EFFECT OF POSITIVE AND NEGATIVE EXPIRATORY PRESSURE ON RENAL FUNCTION

Br.J. Anaesth. (1977), 49, 199

EFFECT OF POSITIVE AND NEGATIVE EXPIRATORY PRESSURE ON RENAL FUNCTION S. GAMMANPILA, D. R. BEVAN AND R. BHUDU SUMMARY

The effects of positive and negative end expiratory pressure on renal function have been studied in adult greyhounds with a normal blood volume and without evidence of cardiorespiratory disease. Positive expiratory pressure (+10cmH 2 O) resulted in a decrease of urine volume, glomerular nitration rate and renal blood flow which returned towards normal following removal of the positive pressure. Negative expiratory pressure ( — 6 cm H2O) resulted in opposite changes in renal function.

S. GAMMANPILA, M.B., B.S., F.F.A.R.C.S.; D. R. BEVAN, M.A., M.B., F.F.A.R.C.S., M.R.C.P.; with technical assistance of

R. BHUDU; Department of Anaesthesia, St Mary's Hospital, London W.2.

syndrome to improve arterial oxygenation whilst avoiding a high inspired oxygen concentration (Ashboroughetal., 1967;Kafer, 1971). We have been concerned that PEEP is used indiscriminately in intensive therapy units. Often, success is measured as an improvement in arterial Po 2 , ignoring possible deleterious effects on the circulation. Consequently, this present study was designed to reassess the effects of PEEP and NEEP in experimental animals with no cardiorespiratory disease, on the function of the kidney, which is particularly susceptible to haemodynamic disturbances (Trueta et al., 1947). Previous work of this type has been concerned with the effect of either PEEP or NEEP in different animals. In this study, the effect of PEEP and NEEP has been studied in the same animal. METHODS

The studies were performed on six unpremedicated greyhound dogs weighing between 23 and 32 kg. Anaesthesia was induced with 5% thiopentone i.v. (mean dose 35 mg/kg). The trachea was intubated under direct vision with a cuffed plastic endotracheal tube. Mechanical ventilation was commenced, immediately after inflating the cuff, with a Blease anaesthetic ventilator. Approximately 75% nitrous oxide in oxygen was administered at a rate of 12 b.p.m. and the tidal volume was adjusted to maintain .Paco., of approximately 5 kPa*. Ketamine HC1 10 mg/kg i.m. initially followed by 5 mg/kg at hourly intervals was used to maintain anaesthesia. It has been established previously that ketamine HC1 has no effect on renal perfusion (Bevan and Bhudu, 1975). An incision was made in the right groin and a catheter was passed into the abdominal aorta via the *1 kPa= 7.5 mm Hg.

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Following the widespread use of intermittent positive pressure ventilation (IPPV) in the last 20 years, much controversy has focused on the optimal pattern of ventilation, particularly with regard to the expiratory phase. Alterations in ventilatory pressure patterns may lead to opposite effects on ventilation and tissue perfusion. Early in the development of ventilators it was anticipated that the abolition of the negative intrathoracic pressure in inspiration which occurs during spontaneous ventilation and its replacement with a positive pressure would cause a decrease in venous return with a subsequent reduction in cardiac output (Cournand et al., 1948). Consequently, most early ventilators had the facility to produce a negative end expiratory pressure (NEEP) to compensate for the net increase in intrathoracic pressure during IPPV. However, applying a negative pressure to the airways often resulted in a decrease in Pa Oj , probably as a result of closure of small airways and associated airtrapping (Nunn, 1958; Watson, 1962). It was stated subsequently that the cardiac output was depressed only minimally by IPPV in the normovolaemic patient. Thus NEEP is now seldom used (Adams, 1968). Recently the emphasis has shifted towards the provision of positive end expiratory pressure (PEEP) to prevent airway closure and improve pulmonary ventilation-perfusion ratios. Such therapy seems to be of particular benefit in the neonatal respiratory distress syndrome (Spiedel and Dunn, 1975) where PEEP is provided with either a Gregory box (Gregory et al., 1971) or a PEEP valve in the ventilator circuit. PEEP is used also in the adult respiratory distress

200

BRITISH JOURNAL OF ANAESTHESIA removed for sampling, 12 ml/sample, was replaced with 24 ml of Ringer-lactate. Dextrose 2.5% in water, containing PAH and inulin, was infused at the rate of 0.8 ml/min during the experiment. Blood-gas analysis

Arterial and renal venous blood were analysed immediately after withdrawal. Po 2 was measured with a Radiometer E 5406 oxygen electrode (Radiometer Ltd, Copenhagen), calibrated with oxygen, air and "white spot" nitrogen. pH and Pco2 (by interpolation) were measured with a Radiometer microelectrode apparatus calibrated with pH 6.840 and 7.383 buffers of the National Bureau of Standards. Temperature correction factors were used as described by Kelman and Nunn (1966). Experimental procedure

After all cannulae were in position, the animals were allowed to stabilize for 30 minutes. In three dogs the experiment was conducted as follows:

Measurement of renal blood flow

Renal blood flow (RBF) was measured by PAH clearance after determining renal PAH extraction. A stable plasma concentration of PAH of less than 10 mg/dl was obtained by infusing a solution of PAH and inulin in 2.5% dextrose with a constant infusion pump (MHRE 22) (Watson Marlow Ltd, Falmouth, Cornwall). Urine collections were made from the left ureter, over 20-min periods, and the volume was measured. At the mid-point of each urine collection, arterial and renal venous blood were sampled. PAH concentration of the blood and urine samples was estimated by a standard technique (Smith et al., 1945). After measuring the haematocrit (PCV), renal bloodflowwas estimated as follows: RBF =

•'PAH' • " P A TT — * P1 A H

1 ml/min i-PCV

where, C/PAH = urine PAH concentration AFAn = arterial PAH concentration P A H = renal venous PAH concentration F u = urine volume

30 min stabilization 2x20minIPPV 2x 20 min NEEP at - 6 cm H 2 O 2x20minIPPV 2 x 20 min PEEP at +10 cm H2O 2 x 20 min IPPV In the other three dogs, the periods of NEEP and PEEP were reversed. Blood was sampled at the mid-point of each 20min period and urine was sampled at the end. A PEEP valve from an Elema-Schonander Servo 900 ventilator was used to maintain PEEP. NEEP was produced using the mechanism of the Blease ventilator. Statistical analysis

Evaluation of the data was performed employing Student's t test.

RESULTS

Measurement ofglomerularfiltration

rate

Inulin was infused at a constant rate during the experiment and the inulin clearance was measured by a standard method (Davidson and Sackner, 1963). Fluid replacement

When all the catheters were positioned, Ringerlactate 25 ml/kg, was infused during 30 min Blood

Urine volume

There was no significant change in urine volume from the initial control value of 0.59 ml/min during any of the control periods throughout the experiments. When PEEP was applied, urine volume decreased in all six dogs (P<0.05) and increased towards prePEEP control values following its removal (tables I

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femoral artery. A wide-bore metal cannula with a curved tip was passed into the inferior vena cava via the femoral vein. At laparotomy, the tip of this cannula was placed near the left renal vein and a fine plastic catheter was passed through it to be positioned within the renal vein. The position of this catheter was checked at the conclusion of each experiment. Both ureters were cannulated for collection of urine. The catheters from the abdominal aorta and the left renal vein and another connected to the catheter mount of the endotracheal tube (airway pressure) were connected to strain gauge transducers (Devices Instruments Ltd, Welwyn Garden City, Herts) whose output was amplified and fed into a fourchannel heated stylus recorder (Devices Ltd) and displayed on an oscilloscope (Airmec Ltd, High Wycombe, Bucks). Rectal temperature was monitored using a mercury-filled glass thermometer. Cannulae were placed in a forelimb and a hindlimb vein for fluid replacement and constant infusion of para-amino hippuric acid (PAH) and inulin.

EXPIRATORY PRESSURE AND RENAL FUNCTION

201

TABLE I. Renal function data in dogs in which negative end-expiratory pressure was employed first End expiratory pressure (cm H 2 O) Cl C2

C3 C4

0 0 -6 -6 0 0

C5 C6

0 0

1.1

1.035 0.72 0.195 0.18 0.385 0.41

RBF

Cm

350 421 520 296 265 270 176 283 362 289

29.4 41.2 60.3 45.2 41.2 45.2 19.5 16.7 23.2 27.3

0.49 0.305 0.235 0.175 0.11 0.11 0.055 0.04 0.09 0.04

RBF

Cm

393 185 431 367 276 459 75 42 210 97

23.9

18.3

0.275 0.155 0.205 0.145 0.075 0.055 0.01 0.01 0.025

7.8

—

8.7

12.8 10.1 1.2 1.7

11.6 7.4

RBF

Cm

329 359 780 414 337 238 79 83 39 —

40.5 51.1 45.6 25.9 22.9 21 3.3 2.9 4.1 —

Vn= urine volume (ml/min); RBF= renal blood flow (ml/min); Cm= inulin clearance (ml/min).

TABLE II. Renal function data in dogs in which positive end-expiratory pressure was employed first

Cl C2

End expiratory

Dog no. 12/75

(cm H 2 O)

RBF

Cm

662 551 350 505 566 616 505 604 538 719

22.2

0 0

+ 10 + 10 C3 C4

0 0 -6 -6

C5 C6

0 0

0.9

0.79 0.15 0.19 0.34 0.49 0.96 1.31 1.34 1.6

Dog no. 14/75

33

10.1 20

17.8 8.7

17.3 11.3 32.2 36.5

0.62 0.96 0.605 0.425 0.45 0.55 0.955 1.19 0.76 0.775

Dog no. 23/75

RBF

Cm

239 421 367 482 360 362 753 884 729 837

39.4 81.2 34.1 35.6 31.6 48.9 40

59.5 39.2 49.3

0.325 0.42 0.14 0.2

0.255 0.255 0.32 0.5

0.275 0.095

RBF

Cm

593 639 428 565 550 398 436 439 395 337

59.5 54.1 29.9 41.9 74.2 48

56.9 56.9 39.1 20.9

Ku= urine volume (ml/min); RBF= renal blood flow (ml/min); 0 ^ = inulin clearance (ml/min).

and II, fig. 1). In the figures, all values for PEEP, and also NEEP, have been aggregated although in half the dogs the NEEP periods preceded those of PEEP. Glomerular filtration rate

During the study period, there was a gradual decrease in inulin clearance (C In ) in the control periods from an initial value of 36.8 ml/min to a final value of 28.3 ml/min. This decrease was not statistically significant. Institution of PEEP resulted in a decrease in C I n in five of the six dogs and, in three of

these, removal of PEEP resulted in a restoration of C I n towards control values. The decrease in C l n was statistically significant (P<0.05). Institution of NEEP resulted in an increase in C In in four of the six dogs (P<0.05) and on its removal C I n decreased infiveof the dogs (tables I and II,fig.2). Renal blood flow

There was a gradual reduction in RBF during the day from an initial mean value of 427 ml/min to a final value of 181 ml/min. With PEEP, RBF decreased in all six dogs (P<0.05). The decrease was greatest

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+ 10 + 10

0.95 0.495 1.005

Dog no. 22/75

Dog no. 15/75

Dog no. 13/75

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202

s

o.e

•H

E

I

0.6

0.4 >

0.2

\ Ir •

FIG. 1. Effect of PEEP and NEEP on urine production. Control periods: C1-C6; PEEP, +10 cm H 2 O: + + ; NEEP, - 6 c m H , O : .

200

Cl

C2

+

+

C3

C4

-

-

CS

C6

FIG. 3. Effect of PEEP and NEEP on renal blood flow.

oxygen. No change was made in the Rotameter setting throughout the day. Pa Oi never decreased more than 2 kPa below the initial control value in any dog and was always sufficient to achieve more than 90% arterial saturation. In five dogs Pa Oi decreased slightly with PEEP and returned towards normal on its removal although the changes were not statistically significant. No obvious change was seen with NEEP (table III, fig. 4). Renal oxygenation

Renal venous Po 2 remained stable throughout the day (initial mean value 8.7 kPa, final value 9.0 kPa)

FIG. 2. Effect of PEEP and NEEP on glomerular filtration rate.

X

I

RENAL VENOUS (mean -

PO,

SEH)

in those three dogs in which PEEP followed NEEP (65% mean reduction compared with 20%). With NEEP, RBF increased in all six dogs (P<0.05) and returned towards control values after its removal (tables I and II, fig. 3). Arterial oxygenation No attempt was made to maintain PiOi constant, the oxygen and nitrous oxide Rotameters being adjusted to give approximately 75% nitrous oxide in

FIG. 4. Arterial and renal venous oxygen tension during PEEP and NEEP.

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5

E

EXPIRATORY PRESSURE AND RENAL FUNCTION

203

TABLE III. Arterial and renal venous Po2 (kPa) associated with changes in end-expiratory pressure End expiratory pressure (cm H 2 O) Cl C2

C3 C4

Dog no. 23/75

Dog: no. 14/75

Dog no.

13/75

•Pao,

Pvo,

P*O,

^vo,

^a 0 ,

Pvo.

P^o.

13.24 13.50 12.44 13.24 14.43 14.44 11.23 11.64 11.77 12.63

8.2 8.06 8.26 8.93 8.6 8.67 6.87 7.40 7.33 11.07

13.51 14.31 13.91 13.77 14.44 14.71 14.84 14.71 15.11 15.24

9.6

13.47

7.73 7.47 8.67 8.53

11.91 11.96 9.36 10.63 9.76 8.83 10.43 9.36 10.83 10.43

9.67 9.47 9.73 9.73 9.67 9.67 12.53 9.67 9.33

12

13.13 12.8 14.67 12.53 12.2 11.87 12

13.07

8.4 —

8.13 7.87 7.73 8.53

^vo, 9.07 9.2 8.73 9.2 8.8 8.27 9 8.47 9.2 8.93

Dog no. 15/75

P*o,

P&O. 13.91 14.05 11.91 11.77 14.17 11.64 13.37 13.37 11.51 11.77

Dog no. 22/75

8.8 9.07 8.27 7.33 9.07 8.67 8.67 9.2 7.73 7.47

15.2 15.2 12.53 12.27 13.87 13.07 12.67 12.67 12.67 —

Pvo. 8.53 8.4 7.2 9.2

8.87 8.27 8.47 8.8

6.93 —

= renal venous Po2

suggesting that despite a decrease in renal perfusion there was no evidence of renal hypoxia (table III, fig. 4). DISCUSSION

This study showed that renal function, as assessed by urine output, glomerular filtration rate and renal blood flow, was affected by alteration in expiratory pressure during IPPV in greyhounds. Positive pressure produced a reduction in these indices which was abolished on return to zero expiratory pressure and reversed in the presence of a negative phase. There was no evidence of renal ischaemia, as assessed by renal venous Po2 because the reduced oxygen delivery during PEEP was matched by an overall decrease in renal function, and therefore oxygen requirement. Such changes, if they occur in man also, —and there is good reason to suspect that they do— would lead to considerable problems in the maintenance of fluid balance. Sladen, Laver and Pontoppidan (1968), Gett, Sherwood-Jones and Shepherd (1971), Styles, Robinson and Jones (1970) and Qvist and colleagues (1975) have described the water and sodium retention which occurs both in man and animals during IPPV. This retention is accentuated when PEEP is applied (Murdaugh, Sieker and Manfredi, 1959; Baratz, Philbin and Patterson, 1971; Ueda et al., 1972). With the application of NEEP oliguria is abolished and even a diuresis may occur (Gauer et al., 1954; Murdaugh, Sieker and Manfredi, 1959). Debate has arisen about the aetiology of such changes. Baratz and Ingraham (1960) suggested that PEEP caused oliguria by the reflex secretion of

antidiuretic hormone (ADH) as a consequence of changes in left atrial pressure. Kumar and others (1974) and Khambatta and Baratz (1972) showed that, in humans, PEEP produced a twofold increase in secretion of ADH, sufficient to cause oliguria, but that inconsistent changes in free water and osmolar clearances and urine osmolality pointed to an inappropriate response to ADH, suggesting that other factors were concerned in the oliguria. In the present study it was a striking observation that, when PEEP was removed, urine flow rate increased almost immediately. As the half-life of ADH is 7-8 min (Morton, Padfield and Forsling, 1975) it is unlikely that oliguria associated with PEEP is induced by ADH. The observations of Baratz and Ingraham, that there was a 15-20 min delay before NEEP induced diuresis in ventilated dogs was not confirmed in the present study. As the changes in renal function occur so rapidly with a change in expiratory pressure, it seems more likely that there is a haemodynamic reason for the change. However, Hall, Johnson and Hedley-White (1974) were unable to demonstrate any change in total renal blood flow during PEEP in animals, but showed that there was a redistribution of blood flow from the superficial to the deeper renal cortical regions. Such a redistribution would be associated with sodium and water retention as the deeper, juxtamedullary nephrons conserve sodium, and consequently water (Thurau, 1969). In the present study total renal blood flow was measured after calculation of renal PAH extraction. When measured in this way PEEP (+ 10 cm H2O)-induced oliguria was associated with a mean decrease in RBF of 42%

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C5 C6

0 0 + 10 + 10 0 0 -6 -6 0 0

Dog no. 12/75

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ACKNOWLEDGEMENTS

This study was supported by a grant from the St Mary's Hospital Joint Standing Research Committee. We are also grateful to Miss A. Colbran for secretarial assistance. REFERENCES

Adams, A. P. (1968). Ventilators for use in anaesthesia. Br.J.Hosp.Med., 4,23. Ashborough, D. G., Bigelow, D. B., Petty, T. L., and Levine, B. E. (1967). Acute respiratory distress in adults. Lancet, 2,319. Baratz, R. A., and Ingraham, R. C. (1960). Renal hemodynamics and antidiuretic hormone release associated with volume regulation. Am.J. Physiol., 198,565. Philbin, D. M., and Patterson, R. W. (1971). Plasma antidiuretic hormone and urinary output during continuous positive pressure breathing in dogs. Anesthesiology, 34,510. Bevan, D. R., and Bhudu, R. (1975). The effect of ketamine on renal blood flow in greyhounds. Br. J. Anaesth., 47, 634. Colgan, F. J., Barrow, R. E., and Fanning, G. L. (1971). Constant positive pressure breathing and cardiorespiratory function. Anesthesiology, 34,145. Cournand, A., Motley, H. L., Wenko, L., and Richards, D. W. (1948). Physiological studies of the effects of intermittent positive pressure breathing on cardiac output in man. Am.J. Physiol., 152,162. Davidson, W. D., and Sackner, M. A. (1963). Simplification of the anthrone method for the determination of inulin in clearance studies. .7. Lab. Clin. Med., 62,351. Gauer, O. H., Henry, J. P., Seiker, H. O., and Wendt, W. E. (1954). The effect of negative pressure breathing on urineflow.J . Clin. Invest., 33,287. Gett, P. M., Sherwood-Jones, J. G., and Shepherd, G. F. (1971). Pulmonary oedema associated with sodium retention during ventilator treatment. Br. J. Anaesth., 43,460.

Morgan, B. C , Crawford, E. W., and Guntherath, W. G. (1969). The hemodynamic effects of changes in blood volume during intermittent positive pressure ventilation. Anesthesiology, 30,299. Morton, J. J., Padfield, P. L., and Forsling, M. L. (1975). A radio-immunoassay for plasma arginine-vasopressin in man and dog: application to physiological and pathological states. J. Endocrinol., 65,411. Murdaugh, H. V., Seiker, H. O., and Manfredi, F. (1959). Effect of altered intrathoracic pressure on renal hemodynamics, electrolyte excretion and water clearance. J. Clin. Invest., 38,834. Nunn, J. F. (1958). The anaesthetist and the emphysematous patient. Br.J. Anaesth., 30,134. Qvist, J., Pontoppidan, H., Wilson, R. S., Lowenstein, E., and Laver, M. B. (1975). Hemodynamic responses to mechanical ventilation with PEEP. The effect of hypervolemia. Anesthesiology, 42,45. Scott, D. B., Stephen, G. W., and Davie, I. T. (1972). Haemodynamic effects of negative (sub-atmospheric) pressure expiratory phase during artificial ventilation. Br.J. Anaesth., AA, 171. Sladen, A., Laver, M. B., and Pontoppidan, H. (1968). Pulmonary complications and water retention in prolonged mechanical ventilation. N. Engl.J. Med., 279,448. Smith, H. W., Finkelstein, N., Alminosa, L., Crawford, R., and Graher, M. (1945). The renal clearances of substituted hippuric acid derivatives and other aromatic acids in dog and man. J. Clin. Invest., 24,388. Spiedel, B. D., and Dunn, P. M. (1975). Effect of continuous positive airway pressure on breathing pattern of infants with respiratory-distress syndrome. Lancet, 1,302. Styles, J., Robinson, J. S., and Jones, J. G. (1970). Continuous ventilation and oedema. Br.J. Med., 2,522. Thurau, K. (1969). The dependancy of intrarenal distribution of single nephron filtration rates on dietary salt intake (micropuncture studies). Proc. R. Soc. Med., 62,1118. Trueta, J., Barclays, A. E., Franklin, K. H., Daniel, P. M., and Prichard, M. L. (1947). Studies of the Renal Circulation. Springfield, Illinois: Thomas.

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and NEEP (— 6 cm H2O)-induced diuresis with a Gregory, G. A., Kitterman, J. A., Phibbs, R. H., Tooley, W. H., and Hamilton, W. K. (1971). Treatment of the mean increase in RBF of 45%. idiopathic respiratory distress syndrome with continuous The alterations in renal function are compatible positive airway pressure. N. Engl.J. Med., 284,1333. with haemodynamic changes resulting from changes Hall, S. V., Johnson, E. E., and Hedley-White, J.(1974). in intrathoracic pressure. Many authors (Morgan, Renal hemodynamics and function with continuous positive pressureventilation in dogs. Anesthesiology, 41,452. Crawford and Guntherath, 1969; Scott, Stephen and Davie, 1972; Qvist et al., 1975) have reported a Kafer, E. (1971). Pulmonary oxygen toxicity. A review of the evidence for acute and chronic oxygen toxicity in man. decrease in cardiac output associated with PEEP and Br. J. Anaesth., 43,687. accompanied by an increase in central venous pres- Kelman, G. R., and Nunn, J. F. (1966). Nomograms for sure, and a decrease in central blood volume and correction of blood Poa Pco2, pH and base excess for stroke volume. In contrast NEEP results in an time and temperature. J. Appl. Physiol., 21,1484. increase in central blood volume, stroke volume and Khambatta, H. J., and Baratz, R. A. (1972). IPPB, plasma ADH, and urine flow in conscious man. J. Appl. Physiol., cardiac output (Kilburn and Seiker, 1960; Colgan, 33,362. Barrow and Fanning, 1971). These experiments with Kilburn, K. H., and Seiker, H. O. (1960). Hemodynamic normovolaemic dogs suggest that such changes may effects of continuous positive and negative pressure breathing in normal man. Circ. Res., 8,660. be of importance in the maintenance of organ function and that physiological consequences of Kumar, W., Pontoppidan, H., Baratz, R. A., and Laver, M. B. (1974). Inappropriate response to increased plasma alteration of expiratory pressure during IPPV merit ADH during mechanical ventilation in acute respiratory greater consideration. failure. Anesthesiology, 40,215.

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EXPIRATORY PRESSURE AND RENAL FUNCTION Ueda, H., Neclerio, M., Leather, R. P., and Powers, S. R. (1972). Effect of positive end expiratory pressure ventilation on renal function. Surg. Forum., 23,209. Watson, W. E. (1962). Observations on physiological deadspace during intermittent positive pressure respiration. Br.J. Anaesth., 34,502.

RESUME

On a 6tudi6 sur des levriers adultes ayant un volume sanguin normal et ne prSsentant aucun symptome de maladie cardiorespiratoire les effets de la pression expiratoire finale, positive et negative, sur la fonction renale. La pression expiratoire positive (+10 cm H 2 O) a produit une diminution du volume d'urine, du taux de nitration glom£rulaire et de l'ecoulement de sang renal qui sont retourne's a la normale apres retrait de la pression positive. La pression expiratoire negative (— 6 cm H2O) a donn6 pour resultat des variations opposees dans la fonction renale.

18

ZUSAMMENFASSUNG

Die Wirkungen des positiven und negativen Ausatmungsdruckes auf die Nierenfunktion wurden studiert bei ausgewachsenen Windhunden mit normalem Blutvolumen und ohne Anzeichen von Herz- und Atmungskrankheiten. Der positive Ausatmungsdruck (+10 cm H 2 O) fuhrte zu einer Verringerung des Urinvolumens, der glomerularen Filtriergeschwindigkeit und des Nieren-Blutdurchflusses; diese Werte wurden wieder normal, sobald der positive Druck ausgesetzt wurde. Der negative Ausatmungsdruck (— 6 cm H 2 O) fuhrte zu gegenteiligen Veranderungen der Nierenfunktion. EFECTO DE PRESION ESPIRATORIA POSITIVA Y NEGATIVA SOBRE LA FUNCION RENAL SUMARIO

Los efectos de la presi6n espiratoria positiva y negativa sobre la funcion renal han sido estudiados en galgos adultos con una volemia normal y sin evidencia de afeccion cardiorrespiratoria. La presi6n espiratoria positiva (+10 cm H a O) resulto en disminucion del volumen de orina, indice de filtrado glomerular y deflujo hematico renal, que retornaron a la normalidad tras suspender la presion positiva. La presi6n espiratoria negativa ( — 6 cm H2O) result6 en cambios opuestos en la funcidn renal.

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EFFET DE LA PRESSION EXPIRATOIRE POSITIVE ET NEGATIVE SUR LA FONCTION RENALE

DIE WIRKUNG DES POSITIVEN UND NEGATIVEN EXPIRATORISCHEN DRUCKES AUF DIE NIERENFUNKTION

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