Hydrops fetalis in nephrectomized fetal lambs infused with angiotensin I

1994 ◽  
Vol 267 (6) ◽  
pp. R1522-R1527 ◽  
Author(s):  
J. J. Faber ◽  
D. F. Anderson
Keyword(s):  
Blood Pressure ◽  
Venous Pressure ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Hydrops Fetalis ◽  
Angiotensin I ◽  
Fetal Sheep ◽  
Gradual Rise ◽  
Arterial Blood ◽  
Excess Water

Nine bilaterally nephrectomized fetal sheep were infused for 6 days with angiotensin I in sterile water, and five nephrectomized fetal sheep were infused for 6 days with water alone. Total dose of angiotensin was 13.8 +/- 8.6 (SD) mg/kg fetal dry wt, and the total volumes of infused water were 303 +/- 201 and 423 +/- 164 ml, respectively. Of the fetuses infused with angiotensin I, one was of normal appearance, two showed moderate hydrops fetalis, and the remaining fetuses were grossly hydropic. All water-infused fetuses were normal. Their wet-to-dry weight ratios were 7.98 and 6.36 (P < 0.015), representing a 25% of normal body weight excess of water in the angiotensin I-infused fetuses. Six days of angiotensin I infusion caused a gradual rise in fetal arterial blood pressure from 37 +/- 15 to 81 +/- 15 mmHg (P < 0.05) and a gradual rise in venous blood pressure from 2.7 +/- 1.0 to 10.5 +/- 1.7 mmHg (P < 0.05). It was concluded that the fetal edema was due to the elevation in venous pressure. Plasma concentrations of Na+, K+, Cl-, HCO3-, total alpha-amino acids, fructose, glucose, and lactate in the fetus and the ewe did not identify an osmotically active solute responsible for the transplacental attraction of excess water into the conceptus, and the mechanism that attracted this excess water across the placenta remains unclear.

The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

Renal, hormonal, and cardiovascular responses to chronic angiotensin I infusion in the ovine fetus

1997 ◽  
Vol 272 (6) ◽  
pp. R1912-R1917 ◽  
Author(s):  
K. M. Moritz ◽  
K. Tangalakis ◽  
E. M. Wintour
Keyword(s):  
Plasma Concentrations ◽  
Allantoic Fluid ◽  
Cardiovascular Responses ◽  
Urine Flow ◽  
Angiotensin I ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Urine Production ◽  
Fetal Urine ◽  
Ovine Fetus

Long-term infusion of angiotensin I (ANG I) into the ovine fetus has been shown to cause excess accumulation of fetal fluid in the allantoic compartment. It was hypothesized that this resulted from sustained increases in fetal urine production, and the hormonal basis was examined. ANG I (6.7 micrograms/h, n = 6) or isotonic saline (n = 6) was infused for 3 days into chronically cannulated ovine fetuses (112-122 days of gestation). ANG I caused an immediate and progressive increase in mean arterial blood pressure (from 42 +/- 2 to 57 +/- 4 mmHg), increased urine flow rate (from 15 +/- 3 to 48 +/- 8 ml/h), and increased glomerular filtration rate (from 97 +/- 15 to 146 +/- 24 ml/h), without significant changes in fetal plasma concentrations of aldosterone, atrial natriuretic factor (ANF), adrenocorticotropin, or cortisol. There were substantial increases in sodium and chloride excretion, due to both increased fetal urine concentrations and fetal urine flow, without significant changes in urine osmolality (from 134 +/- 9 to 147 +/- 12 mosmol/kg water). There were no significant changes in any parameter in the saline-infused fetuses. Neither amniotic or allantoic fluid volume was significantly changed by ANG I infusion, but allantoic fluid Cl- concentration increased significantly. The conclusions are that ANG I caused a diuresis and natriuresis in the fetal sheep independent of changes in cortisol or ANF.

Physiological Amounts of Angiotensinogen Increase Blood Pressure in Sprague Dawley Rats After I.V. Administration.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 694-694
Author(s):  
Christoph P R Klett ◽  
Joey P Granger
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Transit Time ◽  
Mean Arterial Blood Pressure ◽  
Time Lag ◽  
Plasma Concentrations ◽  
Sprague Dawley ◽  
Angiotensin I ◽  
Arterial Blood ◽  
Sprague Dawley Rats

P9 The synthesis and secretion of hepatic angiotensinogen is controlled by a complex pattern of physiologic and pathophysiologic mediators including glucocorticoids, estrogens, thyroid hormones, cytokines, glucagon,insulin, and prostaglandins. Since plasma concentrations of angiotensinogen are close to the Michaelis Menten constant, it was hypothesized that changes in angiotensinogen plasma concentrations have an influence on the formation rate of angiotensin I and angiotensin II and, therefore, on blood pressure. To further test this hypothesis we injected purified rat angiotensinogen i.v. in Sprague Dawley rats via the femoral vein. Mean arterial blood pressure was measured after arterial cathederization. Control animals had a mean arterial pressure of 131 ± 2 mm Hg before and after the injection of vehicle (saline). The injection of 0.8, 1,2, and 2.9 mg/kg angiotensinogen caused a dose dependend increase in mean arterial blood pressure of 8 ± 0.4, 19.3 ± 2.1, and 32 ± 2.4 mm Hg, respectively. In contrast, the injection of a purified rabbit anti-rat-angiotensinogen antibody 1.4 mg/kg resulted in a significant decrease in blood pressure (-52 ± 3.2 mmHg). In an attempt to analyze how fast and efficient angiotensinogen production can sense regulatory input and convert into adaptation of secretion rate we determined the transit time (time needed for translation and post-translational modifications) for angiotensinogen in a pulse chase experiment employing 35 [S]-methionine as label in freshly isolated hepatocytes. During the chase periode, after quantitative immunoprecipitation, we determined the transit time for angiotensinogen with 2.5 h which is consistent with the constitutive type of angiotensinogen secretion and the time lag found for plasma concentrations to respond to regulatory mediators. In summary we conclude that variations in angiotensinogen plasma concentrations can result in changes in blood pressure. In contrast to renin known as a tonic regulator for the generation of angiotensin I, angiotensinogen seems to be a factor rather important for long-term control of the basal activity of the renin angiotensin system.

Fetal cardiovascular reflex responses to hypoxaemia

1994 ◽  
Vol 6 (1) ◽  
pp. 17-37 ◽  
Author(s):  
Dino A Giussani ◽  
John AD Spencer ◽  
Mark A Hanson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Plasma Concentrations ◽  
Late Pregnancy ◽  
Intrauterine Environment ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Cardiovascular Reflex ◽  
Transient Bradycardia

The fetus mounts a coordinated cardiovascular response to an insult of acute hypoxaemia which involves neural and endocrine components. During acute hypoxaemia in late pregnancy there is a transient bradycardia, a gradual increase in arterial blood pressure and an increase in heart rate variability. In addition, there is a redistribution of the combined ventricular output favouring the cerebral, myocardial and adrenal circulations by shunting blood away from the peripheral circulations. A component of the increase in peripheral vascular resistance and the increase in arterial blood pressure during acute hypoxaemia is mediated via increases in plasma concentrations of vasoconstrictor hormones such as vasopressin, angiotensin II and neuropeptide Y. Whilst an increase in plasma ACTH and cortisol is also seen during acute hypoxaemia, their contribution to cardiovascular control in fetal sheep is less clear.Evidence has been presented to suggest that a number of these cardiovascular and endocrine responses to acute hypoxaemia are chemorefiex in nature, mediated principally by carotid chemoreceptor afferents. In addition, this reflex may be modifiable in terms of changes in magnitude and gain: first, by an influence of the intrauterine environment during chronic hypoxaemia and second, through genetic influences, in animals adapted to life at high altitude.

Static filling pressure in patients during induced ventricular fibrillation

2003 ◽  
Vol 285 (6) ◽  
pp. H2510-H2515 ◽  
Author(s):  
J. D. Schipke ◽  
G. Heusch ◽  
A. P. Sanii ◽  
E. Gams ◽  
J. Winter
Keyword(s):  
Blood Pressure ◽  
Time Constant ◽  
Pressure Difference ◽  
Venous Pressure ◽  
Venous Blood ◽  
Central Venous ◽  
Equilibrium Pressure ◽  
Arterial Blood ◽  
Cardiac Pumping ◽  
Blood Pressure Difference

The static pressure resulting after the cessation of flow is thought to reflect the filling of the cardiovascular system. In the past, static filling pressures or mean circulatory filling pressures have only been reported in experimental animals and in human corpses, respectively. We investigated arterial and central venous pressures in supine, anesthetized humans with longer fibrillation/defibrillation sequences (FDSs) during cardioverter/defibrillator implantation. In 82 patients, the average number of FDSs was 4 ± 2 (mean ± SD), and their duration was 13 ± 2 s. In a total of 323 FDSs, arterial blood pressure decreased with a time constant of 2.9 ± 1.0 s from 77.5 ± 34.4 to 24.2 ± 5.3 mmHg. Central venous pressure increased with a time constant of 3.6 ± 1.3 s from 7.5 ± 5.2 to 11.0 ± 5.4 mmHg (36 points, 141 FDS). The average arteriocentral venous blood pressure difference remained at 13.2 ± 6.2 mmHg. Although it slowly decreased, the pressure difference persisted even with FDSs lasting 20 s. Lack of true equilibrium pressure could possibly be due to a waterfall mechanism. However, waterfalls were identified neither between the left ventricle and large arteries nor at the level of the diaphragm in supine patients. We therefore suggest that static filling pressures/mean circulatory pressures can only be directly assessed if the time after termination of cardiac pumping is adequate, i.e., >20 s. For humans, such times are beyond ethical options.

Substantial reductions in blood pressure after bilateral nephrectomy in fetal sheep

1994 ◽  
Vol 266 (1) ◽  
pp. H17-H20 ◽  
Author(s):  
D. F. Anderson ◽  
A. Barbera ◽  
J. J. Faber
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Venous Blood ◽  
Bilateral Nephrectomy ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Pregnant Sheep ◽  
Blood Pressures ◽  
Twin Pregnancies

The role of the kidneys in the maintenance of arterial blood pressure was examined in fetal sheep. Surgery was performed on 11 pregnant sheep (8 twin pregnancies) at approximately 125 days. All 19 fetuses were instrumented with hindlimb arterial and venous catheters. Eleven of the fetuses (but only 1 of each twin) were also bilaterally nephrectomized. Fetal arterial blood pressure was measured several times between 2 and 14 days after surgery. Arterial blood pressure in the intact fetuses increased from 44 +/- 1 to 47 +/- 1 mmHg (SE) but gradually decreased from 37 +/- 4 to 25 +/- 3 mmHg in the nephrectomized group. Whereas the arterial blood pressures measured on the first day of the experiment were not statistically significantly different between the two groups, by the final day of the experiment the arterial blood pressure of the intact fetuses was much higher than that of the nephrectomized fetuses. Venous blood pressure was similar in the two groups. We conclude that bilateral nephrectomy in fetal sheep not only stops the normal gestational increase in arterial blood pressure but also leads to a progressive decline.

Hemorrhage in newborn lambs: effects on arterial blood pressure, ACTH, cortisol, and vasopressin

1981 ◽  
Vol 240 (6) ◽  
pp. E585-E590 ◽  
Author(s):  
J. C. Rose ◽  
M. Morris ◽  
P. J. Meis
Keyword(s):  
Blood Pressure ◽  
Central Venous Pressure ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Venous Pressure ◽  
Plasma Concentrations ◽  
Central Venous ◽  
Arterial Blood ◽  
Age Related ◽  
Mean Pressure

Arterial blood pressure, central venous pressure, and plasma concentrations of ACTH, cortisol, and vasopressin (AVP) were monitored in chronically prepared, unanesthetized newborn and weanling lambs at rest and during and after hemorrhage of 15% of estimated blood volume at 1.5%/min. Differences in the endocrine and blood pressure responses to hypovolemia were noted in the two groups of animals. Hemorrhage did not change arterial mean pressure, reduced central venous pressure, and caused a delayed increase in the plasma concentrations of ACTH, cortisol, and AVP in the newborn lambs. In weanling lambs, hemorrhage reduced arterial mean pressure and central venous pressure and promptly increased plasma ACTH and cortisol levels while plasma AVP concentrations again showed a delayed increase. The data indicate that certain hormonal mechanisms for the defense of blood volume are present and operational within 3 days of birth and that age-related differences in the responses to hemorrhage exist in the lamb.

On venous pressure in arterial and "isolated" venous hypertension

1927 ◽  
Vol 23 (6-7) ◽  
pp. 632-640
Author(s):  
P. N. Nikolaev
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Venous Blood ◽  
Venous Hypertension ◽  
Clinical Use ◽  
Arterial Blood

If the determination of arterial blood pressure has entered clinical use as an indispensable method for the recognition and interpretation of various diseases, the same cannot be said about the determination of venous blood pressure. Only the first steps are still being taken.

Effects of diltiazem on atrioventricular conduction and arterial blood pressure: correlation with plasma drug concentrations

1984 ◽  
Vol 62 (12) ◽  
pp. 1479-1486 ◽  
Author(s):  
Jean-Paul Clozel ◽  
Jacques Billette ◽  
Gilles Caillé ◽  
Pierre Théroux ◽  
Richard Cartier
Keyword(s):  
Blood Pressure ◽  
Plasma Concentration ◽  
Refractory Period ◽  
Plasma Concentrations ◽  
Atrioventricular Conduction ◽  
Gas Liquid Chromatography ◽  
Conduction Time ◽  
Arterial Blood ◽  
Drug Concentrations ◽  
Atrial Conduction Time

Atrial and atrioventricular conduction variables were studied at control and at the end of each of six consecutive 45-min diltiazem administration periods in eight closed chest-anesthetized dogs. Diltiazem was given as a bolus (50 μg/kg, i.v.) followed by an infusion (0.5 μg∙kg−1∙min−1); doses were doubled in subsequent periods. The plasma concentrations, measured by gas–liquid chromatography, ranged from 8 to 1400 ng/mL and correlated strongly with the doses (r = 0.92; p < 0.01). The Wenckebach cycle length, basic conduction time, and functional refractory period of the atrioventricular (AV) node increased proportionally with plasma concentration (respective r = 0.90, 0.89, 0.80; p < 0.01). The minimum mean plasma concentrations affecting these variables significantly were 37, 83, and 175 ng/mL, respectively. Second or third degree AV blocks developed in all dogs for plasma concentrations between 379 and 1400 ng/mL. In four dogs which were given isoproterenol (0.2 μg∙kg−1∙min−1), these blocks disappeared within 1 min. Atrial conduction time and functional refractory period were slightly but significantly shortened by diltiazem with mean plasma concentrations of 175 ng/mL and over. His–Purkinje intervals were not significantly changed by diltiazem. Systolic and diastolic arterial pressures were decreased by diltiazem (r = −0.64, r = −0.79; p < 0.01) starting with a mean plasma concentration of 83 ng/mL. We conclude that AV nodal conduction variables are progressively prolonged with increasing plasma concentrations of diltiazem; plasma concentrations affecting blood pressure and AV nodal variables overlap; and the AV blocks produced by toxic concentrations of diltiazem can be corrected by isoproterenol.

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