Effect of epinephrine on alveolar liquid clearance in the rat.
Adrenergic; Adrenergic beta-Agonists/*pharmacology; Amiloride/pharmacology; Animals; beta/metabolism; Bronchoalveolar Lavage Fluid/chemistry; Epinephrine/blood/*pharmacology; Male; Norepinephrine/blood; Propranolol/pharmacology; Pulmonary Alveoli/*drug effects; Rats; Receptors; Serum Albumin/metabolism; Sprague-Dawley; Time Factors
Endogenous epinephrine has been found to increase alveolar liquid clearance (ALC) in several pulmonary edema models. In this study, we infused epinephrine intravenously for 1 h in anesthetized rats to produce plasma epinephrine concentrations commonly observed in this species under stressful conditions and measured ALC by mass balance. Epinephrine increased ALC from 31.5 +/- 3.2 to 48.9 +/- 1.1 (SE)% of the instilled volume (P \textless 0.05). The increased ALC was prevented by either propranolol or amiloride. To determine whether ALC returns to normal after plasma epinephrine concentration normalizes, we measured ALC 2 h after stopping an initial 1-h epinephrine infusion and found ALC to be at baseline values. Finally, to determine whether desensitization of the liquid clearance response occurs, we evaluated the effects of both repeated 1-h infusions and a continuous 4-h infusion of epinephrine on ALC and found no reduction in ALC under either condition. We conclude that epinephrine increases ALC by stimulating beta-adrenoceptors and sodium transport, that the increase is reversible once plasma epinephrine concentration normalizes, and that desensitization of the ALC response does not appear to occur after 4 h of continuous epinephrine exposure.
Charron P D; Fawley J P; Maron M B
Journal of applied physiology (Bethesda, Md. : 1985)
1999
1999-08
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jappl.1999.87.2.611" target="_blank" rel="noreferrer noopener">10.1152/jappl.1999.87.2.611</a>
Cardiac afferents attenuate the muscle metaboreflex in the rat.
Afferent/drug effects/*physiology; Animals; Aorta/drug effects/physiology; Blood Pressure/drug effects/physiology; Blood Volume/drug effects/physiology; Heart Rate/drug effects/physiology; Heart/drug effects/*innervation/physiology; Muscles/drug effects/*metabolism; N-Methylscopolamine; Neurons; Parasympatholytics/pharmacology; Physical Exertion/physiology; Procainamide/pharmacology; Propranolol/pharmacology; Rats; Reflex/drug effects/*physiology; Scopolamine Derivatives/pharmacology; Specimen Handling
The influence of cardiac afferents on the muscle metaboreflex was examined in 16 rats instrumented with a Silastic-tipped catheter in the pericardial space and right atrium, Doppler ultrasonic flow probe and a pneumatic vascular occluder around the terminal aorta, and a Teflon catheter in the thoracic aorta. In protocol I (cardiac efferent and afferent blockade), the muscle metaboreflex was examined under three experimental conditions: 1) control, 2) cardiac autonomic efferent blockade [intrapericardial methylscopolamine (10 micrograms/kg) and propranolol (50 micrograms/kg)], and 3) combined cardiac autonomic efferent and afferent blockade (intrapericardial procainamide, 2%). In protocol II (blood volume expansion), the muscle metaboreflex was examined before and after 15% blood volume expansion. Mild treadmill exercise (9 m/min, 10% grade) increased heart rate (71 +/- 9.4 beats/min), mean arterial pressure (12 +/- 2.0 mmHg), and terminal aortic blood flow velocity (6 +/- 1.0 kHz). During exercise, a reduction of terminal aortic blood flow velocity (10.5 +/- 1.1%) reduced mixed venous PO2 18 +/- 6%. The gain of the muscle metaboreflex in the control condition was 14.6 +/- 2.9 mmHg/kHz. Efferent blockade reduced the gain 51 +/- 7%. However, combined cardiac efferent and afferent blockade increased the gain 207 +/- 64% above the efferent blocked condition and restored the gain to levels above those obtained in the control condition (18.3 +/- 4.6 mmHg/kHz). In addition, 15% blood volume expansion reduced the gain of the muscle metaboreflex regulation of mean arterial pressure and heart rate (44 +/- 9.5% and 41 +/- 12.0%, respectively). Thus cardiac afferents tonically inhibit the pressor response to a reduction in terminal aortic blood flow velocity during exercise.
Collins H L; DiCarlo S E
Journal of applied physiology (Bethesda, Md. : 1985)
1993
1993-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jappl.1993.75.1.114" target="_blank" rel="noreferrer noopener">10.1152/jappl.1993.75.1.114</a>
Distal air space epithelial fluid clearance in near-term rat fetuses is fast and requires endogenous catecholamines.
Adrenergic beta-Antagonists/pharmacology; Aging/metabolism; Animals; Body Fluids/*metabolism; Body Water/metabolism; Catecholamines/*physiology; Embryonic and Fetal Development; Epinephrine/blood; Epithelium/metabolism; Female; Fetus/drug effects/metabolism; Gestational Age; Lung/drug effects/*embryology/metabolism; Male; Newborn/metabolism; Propranolol/pharmacology; Rats; Sprague-Dawley; Time Factors
Knowledge about the conversion of the epithelium in the distal air spaces of the lung from secretion to absorption is imperative to the understanding of postnatal lung development; little such information is available in rats. Distal air space fluid clearance was therefore measured in 21- to 22-day gestation rat fetuses and newborn (40 h) rats. Distal air space fluid clearance was measured from the increase in (131)I-albumin concentration in an isosmolar, physiological solution instilled into the developing lungs. There was no net fluid movement across the distal air space epithelium in the lungs of 21-day gestation fetuses. Twenty-four hours later, distal air space fluid was cleared at a rapid rate in the 22-day gestation fetuses. Within the first 40 h after birth, the rate rapidly declined to adult levels. The high distal air space fluid clearance at 22 days gestation and at 40 h after birth was mediated by beta-adrenergic receptors as demonstrated by elevated plasma epinephrine levels and inhibition by propranolol. Interestingly, the elevated distal air space fluid clearance in the 22-day gestation fetuses was only minimally amiloride sensitive; however, amiloride sensitivity increased over the first 40 h after birth. In conclusion, these studies demonstrate that 1) rapid rates of net alveolar fluid clearance occur late in gestation in the rat and 2) this clearance is driven by elevations of endogenous epinephrine.
Folkesson Hans G; Matthay Michael A; Chapin Cheryl J; Porta Nicolas F M; Kitterman Joseph A
American journal of physiology. Lung cellular and molecular physiology
2002
2002-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajplung.00183.2001" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00183.2001</a>
Congenital diaphragmatic hernia prevents absorption of distal air space fluid in late-gestation rat fetuses.
*Gestational Age; *Hernias; Absorption; Amiloride/pharmacology; Animals; Body Fluids/*metabolism; Congenital; Diaphragmatic; Diaphragmatic/*metabolism; Epinephrine/metabolism; Epithelial Sodium Channels; Female; Fetal Organ Maturity; Fetus/*metabolism; Hernia; Male; Newborn; Phenyl Ethers/administration & dosage; Pregnancy; Propranolol/pharmacology; Rats; Respiratory System Abnormalities; Sodium Channels/metabolism; Sodium-Potassium-Exchanging ATPase/metabolism; Sprague-Dawley
We hypothesized that congenital diaphragmatic hernia (CDH) may decrease distal air space fluid absorption due to immaturity of alveolar epithelial cells from a loss of the normal epithelial Na+ transport, as assessed by amiloride and epithelial Na+ channel (ENaC) and Na-K-ATPase expression, as well as failure to respond to endogenous epinephrine as assessed by propranolol. Timed-pregnant dams were gavage fed 100 mg of nitrofen at 9.5-day gestation to induce CDH in the fetuses, and distal air space fluid absorption experiments were carried out on
Folkesson Hans G; Chapin Cheryl J; Beard LaMonta L; Ertsey Robert; Matthay Michael A; Kitterman Joseph A
American journal of physiology. Lung cellular and molecular physiology
2006
2006-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajplung.00124.2005" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00124.2005</a>
Impaired alveolar liquid clearance after 48-h isoproterenol infusion spontaneously recovers by 96 h of continuous infusion.
*Pulmonary Alveoli/drug effects/metabolism; Adrenergic; Adrenergic beta-Antagonists/pharmacology; Animals; beta-2/metabolism; Bronchodilator Agents/administration & dosage/*pharmacology; Isoproterenol/administration & dosage/*pharmacology; Lung/drug effects/metabolism; Male; Propranolol/pharmacology; Rats; Receptors; Sprague-Dawley; Terbutaline/pharmacology; Time Factors
We previously demonstrated that 48-h isoproterenol (Iso) infusion in rats impaired the ability of beta-adrenoceptor (beta-AR) agonists to increase alveolar liquid clearance (ALC). In this study, we determined whether this impairment persisted over longer time periods by infusing 400 mug.kg(-1).h(-1) Iso by osmotic minipump for 24-144 h (n = 6-7/group). ALC in control rats was 19.0 +/- 2.4 (SD)% of instilled volume absorbed per hour. In Iso-infused rats, ALC was elevated at 24 h (34.9 +/- 2.4%) and decreased at 48 h (15.2 +/- 4.4%) and had recovered to 24 h values at 96 h (37.3 +/- 3.8%) and 144 h (35.2 +/- 3.3%). Plasma Iso concentrations remained elevated at all Iso infusion times. Peripheral lung beta(2)-AR expression exhibited a parallel time course, with a reduction in expression observed at 48 h, followed by an increase to 24 h values at 96 and 144 h. Propranolol prevented the increase in ALC observed at 96 and 144 h, indicating that the recovery in ALC was mediated by a recovery of beta-AR function and beta-AR signaling. ALC at 96 and 144 h could not be further increased by terbutaline, indicating that ALC was maximally stimulated. These data indicate that recovery of beta-AR-stimulated ALC can occur in the continued presence of Iso and is mediated by a recovery of the ability of the distal lung epithelium to respond to beta-AR stimulation.
Maron Michael B; Folkesson Hans G; Stader Sonya M; Hodnichak Cheryl M
American journal of physiology. Lung cellular and molecular physiology
2006
2006-08
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajplung.00022.2006" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00022.2006</a>
Stimulation of distal airspace fluid clearance in guinea pigs involves bumetanide-sensitive ion transport.
*Ion Transport; Absorption; Adrenergic; Adrenergic beta-Antagonists/pharmacology; Animals; beta/physiology; Body Fluids/*metabolism; Bumetanide/*pharmacology; Diuretics/*pharmacology; Epinephrine/blood; Epithelium; Fetus/metabolism; Gestational Age; Guinea Pigs; Lung/*embryology/metabolism; Newborn; Propranolol/pharmacology; Receptors
OBJECTIVE: This study was undertaken to test the hypothesis that beta-adrenoceptor stimulation of fetal lung fluid absorption in near-term guinea pig fetuses involves bumetanide-sensitive ion transport. STUDY DESIGN: Fetuses were obtained from timed-pregnant guinea pigs at 61 to 69 days' gestation with and without oxytocin-induced preterm labor. The fetuses were placed on continuous positive airway pressure oxygenation, and an isosmolar 5% albumin solution was instilled into the lungs. Distal airspace fluid clearance was measured over 1 hour from the increase in distal airspace protein concentration as fluid was reabsorbed with and without the Cl(-) transport inhibitor bumetanide. RESULTS: Fetal lungs began to absorb distal airspace fluid at 64 to 66 days' gestation, and at birth, distal airspace fluid clearance rapidly quadrupled. Labor induction by oxytocin stimulated distal airspace fluid clearance. Distal airspace fluid clearance, when present, was sensitive to propranolol-inhibition and depended on beta-adrenoceptor stimulation. Fluid secretion at 61 days' gestation was reduced by bumetanide instillation. Bumetanide addition was only inhibitory when distal airspace fluid clearance was propranolol-sensitive. CONCLUSION: Beta-adrenoceptor stimulation from endogenous fetal epinephrine increased fetal distal airspace fluid clearance and involved bumetanide-sensitive ion transport.
Ye Xin; Norlin Andreas; Folkesson Hans G
American journal of obstetrics and gynecology
2004
2004-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.ajog.2003.09.074" target="_blank" rel="noreferrer noopener">10.1016/j.ajog.2003.09.074</a>