scholarly journals Habituation of the cardiac response to involuntary diving in diving and dabbling ducks

1987 ◽  
Vol 131 (1) ◽  
pp. 403-415 ◽  
Author(s):  
G. R. Gabbott ◽  
D. R. Jones

1. Bradycardia in response to forced submergence was habituated in dabbling (Anas platyrhynchos, Linnaeus) and diving (Aythya americana, Eyton) ducks by repetitively submerging the animals, each day for several days, for periods of 40 and 20 s, respectively. The onset of pronounced bradycardia was delayed with each successive trial, until little or no bradycardia occurred during submergence. Diving bradycardia is driven by chemoreceptors in the dabbler and caused by stimulation of narial receptors in the diver. 2. Mean arterial blood pressure in dives was unchanged from pre-dive levels in both naive and trained dabbling ducks. PaO2, PaCO2 and pHa at the end of a dive were similar before and after habituation training. 3. Bradycardia occurred in dives by habituated dabbling ducks if the animal breathed 15% O2 before submergence. The ventilatory responses to breathing high and low levels of oxygen were unaffected by habituation training. 4. The changes in blood gases during dives by naive and habituated dabbling ducks were the same: therefore, in the absence of a demonstrated decrement in receptor chemosensitivity or efferent potency, the locus of habituation must reside in the central nervous system.

1985 ◽  
Vol 59 (6) ◽  
pp. 1955-1960 ◽  
Author(s):  
B. R. Walker ◽  
E. M. Adams ◽  
N. F. Voelkel

As a fossorial species the hamster differs in its natural habitat from the rat. Experiments were performed to determine possible differences between the ventilatory responses of awake hamsters and rats to acute exposure to hypoxic and hypercapnic environments. Ventilation was measured with the barometric method while the animals were conscious and unrestrained in a sealed plethysmograph. Tidal volume (VT), respiratory frequency (f), and inspiratory (TI) and expiratory (TE) time measurements were made while the animals breathed normoxic (30% O2), hypercapnic (5% CO2), or hypoxic (10% O2) gases. Arterial blood gases were also measured in both species while exposed to each of these atmospheric conditions. During inhalation of normoxic gas, the VT/100 g was greater and f was lower in the hamster than in the rat. Overall minute ventilation (VE/100 g) in the hamster was less than in the rat, which was reflected in the lower PO2 and higher PCO2 of the hamster arterial blood. When exposed to hypercapnia, the hamster increased VE/100 g solely through VT; however, the VE/100 g increase was significantly less than in the rat. In response to hypoxia, the hamster and rat increased VE/100 g by similar amounts; however, the hamster VE/100 g increase was through f alone, whereas the rat increased both VT/100 g and f. Mean airflow rates (VT/TI) were no different in the hamster or rat in each gas environment; therefore most of the ventilatory responses were the result of changes in TI and TE and respiratory duty cycle (TI/TT).


2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.


2016 ◽  
Vol 82 (3) ◽  
pp. 266-270
Author(s):  
Matthew B. Bloom ◽  
Derek Serna-Gallegos ◽  
Mark Ault ◽  
Ahsan Khan ◽  
Rex Chung ◽  
...  

Pleural effusions occur frequently in mechanically ventilated patients, but no consensus exists regarding the clinical benefit of effusion drainage. We sought to determine the impact of thoracentesis on gas exchange in patients with differing severities of acute lung injury (ALI). A retrospective analysis was conducted on therapeutic thoracenteses performed on intubated patients in an adult surgical intensive care unit of a tertiary center. Effusions judged by ultrasound to be 400 mL or larger were drained. Subjects were divided into groups based on their initial P:F ratios: normal >300, ALI 200 to 300, and acute respiratory distress syndrome (ARDS) <200. Baseline characteristics, physiologic variables, arterial blood gases, and ventilator settings before and after the intervention were analyzed. The primary end point was the change in measures of oxygenation. Significant improvements in P:F ratios (mean ± SD) were seen only in patients with ARDS (50.4 ± 38.5, P = 0.001) and ALI (90.6 ± 161.7, P = 0.022). Statistically significant improvement was observed in the pO2 (31.1, P = 0.005) and O2 saturation (4.1, P < 0.001) of the ARDS group. The volume of effusion removed did not correlate with changes in individual patient's oxygenation. These data support the role of therapeutic thoracentesis for intubated patients with abnormal P:F ratios.


1978 ◽  
Vol 44 (1) ◽  
pp. 76-80 ◽  
Author(s):  
R. C. Doekel ◽  
E. K. Weir ◽  
R. Looga ◽  
R. F. Grover ◽  
J. T. Reeves

Pulmonary and systemic hemodynamics and arterial blood gases were measured in anesthetized and mechanically ventilated dogs before and after oral or intravenous administration of ethanol. Increases in mean pulmonary artery pressure and pulmonary vascular resistance occurred. Platelet antiserum-induced thrombocytopenia inhibition of prostaglandin synthesis with meclofenamate, or alpha-adrenergic blockade did not alter the pulmonary pressor response to ethanol. However, the increase in resistance following ethanol was abolished by hyperoxia and potentiated by hypoxia. Thus, it appears that the effect of ethanol is to augment hypoxic pulmonary vasoconstriction, whereas ethanol per se has no independent pulmonary pressor activity.


1986 ◽  
Vol 121 (1) ◽  
pp. 227-238 ◽  
Author(s):  
R. A. Furilla ◽  
D. R. Jones

In restrained redhead ducks, forced submergence caused heart rate to fall from 100 +/− 3 beats min-1 (mean +/− S.E.M., N = 12) to a stable underwater rate of 35 +/− 4 beats min-1 (N = 12) within 5 s after submergence. Bradycardia was unaffected by breathing oxygen before a dive, but was virtually eliminated by local anaesthesia of the narial region. In contrast, in a dabbling duck (Anas platyrhynchos) bradycardia in short dives was eliminated by breathing oxygen before a dive. In unrestrained diving, on a man-made pond, heart rate in redheads diving voluntarily (y) was related to pre-dive heart rate (x) by the equation y = 76 + 0.29 +/− 0.05x +/− 17 (r2 = 0.71). Chasing, to induce submergence, had variable effects on this relationship. Local anaesthesia of the narial region inhibited voluntary diving but heart rates in chase-induced dives after nasal blockade were significantly higher, by 10–30%, than those obtained from untreated ducks in chase-induced dives. Breathing oxygen before voluntary dives had no apparent effect on heart rate after 2–5 s submergence. Voluntary head submersion by dabbling ducks caused no change in heart rate. We conclude that nasal receptors make only a minor contribution to cardiac responses in unrestrained dives, compared with forced dives, in diving ducks. Furthermore, these results show that little can be learned about cardiac responses in free diving ducks from studies of forced dives in dabblers or divers.


1983 ◽  
Vol 244 (4) ◽  
pp. R487-R491
Author(s):  
B. R. Walker

Both in vitro and in vivo experiments suggest that prostaglandins may affect antidiuretic hormone (ADH) release centrally. In addition, other studies show that prostaglandins administered peripherally may cause ADH release. However, these latter studies have been flawed by hemodynamic alterations and the use of anesthetics, which make interpretation difficult. The present study was designed to test for involvement of prostaglandins produced outside the central nervous system in ADH release in conscious dogs. Administration of meclofenamate (2 mg/kg and 2 mg X kg-1 X h 1, iv) resulted in a consistent fall in plasma ADH levels in five dogs. This diminution of ADH release occurred with no change in systemic hemodynamics, arterial blood gases, or plasma osmolality, suggesting that prostaglandins are important mediators of basal ADH release in the conscious dog. Because meclofenamate does not cross the blood-brain barrier, prostaglandins produced outside the central nervous system appear to be involved in this process. The specific prostaglandin involved or the site of action of prostaglandins on ADH release is not clear at this time.


1979 ◽  
Vol 46 (6) ◽  
pp. 1171-1177 ◽  
Author(s):  
R. W. Stremel ◽  
B. J. Whipp ◽  
R. Casaburi ◽  
D. J. Huntsman ◽  
K. Wasserman

The ventilatory responses to diminished pulmonary blood flow (Qc), as a result of partial cardiopulmonary bypass (PCB), were studied in chloralose-urethan-anesthetized dogs. Qc was reduced by diverting vena caval blood through a membrane gas exchanger and returning it to the ascending aorta. PCB flows of 400--1,600 ml/min were utilized for durations of 2--3 min. Decreasing Qc, while maintaining systemic arterial blood gases and perfusion, results in a significant (P less than 0.05) decrease in expiratory ventilation (VE) (15.9%) and alveolar ventilation (VA) (31.0%). The ventilatory decreases demonstrated for this intact group persist after bilateral cervical vagotomy (Vx), carotid body and carotid sinus denervation (Cx), and combined Vx and Cx. The changes in VE and VA were significantly (P less than 0.001) correlated with VCO2 changes, r = 0.80 and r = 0.93, respectively. These ventilatory changes were associated with an overall average decrease in left ventricular PCO2 of 2.1 Torr; this decrease was significant (P less than 0.05) only in the intact and Cx groups. Decreasing pulmonary blood flow results in a decrease in ventilation that may be CO2 related; however, the exact mechanism remains obscure but must have a component that is independent of vagally mediated cardiac and pulmonary afferents and peripheral baroreceptor and chemoreceptor afferents.


1993 ◽  
Vol 74 (2) ◽  
pp. 853-858 ◽  
Author(s):  
F. Xu ◽  
R. F. Taylor ◽  
T. McLarney ◽  
L. Y. Lee ◽  
D. T. Frazier

This study examines the extent to which the cerebrum and other suprapontine structures modulate the respiratory response to added mechanical resistive loads to breathing. Nine adult cats were anesthetized with thiopental sodium, tracheotomized, and instrumented with diaphragm electromyographic (EMGdi) recording electrodes. Two levels of resistive loads and tracheal occlusion were applied at the onset of inspiration in random order before and after decerebration. The integrated signal of the EMGdi (integral of EMGdi) was used to detect changes in respiratory timing and as an index of respiratory motor drive. The results showed that, compared with intact cats, decerebration did not significantly change baseline values for peak integral of EMGdi, respiratory timing, systemic blood pressure, or arterial blood gases. Although the percent changes in the peak integral of EMGdi elicited by the added loads were still significantly greater than those elicited by unloaded control breaths after decerebration, the magnitude of the responses was significantly attenuated at all load levels compared with the intact preparation. It is concluded that the cerebrum and/or other suprapontine structures provide information that is facilitatory to the respiratory pattern generator with little effect on timing.


1982 ◽  
Vol 52 (5) ◽  
pp. 1216-1222 ◽  
Author(s):  
G. E. Bisgard ◽  
H. V. Forster ◽  
J. Mesina ◽  
R. G. Sarazin

In the present study the ventilatory response to exercise was measured in goats before and after carotid body excision (CBE) (n = 7) or sham operation (n = 1). Nine-minute periods of moderate treadmill walking were carried out under three conditions: 4.8 kph, 0% grade during normoxia and hypoxia (arterial O2 tension approximately 43 Torr) and 4.8 kph, 5% grade during normoxia. Ventilatory variables, metabolic rate, and arterial blood acid-base and blood gases were measured at 30-s intervals for the first 3 min and again during the 6th and 9th min of exercise. In normal goats during exercise in normoxia, ventilation changed in proportion to changes in metabolic rate resulting in arterial CO2 tension (PaCO2) and arterial pH (pHa) homeostasis throughout exercise. CBE resulted in nearly equivalent hypoventilation during steady-state rest and exercise (delta PaCO2 approximately equal to 5--7 Torr) during normoxia and loss of the positive interaction between hypoxia and exercise. There was also a significant disruption of PaCO2-pHa homeostasis during the first 30 s of exercise after CBE when PaCO2 was 3 Torr below rest and pHa was 0.03 units above rest. Our data indicate: 1) that the carotid chemoreceptors may contribute a similar proportional drive to breathe during rest and exercise; 2) that transient hyperventilation at the onset of exercise after CBE may indicate an important neural drive to breathe that is normally damped by intact peripheral chemoreceptors; and 3) that the mechanism linking ventilation to CO2 production remains intact after CBE.


1985 ◽  
Vol 249 (1) ◽  
pp. H164-H173 ◽  
Author(s):  
W. C. Seyde ◽  
L. McGowan ◽  
N. Lund ◽  
B. Duling ◽  
D. E. Longnecker

Twenty-nine male Sprague-Dawley rats were divided into four groups based on anesthetic exposure, i.e., awake animals and those receiving anesthesia produced by chloralose-urethan, pentobarbital, or by midcollicular brain stem transsection. Before and after hemorrhage (30% of the estimated blood volume), cardiac output (CO) and regional blood flows were measured by the microsphere method. Arterial blood gases and lactate (L) and pyruvate (P) were also determined. CO and regional blood flows were greatest and the L/P ratio was least in awake animals both before and after hemorrhage. In normovolemic rats, the frequency of altered values (as compared with those in awake animals) was similar for all anesthetic techniques, whereas the CO and regional blood flow responses to hemorrhage were altered less frequently in decerebrated animals. Decerebration may be the preferable procedure if the intent is to produce responses in anesthetized animals similar to those in awake rats. If the intent is to study hemodynamics in a specific organ, the selection of an anesthetic technique should be guided by the individual anesthetic effects on that particular tissue.


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