Immersion diuresis in dogs

1977 ◽  
Vol 42 (6) ◽  
pp. 915-922 ◽  
Author(s):  
J. T. Davis ◽  
A. B. DuBois

The mechanism of diuresis during the 1st h of immersion was investigated using anesthetized dogs. Four different experiments were carried out. First, left atrial transmural pressure was measured before, during, and after immersion. The data suggest that, although the left atrium may or may not be stretched depending on the conditions of immersion, the amount of diuresis is independent of the amount of left atrial stretch, and therefore a causal relationship between diuresis and left atrial stretch could not be established. Second, bilateral cervical vagotomy was carried out. Immersion diuresis sometimes occurred despite this vagotomy, suggesting that the left atrial stretch reflex was not participating in those cases. Third, negative-pressure breathing was carried out to simulate the negative transthoracic pressure associated with uncompensated immersion. The average left atrial transmural pressure did not change. A slight hemodilution and a moderate diuresis occurred. There was no correlation between changes in left atrial transmural pressure and changes in urine ouput. Fourth, blood studies were done on splenectomized dogs subjected to immersion. Hemodilution occurred and was most marked in dogs which had had their kidneys removed. The hemodilution is sufficient to explain the early phase of the immersion diuresis. The data suggest that, in anesthetized dogs, hemodilution is the probable initiator of diuresis upon immersion and that, in dogs, left atrial stretch is unrelated to diuresis during immersion or negative-pressure breathing.

1967 ◽  
Vol 22 (6) ◽  
pp. 1053-1060 ◽  
Author(s):  
Maylene Wong ◽  
Edgardo E. Escobar ◽  
Gilberto Martinez ◽  
John Butler ◽  
Elliot Rapaport

We measured the end-diastolic volume (EDV) and stroke volume (SV) in the right ventricle of anesthetized dogs during continuous pressure breathing and compared them to measurements taken during breathing at atmospheric pressure. During intratracheal positive-pressure breathing, EDV, and SV decreased and end-diastolic pressure became more positive relative to atmospheric pressure. During intratracheal negative-pressure breathing, EDV enlarged and SV tended to increase; end-diastolic pressure became more negative. During extrathoracic negative-pressure breathing SV decreased, EDV fell, though not significantly, and end-diastolic pressure rose, but insignificantly. Changes in EDV observed during intratracheal positive-pressure breathing and intratracheal negative-pressure breathing were associated with minor shifts in transmural pressure (end-diastolic pressure minus intrapleural pressure) in the expected directions, but during extrathoracic negative-pressure breathing a large increase in transmural pressure took place with the nonsignificant reduction in EDV. We believe that intrathoracic pressure influences right ventricular filling by changing the peripheral-to-central venous pressure gradient. The cause of the alteration in diastolic ventricular distensibility demonstrated during extra-thoracic negative-pressure breathing remains unexplained. positive-pressure breathing; negative-pressure breathing; extrathoracic negative-pressure breathing Submitted on August 16, 1966


1979 ◽  
Vol 47 (3) ◽  
pp. 582-590 ◽  
Author(s):  
S. M. Scharf ◽  
R. Brown ◽  
N. Saunders ◽  
L. H. Green

To assess the hemodynamic effects of spontaneous inspiration, we studied 12 anesthetized mongrel dogs during normal and loaded inspiration, before and after bilateral cervical vagotomy. Peak aortic flow fell (15--20%) whereas peak pulmonary artery flow rose (15--20%) under all conditions. When aortic flow fell, left ventricular diastolic size decreased whereas aortic and left atrial transmural pressures increased slightly. Right ventricular diastolic size and right atrial transmural pressure increased. During inspiratory loading transmural pressures rose more, but the fall in aortic flow remained the same. After vagotomy, inspiration was prolonged, allowing aortic flow to return to preinspiratory levels. At this time left ventricular diastolic size was increased compared to preinspiratory levels and there were further increases in left atrial and aortic transmural pressures. We have concluded that at least two factors affect aortic flow during inspiration: 1) a decrease in left ventricular preload that is associated with decreased left ventricular compliance, and 2) increased impedance to left ventricular emptying as reflected by the increase in aortic transmural pressure. This may play a greater role during inspiratory loading and when inspiration is prolonged.


1975 ◽  
Vol 229 (6) ◽  
pp. 1486-1491 ◽  
Author(s):  
J Boykin ◽  
P Cadnapaphornchai ◽  
KM McDonald ◽  
RW Schrier

Left atrial pacing was performed in three groups of anesthetized dogs. In the first group of eight intact dogs a mean increase in atrial rate (AR) from 140 +/- 7 to 244 +/- 6 was associated with a decrease in urinary osmolality (U osmol) from 631 +/- 72 to 264 +/- 43 mosmol/kg (P less than .001), and free-water clearance (CH20) increased from -.325 +/- .06 to +.355 +/- .15 ml/min (P less than .001). At the same time left atrial pressure (LAP) increased from 6 +/- 1 to 15 +/- 1 mmHg (P less than .001). A second group of studies was performed in six hypophysectomized, steroid-replaced animals receiving 40-50 muU/kg per min of antidiuretic hormone (ADH). In these animals AR was increased from 148 +/- 17 to 250 +/- 17 but diuresis did not occur. In these studies Uosmol was 690 +/- 55 before and 704 +/- 49 mosmol/kg after atrial pacing and CH20 also did not change. Left atrial pressure increased from 10 +/- 2 to 19 +/- 2 mmHg during atrial pacing. A third group of studies was performed in five animals with bilateral cervical vagotomy. In these animals AR was increased from 159 +/- 6 to 258 +/- 17 and LAP increased from 7 +/- 1 to 16 +/- 2 mmHg. Osmolality increased from 808 +/- 72 to 1,049 +/- 65 musmol/kg (P less than .005) and CH20 was unchanged. These results, therefore, indicate that atrial tachycardia primarily increases renal water excretion by suppressing ADH release. This reflex is dependent on the integrity of cervical vagal pathways.


1964 ◽  
Vol 19 (4) ◽  
pp. 665-671 ◽  
Author(s):  
Tulio Velasquez ◽  
Leon E. Farhi

Anesthetized dogs in the supine position show a spontaneous decrease in total respiratory compliance and an increase in venous admixture to the pulmonary circulation. Both these changes can be increased by negative-pressure breathing and reversed by positive-pressure breathing. If the changes in total respiratory compliance are due only to changes in lung compliance and these in turn result directly from the closure of alveoli, the relationship between compliance and inspiratory and expiratory pressure allows one to determine the scatter of opening and closing pressures in the alveoli. The venous admixture measures blood flow through collapsed alveoli, and its relationship to the negative pressure applied indicates the perfusion of the alveoli collapsing with each increment in negative pressure. By studying simultaneously changes in compliance and venous admixture, and using two basic assumptions, the dog's lungs can be described as a system composed of some elements receiving nearly 50% of the ventilation and 20% of the perfusion, relatively unstable mechanically, and having a very high Va/ Q ratio, while the remaining air spaces receive the same ventilation, but 80% of the perfusion. lung compliance; atelectasis; ventilation-perfusion ratio Submitted on October 28, 1963


1956 ◽  
Vol 186 (3) ◽  
pp. 501-504 ◽  
Author(s):  
Robert J. Atwell ◽  
Joseph F. Tomashefski ◽  
Joseph M. Ryan

The A-a oxygen pressure gradient was determined in anesthetized dogs. Data obtained when pulmonary ventilation and alveolar oxygen tension are varied independently suggests that: a) the magnitude of the A-a oxygen pressure gradient correlates directly with the Paoo2. b) In the anesthetized dog venous admixture seems to be constant, unrelated to the changes in ventilation produced by positive-negative pressure breathing. c) Venous admixture is the most important factor in producing the A-a gradient in the dog.


2001 ◽  
Vol 281 (4) ◽  
pp. H1583-H1588 ◽  
Author(s):  
Bettina Pump ◽  
Morten Damgaard ◽  
Anders Gabrielsen ◽  
Peter Bie ◽  
Niels Juel Christensen ◽  
...  

During an antiorthostatic posture change, left atrial (LA) diameter and arterial pulse pressure (PP) increase, and plasma arginine vasopressin (AVP) is suppressed. By comparing the effects of a 15-min posture change from seated to supine with those of 15-min seated negative pressure breathing in eight healthy males, we tested the hypothesis that with similar increases in LA diameter, suppression of AVP release is dependent on the degree of increase in PP. LA diameter increased similarly during the posture change and negative pressure breathing (−9 to −24 mmHg) from between 30 and 31 ± 1 to 34 ± 1 mm ( P < 0.05). The increase in PP from 38 ± 2 to 44 ± 2 mmHg ( P < 0.05) was sustained during the posture change but only increased during the initial 5 min of negative pressure breathing from 36 ± 3 to 42 ± 3 mmHg ( P < 0.05). Aortic transmural pressure decreased during the posture change and increased during negative pressure breathing. Plasma AVP was suppressed to a lower value during the posture change (from 1.5 ± 0.3 to 1.2 ± 0.2 pg/ml, P < 0.05) than during negative pressure breathing (from 1.5 ± 0.3 to 1.4 ± 0.3 pg/ml). Plasma norepinephrine was decreased similarly during the posture change and negative pressure breathing compared with seated control. In conclusion, the results are in compliance with the hypothesis that during maneuvers with similar cardiac distension, suppression of AVP release is dependent on the increase in PP and, furthermore, probably unaffected by static aortic baroreceptor stimulation.


1991 ◽  
Vol 261 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
F. L. Belloni ◽  
T. H. Hintze

The effects of the ATP-sensitive K(+)-channel blocker glibenclamide on the cardiovascular responses to adenosine in dogs were determined. Adenosine (0.01-20 mumol/kg iv) caused coronary vasodilatation, arterial hypotension, and bradycardia in dogs with either combined beta-adrenergic and muscarinic receptor blockade or with bilateral cervical vagotomy plus beta-adrenergic receptor blockade. The 50% effective dose for adenosine-induced coronary dilatation was increased from 0.13 +/- 0.04 mumol/kg in the control state to 1.1 +/- 0.5 mumol/kg after 2 mg/kg of glibenclamide (P less than 0.001). Adenosine at 5 mumol/kg reduced heart rate by 19 +/- 5% from a baseline of 158 +/- 6 beats/min in five anesthetized dogs. After glibenclamide (10 mg/kg), this dose of adenosine failed to cause a significant change in heart rate. The arterial hypotensive effects of adenosine were also attenuated by glibenclamide. Thus glibenclamide inhibited adenosine-induced bradycardia, hypotension, and coronary dilatation. On the other hand, glibenclamide did not affect the reductions in heart rate caused by vagus nerve stimulation. The mechanism of this adenosine antagonism is not known but, in the case of bradycardia, it does not appear to involve any of the steps shared in common by both adenosine-induced and vagal responses of the sinoatrial node.


1980 ◽  
Vol 2 (6) ◽  
pp. 761-770 ◽  
Author(s):  
Daniel Cousineau ◽  
Jacques de Champlain ◽  
Réginald Nadeau ◽  
François Péronnet

1965 ◽  
Vol 20 (4) ◽  
pp. 669-674 ◽  
Author(s):  
J. Salzano ◽  
F. G. Hall

Continuous pressure breathing was studied in hypothermic anesthetized dogs. Alveolar ventilation decreased during continuous positive-pressure breathing and increased during continuous negative-pressure breathing. The changes in alveolar ventilation were due to changes in respiratory rate as well as in respiratory dead space. Cardiac output fell significantly during continuous positive-pressure breathing due to a reduction in heart rate and stroke volume. During continuous negative-pressure breathing cardiac output was only slightly greater than during control as a result of a fall in heart rate and an increase in stroke volume. Oxygen consumption was reduced to 60% of control during continuous positive-pressure breathing of 16 cm H2O but was 25% greater than control during continuous negative-pressure breathing. Qualitatively, CO2 production changed as did O2 consumption but was different quantitatively during continuous negative-pressure breathing indicating hyperventilation due to increased respiratory rate. Mean pulmonary artery pressures and pulmonary resistance varied directly with the applied intratracheal pressure. The results indicate that the hypothermic animal can tolerate an imposed stress such as continuous pressure breathing and can increase its oxygen consumption during continuous negative-pressure breathing as does the normothermic animal. hypothermia; respiratory dead space; metabolic rate; cardiac output Submitted on December 8, 1964


1988 ◽  
Vol 64 (3) ◽  
pp. 1060-1067 ◽  
Author(s):  
G. A. Farkas ◽  
R. E. Baer ◽  
M. Estenne ◽  
A. De Troyer

To examine the mechanical effects of the abdominal and triangularis sterni expiratory recruitment that occurs when anesthetized dogs are tilted head up, we measured both before and after cervical vagotomy the end-expiratory length of the costal and crural diaphragmatic segments and the end-expiratory lung volume (FRC) in eight spontaneously breathing animals during postural changes from supine (0 degree) to 80 degrees head up. Tilting the animals from 0 degree to 80 degrees head up in both conditions was associated with a gradual decrease in end-expiratory costal and crural diaphragmatic length and with a progressive increase in FRC. All these changes, however, were considerably larger (P less than 0.005 or less) postvagotomy when the expiratory muscles were no longer recruited with tilting. Alterations in the elastic properties of the lung could not account for the effects of vagotomy on the postural changes. We conclude therefore that 1) by contracting during expiration, the canine expiratory muscles minimize the shortening of the diaphragm and the increase in FRC that the action of gravity would otherwise introduce, and 2) the end-expiratory diaphragmatic length and FRC in upright dogs are thus actively determined. The present data also indicate that by relaxing at end expiration, the expiratory muscles make a substantial contribution to tidal volume in upright dogs; in the 80 degrees head-up posture, this contribution would amount to approximately 60% of tidal volume.


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