Plasma vasopressin during increases and decreases in blood volume in anaesthetized dogs

1985 ◽  
Vol 63 (3) ◽  
pp. 224-229 ◽  
Author(s):  
J. R. Ledsome ◽  
N. Wilson ◽  
C. A. Courneya
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Natural Logarithm ◽  
Plasma Vasopressin ◽  
Logarithmic Relationship ◽  
Atrial Receptors

In chloralose-anaesthetized dogs, plasma vasopressin concentration was measured by radioimmunoassay during step changes in blood volume of 4 mL/kg over a range of blood volume from +20 to −12 mL/kg. Blood volume was both increased and decreased over this range. There was a logarithmic relationship between blood volume and plasma vasopressin concentration over the range of blood volume examined. There was also a logarithmic relationship between blood volume and mean left atrial pressure. Linear regression between the natural logarithm of plasma vasopressin concentration and mean arterial pressure, heart rate, and mean left atrial pressure gave the highest correlation coefficient (r = 0.94) between vasopressin and mean arterial pressure. The results support the hypothesis that there are sensitive mechanisms controlling the release of vasopressin in response to changes in blood volume. Observations were also made of changes in atrial pressure and activity of left atrial receptors during changes in blood volume over the same range. The results suggest that changes in atrial receptor activity are unlikely to be the major cause of the large increases in plasma vasopressin concentration associated with hypovolemia.

Distension of the pulmonary vein – atrial junctions and plasma vasopressin in the chloralose-anaesthetized dog

1983 ◽  
Vol 61 (8) ◽  
pp. 905-910 ◽  
Author(s):  
N. Wilson ◽  
J. R. Ledsome
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pulmonary Vein ◽  
Arginine Vasopressin ◽  
Left Atrial ◽  
Vagus Nerves ◽  
Plasma Vasopressin ◽  
Plasma Arginine ◽  
Atrial Receptors ◽  
Anaesthetized Dog

The effects of localized distension of the pulmonary vein–left atrial junctions on plasma arginine vasopressin (AVP) have been examined in chloralose anaesthetized dogs. Pulmonary vein distension caused an increase in heart rate and a decrease in plasma AVP concentration. Cooling the vagosympathetic nerves to 10 °C caused an increase in arterial pressure and plasma AVP concentration and prevented the changes in heart rate and plasma AVP concentration caused by pulmonary vein distension. Cooling the vagus nerves to 16 °C did not change heart rate, arterial pressure, or plasma AVP concentration but significantly reduced the changes in heart rate and plasma AVP concentration caused by pulmonary vein distension. Propranolol (0.5 mg/kg) decreased heart rate and prevented the increase in heart rate associated with pulmonary vein distension but did not abolish the decrease in plasma AVP concentration. It is concluded that distension of the pulmonary vein – left atrial junctions causes a decrease in plasma AVP concentration by stimulating atrial receptors with myelinated afferent fibres. The decrease in plasma AVP concentration is not secondary to the reflex changes in heart rate caused by pulmonary vein distension.

Effects of left atrial pressure on the pulmonary vascular response to hypoxic ventilation

1991 ◽  
Vol 70 (5) ◽  
pp. 1991-1995 ◽  
Author(s):  
S. A. Gu ◽  
J. Ducas ◽  
U. Schick ◽  
R. M. Prewitt
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Mean Value ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Vascular Response ◽  
Wide Range ◽  
Pulmonary Arterial ◽  
The Mean

We investigated the effects of hypoxic ventilation on the pulmonary arterial pressure- (P) flow (Q) relationship in an intact canine preparation. Mean pulmonary P-Q coordinates were obtained during hypoxic ventilation and during ventilation with 100% O2 at normal and at increased left atrial pressure. Specifically, we tested the hypothesis that, over a wide range, changes in left atrial pressure would alter the effects of hypoxic ventilation on pulmonary P-Q characteristics. Seven dogs were studied. When left atrial pressure was normal (5 mmHg), the mean value of the extrapolated intercept (PI) of the linear P-Q relationship was 10.9 mmHg and the slope (incremental vascular resistance, IR) of the P-Q relationship was 2.2 mmHg.l-1.min. Hypoxic ventilation increased PI to 18 mmHg (P less than 0.01) but did not affect IR. Subsequently, during ventilation with 100% O2, when left atrial pressure was increased to 14 mmHg by inflation of left atrial balloon, PI increased to 18 mmHg. IR was 1.6 mmHg.l-1.min. Again, hypoxic ventilation caused an isolated change in PI. Hypoxia increased PI from 18 to 28 mmHg (P less than 0.01). As in the condition of normal left atrial pressure, hypoxic ventilation did not affect IR. We conclude that, in an anesthetized intact canine preparation, hypoxic ventilation causes an isolated increase in the extrapolated pressure intercept of the pulmonary P-Q relationship. Furthermore the effects of hypoxic ventilation on pulmonary P-Q characteristics are not affected by the resting left atrial pressure.

Methylene blue inhibits neurogenic cholinergic vasodilator responses in the pulmonary vascular bed of the cat

1992 ◽  
Vol 263 (5) ◽  
pp. L575-L584 ◽  
Author(s):  
T. J. McMahon ◽  
P. J. Kadowitz
Keyword(s):  
Methylene Blue ◽  
Arterial Pressure ◽  
Guanylate Cyclase ◽  
Left Atrial ◽  
Vagal Stimulation ◽  
Stimulus Frequency ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Vascular Bed ◽  
Pulmonary Vascular Bed

The effects of methylene blue, an inhibitor of soluble guanylate cyclase, on pulmonary vasodilator responses to efferent vagal stimulation were investigated in the intact-chest cat under conditions of controlled blood flow and constant left atrial pressure. In animals pretreated with reserpine or phenoxybenzamine, under elevated tone conditions, efferent vagal stimulation at frequencies of 2-16 Hz caused stimulus-frequency-dependent decreases in lobar arterial pressure and pulmonary lobar vascular resistance. The vasodilator response to vagal stimulation was reproducible, blocked by atropine, and reduced by methylene blue. Intralobar infusion of methylene blue increased lobar arterial pressure without significantly altering systemic arterial or left atrial pressure. Methylene blue had no significant effect on vasodilator responses to isoproterenol, albuterol, atriopeptin III, lemakalim, adenosine, ATP, and pituitary adenylate cyclase-activating polypeptide-27 but significantly decreased vasodilator responses to acetylcholine, nitric oxide (NO), sodium nitroprusside, and the S-nitrosothiol, S-nitroso-N-acetyl-penicillamine. The effects of methylene blue on responses to vagal stimulation were reversible and were similar with the addition of a NO synthase inhibitor. The present data suggest that vasodilator responses to cholinergic nerve stimulation involve an increase in the production of guanosine 3',5'-cyclic monophosphate in the pulmonary vascular bed. These results provide additional evidence to support the hypothesis that neurogenically released acetylcholine induces endothelium-dependent, muscarinic, guanylate cyclase-mediated vasodilation.

Influence of Zaprinast on vascular tone and vasodilator responses in the cat pulmonary vascular bed

1993 ◽  
Vol 74 (4) ◽  
pp. 1704-1711 ◽  
Author(s):  
T. J. McMahon ◽  
L. J. Ignarro ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Vascular Tone ◽  
Vagal Stimulation ◽  
Phosphodiesterase Inhibitor ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Synthesis Inhibitor ◽  
Vascular Bed ◽  
Pulmonary Vascular Bed

The influence of Zaprinast (M&B 22948), a guanosine 3′,5′-cyclic monophosphate (cGMP)-specific phosphodiesterase inhibitor, was investigated in the pulmonary vascular bed of the cat under conditions of controlled blood flow and constant left atrial pressure. Under baseline conditions, injections of Zaprinast into the perfused lobar artery produced small decreases in lobar arterial pressure without altering systemic arterial or left atrial pressure. When tone was increased with U-46619, Zaprinast caused larger dose-dependent decreases in lobar arterial pressure without altering left atrial pressure. The decreases in lobar arterial pressure were reduced significantly by treatment with the nitric oxide (NO) synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or the guanylate cyclase inhibitor methylene blue. Under elevated tone conditions, efferent vagal stimulation and intralobar injections of acetylcholine, substance P, NO solution, and the S-nitrosothiols [S-nitroso-N-acetylpenicillamine (SNAP) and S-nitroso-L-cysteine (CysNO)] decreased lobar arterial pressure in a frequency-dependent and dose-related manner. After treatment with Zaprinast, the decreases in lobar arterial pressure in response to efferent vagal stimulation, the endothelium-dependent vasodilators, and the nitrovasodilators were not changed, whereas the duration of the vasodilator responses as measured by the half times was increased significantly. Vasodilator responses to adenosine, albuterol, and pinacidil were not altered by Zaprinast. These data suggest that cGMP hydrolysis in the lung is rapid and that endothelium-derived NO is important in stimulating basal cGMP production and in regulating vascular tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Progressive changes in cardiovascular function after unilateral heart irradiation

1964 ◽  
Vol 206 (2) ◽  
pp. 289-293 ◽  
Author(s):  
H. L. Stone ◽  
V. S. Bishop ◽  
A. C. Guyton
Keyword(s):  
Left Ventricle ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Pulse Rate ◽  
Left Atrial ◽  
Pressure Pulse ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Before And After ◽  
The Right

Chronic heart failure was produced by giving 20,000 r Co60 irradiation to either the right or left ventricle in nine closed-chest animals. Measurements of right and left atrial pressures, arterial pressure, pulse rate, body weight, and blood volume were made before and after irradiation. The right and left atrial pressures rose progressively until death in three animals irradiated on the right side. In six animals irradiated on the left side, the left atrial pressure rose progressively, but the right atrial pressure either did not rise or rose only during the latter stages of failure. Declining arterial pressure and increasing pulse rate were common to both groups. Increases in blood volume were observed in all animals, but this increase was only significant in the group irradiated on the left side. At autopsy, 70–100% of the right ventricular muscle was damaged in dogs irradiated on the right side, and 40–70% of the left ventricle in dogs irradiated on the left side. Hydrothorax and liver congestion were found in the right-sided group and pulmonary congestion in the left-sided group.

Pulmonary neutrophil kinetics in sheep: effects of altered hemodynamics

1985 ◽  
Vol 59 (6) ◽  
pp. 1796-1801 ◽  
Author(s):  
J. A. Cooper ◽  
R. Bizios ◽  
A. B. Malik
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Left Atrial ◽  
Recovery Period ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Blood Volume ◽  
Neutrophil Kinetics

We investigated the effect of elevated left atrial pressure and reduced cardiac output on pulmonary neutrophil kinetics in the sheep. Sheep neutrophils were isolated, labeled with 111In-oxine, and reinfused. Erythrocytes were labeled with [99mTc]pertechnetate. A gamma camera measured the lung activities of the labeled neutrophils and erythrocytes. The results indicated that 38.5% of the total injected neutrophils marginated in the lung. Pulmonary hemodynamics were altered by inflating a left atrial balloon three times in each sheep for 15–30 min to achieve 5- to 25-mmHg increments in pulmonary arterial wedge pressure. At least a 30-min recovery period was allowed between inflations. After each left atrial balloon inflation, neutrophil uptake remained unchanged from base line, despite decreased mean cardiac output to 0.67 +/- 0.24 (+/- SD) 1/min and increased pulmonary blood volume. The absence of pulmonary neutrophil uptake was confirmed by arterial-venous measurements. Increased pulmonary blood volume had little effect on lung neutrophil uptake, suggesting that most of the pulmonary neutrophils are marginated. We conclude that the lungs have a large marginated neutrophil pool compared with the circulating pool and that reduced cardiac output and elevated left atrial pressure have no effect on pulmonary neutrophil kinetics in the sheep.

Increased left atrial pressure does not alter renal function in the conscious primate

1982 ◽  
Vol 243 (1) ◽  
pp. R119-R124
Author(s):  
K. G. Cornish ◽  
J. P. Gilmore
Keyword(s):  
Blood Volume ◽  
Nonhuman Primate ◽  
Left Atrial ◽  
Macaca Fascicularis ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Blood Volume Expansion ◽  
Stretch Receptors ◽  
Renal Responses

To study the functional role of the atriorenal reflex in the nonhuman primate, we chronically instrumented six Macaca fascicularis with left atrial snares and left atrial and aortic catheters. After inserting a bladder catheter, we determined hemodynamic and renal responses of the conscious chair-restrained monkey to increased left atrial pressure. In 23 snare experiments, no significant changes in renal or cardiovascular function were observed even though left atrial pressure increased from 6.5 +/- 3.3 to 16.2 +/- 3.4 mmHg. The animals were subjected also to blood volume expansion with isoncotic isotonic dextran solutions (+15% of calculated blood volume). They responded normally to this volume stimulus. Conscious dogs prepared in the same manner as the nonhuman primate exhibited diuresis in response to elevations of atrial pressure. We conclude that left atrial stretch receptors are not importantly involved in volume homeostasis in the nonhuman primate.

Effects of prolonged elevated microvascular pressure on lung fluid balance in sheep

1985 ◽  
Vol 58 (3) ◽  
pp. 869-875 ◽  
Author(s):  
R. E. Parker ◽  
R. J. Roselli ◽  
K. L. Brigham
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Systemic Arterial Pressure ◽  
Protein Fractions ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Total Proteins ◽  
Lung Fluid ◽  
Osmotic Reflection Coefficient

Experiments were conducted in seven chronically instrumented unanesthetized sheep to estimate the osmotic reflection coefficient (sigma d) for total proteins and the solvent-drag reflection coefficients (sigma f) for six endogenous protein fractions. We measured the lymph-to-plasma ratio of total proteins (CL/CP) and six protein fractions during base-line conditions and after left atrial pressure elevations of 24–26 h per elevation. We also monitored pulmonary arterial pressure, left atrial pressure, systemic arterial pressure, and lung lymph flow at the various levels of pulmonary microvascular pressure. Our results indicate the CL/CP may require up to 24 h to reach a true steady state. It was found that sigma d is at least 0.89 for total proteins and sigma f is at least 0.84, 0.87, 0.86, 0.92, 0.95, and 0.96 for protein fractions with effective molecular radii of 36, 39.5, 44, 66, 105, and 123 A, respectively. In addition, the sigma f values for various protein fractions obtained from this investigation are compared with the predicted values of various mathematical models of the lung microcirculation.

Lymph flow and lung weight in isolated sheep lungs

1986 ◽  
Vol 61 (5) ◽  
pp. 1830-1835 ◽  
Author(s):  
W. Mitzner ◽  
J. T. Sylvester
Keyword(s):  
Weight Gain ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Water ◽  
Lung Weight ◽  
Pulmonary Arterial

To study the relationship between lung weight and lymph flow, we used an in situ, isolated sheep lung preparation that allowed these two variables to be measured simultaneously. All lungs were perfused for 4.5 h at a constant rate of 100 ml X min-1 X kg-1. In control lungs, the left atrial pressure (Pla) was kept at atmospheric pressure. In experimental lungs, Pla was kept atmospheric except for a 50-min elevation to 18 mmHg midway through the perfusion. During this period of left atrial hypertension, pulmonary arterial pressure rose from 18 to 31 mmHg, lymph flow rose from 3 to 12 ml/h, and the lymph-to-plasma oncotic pressure ratio (pi L/pi P) fell from 0.7 to 0.48. After left atrial pressure was returned to control, pulmonary arterial pressure, lymph flow, and pi L/pi P all returned to control levels. The rate of weight gain after the return of left atrial pressure to control was also the same as that in the control group. However, during the period of left atrial hypertension 135 ml of fluid were filtered into the lung, and this large increase in lung weight remained after the pressure was lowered. The presence of this substantial excess lung water despite control values for vascular pressures, lymph flow, rate of weight gain, and pi L/pi P suggests that the absolute amount of lung water has little influence on the dynamic aspects of lung fluid balance. These results are consistent with a two-compartment model of the interstitial space, where only one of the compartments is readily drained by the lymphatics.

Analysis of responses to sarafotoxin 6a and sarafotoxin 6c in the pulmonary vascular bed of the cat

1991 ◽  
Vol 71 (5) ◽  
pp. 2019-2025 ◽  
Author(s):  
T. J. McMahon ◽  
J. S. Hood ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Lower Lobe ◽  
Thromboxane A2 ◽  
Aortic Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Lobe ◽  
Vascular Bed ◽  
Pulmonary Vascular Bed

Pulmonary vascular responses to sarafotoxins 6a and 6c (S6a and S6c) were investigated in the intact-chest cat under constant flow conditions. Injections of S6a and S6c into the perfused lobar artery caused dose-related increases in lobar arterial pressure, increased left atrial pressure, and produced biphasic changes in systemic arterial (aortic) pressure. When left atrial pressure was maintained constant, injections of S6a, S6c, and endothelin 1 (ET-1) caused dose-related increases in lobar arterial pressure. The increases in lobar arterial pressure in response to S6a and S6c were not altered by treatment with a cyclooxygenase inhibitor or a thromboxane receptor blocking agent. Increases in lobar arterial pressure in response to S6a and S6c were not altered when airflow to the left lower lung lobe was interrupted by bronchial occlusion, and pressor responses were not diminished when the left lower lobe was perfused with low-molecular-weight dextran. Under conditions of controlled blood flow and constant left atrial pressure, S6a, S6b, S6c, and ET-1 had similar pressor activity, whereas the thromboxane A2 mimic, U-46619, had far greater activity when compared on a nanomolar basis. The present studies demonstrate that S6a and S6c have significant vasoconstrictor activity in the feline pulmonary vascular bed. These data suggest that pulmonary vasoconstrictor responses to the endothelin peptides are not dependent on release of cyclooxygenase products and the activation of thromboxane A2 receptors, alterations in bronchomotor tone, or interaction with formed elements in blood.

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