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At least 289 records · Page 16Linked to original sources
PubMed1986

Pulmonary fluid balance following pulmocutaneous baroreceptor denervation in the toad.

Pulmonary hemodynamics and net transcapillary fluid flux (NTFF) were measured in conscious toads before and following bilateral denervation of the recurrent laryngeal nerves (rLN), which contain afferents from baroreceptors located in the pulmocutaneous arteries. Denervation caused an acute doubling of the arterial-venous pressure gradient across the lung and a threefold increase in pulmonary blood flow. Calculated pulmonary vascular resistance fell and remained below control values through the period of experimentation. NTFF increased by an order of magnitude (0.74-7.77 ml X kg-1 X min-1), as filtration increased in response to the hemodynamic changes caused by rLN denervation. There was a better correlation between NTFF and pulmonary blood flow than between NTFF and pulmonary driving pressure. Our results support the view that tonic neural input from pulmocutaneous baroreceptors protects the anuran lung from edema by restraining pulmonary driving pressure and blood flow and perhaps by reflexly maintaining vascular tone in the extrinsic pulmonary artery, therefore tending to increase the pre-to-postpulmonary capillary resistance ratio and biasing the Starling relationship in the pulmonary capillaries against filtration.

Animals↗
PubMed1994

Effect of hypoxia on lung fluid balance in ferrets.

To determine how hypoxia may alter determinants of pulmonary transvascular fluid flux, adult male ferrets were exposed to either room air (C) or hypoxia (H; FIO2 = 0.12) for 24 h. After anesthesia and ventilation with C or H, the mean pulmonary artery pressures were 18.4 +/- 2.2 (SEM) and 27.3 +/- 2.9 mm Hg, respectively (p < 0.025). The right lung was then removed for gravimetric analysis of lung water and the left lung was blood-perfused (approximately 142 ml/kg/min) and continuously weighed for 15 min at left atrial pressures of 20, 25, and 30 mm Hg. Filtration coefficient (Kf) was estimated from the slopes of the relationships of rate of weight gain versus change in vascular pressure over the last 5 min of each interval. Extravascular lung water/blood-free dry lung weight for C and H were 2.95 +/- 0.06 (SEM) and 3.53 +/- 0.09 ml/g, respectively (p < 0.01). Kf for C and H were 0.0645 +/- 0.0190 (SEM) and 0.0662 +/- 0.0085 ml/min/mm Hg/100 g, respectively (NS). In a second group of experiments, in which lungs were removed from ferrets after 24 h exposures to C or H, protein reflection coefficients (sigma) were estimated by comparing the increases in perfusate hematocrit and protein concentrations during edema formation. Reflection coefficients for albumin were 0.64 +/- 0.03 (SEM) and 0.39 +/- 0.07 with C and H, respectively (p < 0.01). The sigma values for IgG and IgM were not affected.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed2002

Estrogen effects on osmotic regulation of AVP and fluid balance.

To determine estrogen effects on osmotic regulation of arginine vasopressin (AVP) and body fluids, we suppressed endogenous estrogen and progesterone using the gonadotropin-releasing hormone (GnRH) analog leuprolide acetate (GnRHa). Subjects were assigned to one of two groups: 1) GnRHa alone, then GnRHa + estrogen (E, n = 9, 25 +/- 1 yr); 2) GnRHa alone, then GnRHa + estrogen with progesterone (E/P, n = 6, 26 +/- 3). During GnRHa alone and with hormone treatment, we compared AVP and body fluid regulatory responses to 3% NaCl infusion (HSI, 120 min, 0.1 ml. min(-1). kg body wt(-1)), drinking (30 min, 15 ml/kg body wt), and recovery (60 min of seated rest). Plasma [E(2)] increased from 23.9 to 275.3 pg/ml with hormone treatments. Plasma [P(4)] increased from 0.6 to 5.7 ng/ml during E/P and was unchanged (0.4 to 0.6 ng/ml) during E. Compared with GnRHa alone, E reduced osmotic AVP release threshold (275 +/- 4 to 271 +/- 4 mosmol/kg, P < 0.05), and E/P reduced the AVP increase in response during HSI (6.0 +/- 1.3 to 4.2 +/- 0.6 pg/ml at the end of HSI), but free water clearance was unaffected in either group. Relative to GnRHa, pre-HSI plasma renin activity (PRA) was greater during E (0.8 +/- 0.1 vs. 1.2 +/- 0.2 ng ANG I. ml(-1). h(-1)) but not after HSI or recovery. PRA was greater than GnRHa during E/P at baseline (1.1 +/- 0.2 vs. 2.5 +/- 0.6) and after HSI (0.6 +/- 0.1 vs. 1.1 +/- 1.1) and recovery (0.5 +/- 0.1 vs. 1.3 +/- 0.2 ng ANG I. ml(-1). h(-1)). Baseline fractional excretion of sodium was unaffected by E or E/P but was attenuated by the end of recovery for both E (3.3 +/- 0.6 vs. 2.4 +/- 0.4%) and E/P (2.8 +/- 0.4 vs 1.7 +/- 0.4%, GnRHa alone and with hormone treatment, respectively). Fluid retention increased with both hormone treatments. Renal sensitivity to AVP may be lower during E due to intrarenal effects on water and sodium excretion. E/P increased sodium retention and renin-angiotensin-aldosterone stimulation.

Adult↗
PubMed1985

Fluid balance and secretion of antidiuretic hormone following transsphenoidal pituitary surgery. A preliminary series.

Hyponatremia developing some days after transsphenoidal pituitary adenectomy is a treacherous complication of uncertain cause. Of 19 patients monitored in a pilot study at the Wessex Neurological Centre, plasma sodium fell below 125 mmol/liter in three patients at times ranging from 6 to 9 days postoperatively. One patient had evidence of inappropriate secretion of arginine vasopressin (AVP), and the other two probably had steroid insufficiency despite apparently adequate steroid cover. In a more detailed study, the fluid and sodium balance of a further 16 patients was monitored for 7 to 11 days following transsphenoidal surgery together with plasma cortisol, renin, and AVP concentrations. No patient became severely hyponatremic. Three developed partial diabetes insipidus. Two patients with Cushing's disease had evidence of postoperative corticosteroid insufficiency despite normal steroid protection. An inappropriately low plasma cortisol concentration was recorded in both. Plasma AVP concentrations did not show a delayed surge postoperatively. Delayed hyponatremia appears to occur most often in patients with hypoadrenalism, as glucocorticoid cover is decreased. It results from water retention combined with natriuresis, and is reversed by glucocorticoid treatment.

Adenoma↗
PubMed1996

Myocardial fluid balance in acute hypertension.

OBJECTIVES: We hypothesized that (1) acute arterial hypertension increases myocardial microvascular fluid filtration and (2) the combination of acute arterial hypertension and coronary sinus pressure elevation may increase myocardial microvascular filtration sufficiently to estimate the osmotic reflection coefficient of the myocardial exchange vessels. METHODS: In nine mechanically ventilated dogs we cannulated the prenodal major cardiac lymph trunk. With the use of central venous phenylephrine infusion, mean arterial pressure (MAP) was raised progressively to 120, 160, and 180 mm Hg. In five dogs we additionally raised coronary sinus pressure (CSP) to 20 and 40 mm Hg. At each manipulation of MAP and/or CSP, we measured indexes of myocardial lymphatic function and lymph-to-plasma concentration ratios for total protein (CL(TP)/CP(TP) and albumin (CL(alb)/CP(alb)). RESULTS: Myocardial lymph flow rate (QL; microL/min) increased exponentially (QL = 10.9.e0.014.(MAP) and myocardial lymph driving pressure (PL; mm Hg) increased linearly (PL = 2.30 + 0.20 + 0.20 . MAP) following increases, whereas CL(TP)/CP(TP) and CL(alb)/CP(alb) decreases from 0.67 +/- 0.07 (SD) to 0.56 +/- 0.10 and from 0.91 +/- 0.05 to 0.75 +/- 0.11, respectively. Adding CSP elevation increased QL up to 12 times control associated with further CL(TP)/C(TP) and CL(alb)/CP(alb) decreases to 0.49 +/- 0.05 and 0.59 +/- 0.02, respectively. CONCLUSIONS: We conclude that hypertensive arterial pressures are, at least in part, transmitted to the myocardial microvascular exchange vessels in the intact animal leading to increased microvascular fluid filtration. However, the combination of acute arterial hypertension and coronary sinus pressure elevation is not sufficient to produce filtration independence required for myocardial osmotic reflection coefficient determination.

Animals↗
PubMedDate not supplied

[Bases of infusional therapy. Note. I. Fluid balance].

The complex hydroelectrolytic problem is examined by a study of the physiology and physiopathology of fluids, electrolytes and proteins. A number of interesting critical and clinical problems of use in the pre- and postoperative treatment of surgical patients and in cases where a change in the hydroelectric balance takes place, are involved. Therapy is facilitated if needs are calculated on the basis of the three basic principles: 1) daily physiological need; 2) replacement of physiological losses; 3) elimination of the existing deficiency.

Humans↗
PubMedDate not supplied

Fluid balance modelling in patients with kidney failure.

In patients with kidney failure, adequate control of fluid status remains one of the most difficult routine issues to be addressed in the modern style of dialysis. This is primarily due to the lack of quantitative methods for the assessment of fluid status and the reliance on subjective criteria. Fluid is removed from the blood during dialysis treatments using a process called ultrafiltration. The last decade has seen considerable developments in blood volume monitoring (BVM) technology which has enabled responses to ultrafiltration to be continually monitored on an individual basis. This has enabled feedback control of patients' blood volume to be applied with partial success, reducing the number of symptoms. The feedback control algorithms employed have been relatively unsophisticated, using simple proportional control with no attempt to include models of the patient fluid dynamics. This paper describes the development of some prototype fluid kinetic models which may be used in a more advanced control system. Initial results demonstrate the importance of active control processes in the patients' physiological compensatory mechanisms.

Blood Volume↗
PubMed1979

Effect of infusing histamine into pulmonary or bronchial artery on sheep pulmonary fluid balance.

We determined the dose-response curve for the effect of histamine on pulmonary fluid and protein exchange when histamine was infused directly into the bronchial artery or pulmonary circulation in anesthetized sheep with a right thoracotomy and an acutely prepared lung lymph fistula. We measured pulmonary hemodynamics, lung lymph flow, and lymph-to-plasma protein concentration ratios in 14 sheep. We infused histamine at constant rates of 0.1, 1, 3, and 10 micrograms/kg . min until a steady state was achieved at each level for 1 h. In the bronchial circulation the lowest effective dose of histamine was 1 microgram/kg . min, which increased lymph flow at constant ratio of lymph to plasma protein concentration. Lymph flow increased further as the dose of infused histamine increased. Infusions into the pulmonary circulation had similar effects, but in addition, pulmonary vascular resistance decreased. The dose-response curves for the effects of histamine on lung lymph and protein flow were identical for the 2 routes of infusion. The effect of histamine was to increase lung microvascular permeability modestly. We conclude that the site of continued action of histamine is probably in the pulmonary microcirculation, because for any given infusion rate, the local concentration of histamine in the bronchial microcirculation must be much greater than that in the pulmonary microcirculation because the ratio of blood flows is so different.

Animals↗