◽  
Cell Count ◽  
Blood Volume ◽  
Sedimentation Rate ◽  
Color Index ◽  
Peripheral Resistance

Dogs were anesthetized by the intravenous injection of sodium pentobarbital. Viscosity, hematocrit, blood pressure, cardiac index, stroke output, cardiac output, heart rate, peripheral resistance, red blood cell count, blood volume/body surface area, cell volume/area, plasma volume/area, plasma protein, hemoglobin, specific gravity of whole blood, cell size, color index, and sedimentation rate were determined in 16 dogs, before and following hemorrhage, and in seven controls. The following points were demonstrated: following hemorrhage the viscosity, hematocrit, blood pressure, stroke output, minute output, blood volume, and cell volume were markedly decreased. The decrease in blood volume, by limiting the venous return, was probably the cause of the decreased minute output and fall in blood pressure; this, by reducing the capillary flow, deprived the tissues of an adequate supply of oxygen. There was no significant change in the heart rate. The total peripheral resistance (T.P.R.) was greatly increased. The fall in hematocrit indicates a hemodilution which was probably the main factor in reducing the viscosity. It would appear that the decreased blood volume was the primary cause of the fall in blood pressure following hemorrhage and that a lowering of viscosity was not a large factor. There was no significant change following hemorrhage in the cardiac index, color index, cell size, white cell count, specific gravity of plasma, or sedimentation rate.

4. Water, salt, and blood pressure

2014 ◽  
pp. 53-62
Author(s):  
Martin Luck
Keyword(s):  
Blood Pressure ◽  
Blood Vessels ◽  
Blood Volume ◽  
Arginine Vasopressin ◽  
The Body ◽  
Sodium Ions ◽  
Urine Production ◽  
Water Salt ◽  
Blood Change ◽  
Hormone System

‘Water, salt, and blood pressure’ describes how the balance of water in the body is controlled by several hormones, including vasopressin (arginine vasopressin (AVP)). AVP reduces urine production by the kidneys and also causes small blood vessels to contract, raising blood pressure. Blood volume and pressure are also adjusted by changing the amount of sodium ions reclaimed by kidney nephrons. The renin–Ang-II–aldosterone hormone system balances blood volume and circulatory space to keep pressure stable when the volume and dilution of the blood change. But what happens if the concentration of salt (sodium and other ions) in the blood starts to rise? Is there a direct way to get rid of excess salt? A hormone secreted by the heart, called ANP, does exactly this.

IMMEDIATE EFFECTS OF RAPID HEMORRHAGE ON HEMODYNAMICS IN THE DOG

1956 ◽  
Vol 34 (1) ◽  
pp. 827-834
Author(s):  
Russell A. Waud ◽  
Douglas R. Waud
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Index ◽  
Specific Gravity ◽  
Blood Cell ◽  
Cell Count ◽  
Blood Volume ◽  
Sedimentation Rate ◽  
Color Index ◽  
Peripheral Resistance

Dogs were anesthetized by the intravenous injection of sodium pentobarbital. Viscosity, hematocrit, blood pressure, cardiac index, stroke output, cardiac output, heart rate, peripheral resistance, red blood cell count, blood volume/body surface area, cell volume/area, plasma volume/area, plasma protein, hemoglobin, specific gravity of whole blood, cell size, color index, and sedimentation rate were determined in 16 dogs, before and following hemorrhage, and in seven controls. The following points were demonstrated: following hemorrhage the viscosity, hematocrit, blood pressure, stroke output, minute output, blood volume, and cell volume were markedly decreased. The decrease in blood volume, by limiting the venous return, was probably the cause of the decreased minute output and fall in blood pressure; this, by reducing the capillary flow, deprived the tissues of an adequate supply of oxygen. There was no significant change in the heart rate. The total peripheral resistance (T.P.R.) was greatly increased. The fall in hematocrit indicates a hemodilution which was probably the main factor in reducing the viscosity. It would appear that the decreased blood volume was the primary cause of the fall in blood pressure following hemorrhage and that a lowering of viscosity was not a large factor. There was no significant change following hemorrhage in the cardiac index, color index, cell size, white cell count, specific gravity of plasma, or sedimentation rate.

Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress

2005 ◽  
Vol 288 (6) ◽  
pp. R1637-R1648 ◽  
Author(s):  
Peter E. Hammer ◽  
J. Philip Saul
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Blood Volume ◽  
Low Frequency ◽  
Pressure Waves ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Gain Margin ◽  
The Stability

A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.

Weight reduction in the management of hypertension: Epidemiologic and mechanistic evidence

1986 ◽  
Vol 64 (6) ◽  
pp. 818-824 ◽  
Author(s):  
Efrain Reisin
Keyword(s):  
Blood Pressure ◽  
Weight Loss ◽  
Weight Control ◽  
Sodium Intake ◽  
Close Association ◽  
Peripheral Resistance ◽  
Volume Ratio ◽  
Epidemiological Studies ◽  
Left Ventricular ◽  
Normal Weight

A number of studies have established a close association between increased body mass and elevated blood pressure. The presence of obesity in hypertensive subjects is associated with some hemodynamic, metabolic, and endocrinic characteristics: an increased intravascular volume with a high intracellular body water/interstitial fluid volume ratio, increased cardiac output, stroke volume, and left ventricular work while peripheral resistance was reduced or normal. Weight loss of at least 10 kg can reduce blood pressure independently of changes in sodium intake in obese persons of both sexes with mild, moderate, or severe high blood pressure. The fall in arterial pressure in obese hypertensives after weight loss may reverse many of the previously mentioned altered findings and underscore previous epidemiological studies that have shown that weight control could be an important measure in the treatment of hypertension.

Na+, K+ and water balance in young spontaneously hypertensive rats: relationship to blood pressure after high K+ treatment

1987 ◽  
Vol 72 (3) ◽  
pp. 321-327 ◽  
Author(s):  
A. Louise Sugden ◽  
Barbara L. Bean ◽  
James A. Straw
Keyword(s):  
Blood Pressure ◽  
Water Balance ◽  
Spontaneously Hypertensive Rats ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Maximum Level ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High K ◽  
Sufficient Magnitude

1. These studies were designed to investigate the effects of high dietary K+ on electrolyte and water balance in young spontaneously hypertensive rats (SHR) and to relate these effects to changes in blood pressure. 2. The high K+ diet reduced blood pressure by approximately 10 mmHg during the development of hypertension. Blood pressure, however, plateaued at the same maximum level as control by age 13 weeks. 3. Rats fed the high K+ diet showed a significant increase in water intake and urine volume throughout the treatment period but no change in plasma volume or extracellular fluid volume occurred. 4. A slight natriuresis was also observed in rats on the high K+ diet, but this was not of sufficient magnitude to decrease total body Na+. 5. These results confirm previous findings that K+ causes a diuresis and a natriuresis, but demonstrate that the diuretic action of K+ cannot explain its antihypertensive properties in young SHR.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

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