scholarly journals Arterial blood gas levels and cardiovascular function during varying environmental conditions in a mudskipper, periophthalmodon schlosseri

1999 ◽  
Vol 202 (13) ◽  
pp. 1753-1762
Author(s):  
A. Ishimatsu ◽  
N.M. Aguilar ◽  
K. Ogawa ◽  
Y. Hishida ◽  
T. Takeda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Control Level ◽  
Ammonia Concentration ◽  
Blood Gas ◽  
Air Exposure ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Blood Ph ◽  
Periophthalmodon Schlosseri

Changes in blood gas levels, blood pressure and heart rate were studied in chronically cannulated mudskippers, Periophthalmodon schlosseri, subjected to air exposure (6 h), aquatic hypoxia with access to air (water PO2 <0.9 kPa, 6 h) and forced submersion in normoxic water (12 h) at 30 degrees C. Air exposure did not affect either blood O2 and had little effect on blood CO2 levels, but blood pH increased slightly, but significantly. Blood ammonia concentration was elevated sixfold during air exposure. Aquatic hypoxia caused no significant changes in blood gas levels. When the fish was forcibly submerged, blood O2 saturation decreased rapidly to approximately 30 %. Blood PCO2 and total CO2 also decreased, but blood pH was unaffected by forcible submersion. Air exposure did not affect blood pressure or heart rate. Aquatic hypoxia did not affect blood pressure but transiently increased heart rate. In contrast, forced submersion significantly depressed heart rate throughout the period of submersion, while blood pressure decreased only transiently. Upon emersion, the heart rate immediately increased to above the control level when the fish took its first air breath.

Adrenal gland denervation and diving in ducks

1987 ◽  
Vol 252 (6) ◽  
pp. R1143-R1151
Author(s):  
H. J. Mangalam ◽  
D. R. Jones ◽  
A. M. Lacombe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Adrenal Gland ◽  
Plasma Glucose ◽  
Adrenal Glands ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
O2 Partial Pressure ◽  
Before And After

The extreme elevation in plasma levels of free norepinephrine (NE) and free epinephrine (EP), which occurs during forced diving of ducks (Anas platyrhynchos), was studied before and after denervation of the adrenal glands. In intact animals both NE and EP concentration increased by up to two orders of magnitude in a 4-min dive but by a significantly lesser amount if the duck breathed O2 before the dive. Denervating the adrenal glands reduced the amounts of both catecholamines (CA) released during dives, plasma EP decreased to 10%, and NE to 50% of values obtained before denervation. Breathing O2 before a dive virtually eliminated CA release in denervates, indicating that hypoxia was the important non-neural releasing agent. Hypoxia was also the most important neural releasing agent compared with hypercapnia, acidosis, or hypoglycemia. Adrenal denervation did not cause significant changes in heart rate, blood pressure, arterial blood gas tensions, pH, or plasma glucose during dives, although denervation caused increased variation in some of these variables. In ducks CA release in dives is largely due to decreasing arterial O2 partial pressure, and full expression of the response is dependent on intact innervation of the adrenal gland.

Cardiovascular responses to severe hypercapnia of short duration

1964 ◽  
Vol 207 (3) ◽  
pp. 634-640 ◽  
Author(s):  
Emmett S. Manley ◽  
Clinton B. Nash ◽  
R. A. Woodbury
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Short Duration ◽  
Cardiovascular Responses ◽  
Myocardial Contraction ◽  
Contractile Force ◽  
Sympathetic Activation ◽  
Pentobarbital Anesthesia ◽  
Arterial Blood ◽  
Blood Ph

Dogs under pentobarbital anesthesia were employed in an investigation of the effect of abrupt, severe hypercapnia upon blood pressure, heart rate, and force of myocardial contraction. Electrocardiographic activity and arterial blood pH were also monitored. Hypercapnia was induced for 10-min periods with 15 and 30% CO2 in oxygen. The studies were undertaken in nontreated animals and animals treated with atropine, reserpine, chlorisondamine, P-286, or bilateral adrenalectomy. Severe hypercapnia was shown to be depressant to the cardiovascular parameters evaluated, but blood pressure and contractile force normally demonstrated compensation to this depression. Parasympathetic blockade with atropine did not reduce the depression observed in the nontreated dogs during hypercapnia. Results obtained with other pretreated animals indicate that compensation occurs primarily via sympathetic activation. Adrenal activation may assume importance in compensation to 30% CO2, but intact adrenals were not necessary for survival during hypercapnia. No arrhythmias (excluding bradycardia) were observed during or immediately following exposure to either concentration of CO2.

scholarly journals Severe hypoxaemia in field-anaesthetised white rhinoceros (Ceratotherium simum) and effects of using tracheal insufflation of oxygen

2004 ◽  
Vol 75 (2) ◽  
Author(s):  
M. Bush ◽  
J.P. Raath ◽  
D. Grobler ◽  
L. Klein
Keyword(s):  
Blood Pressure ◽  
Tracheal Intubation ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
White Rhinoceros ◽  
Severe Hypoxaemia ◽  
Before And After ◽  
Tracheal Insufflation ◽  
Free Ranging

White rhinoceros anaesthetised with etorphine and azaperone combination develop adverse physiological changes including hypoxia, hypercapnia, acidosis, tachycardia and hypertension. These changes are more marked in field-anaesthetised rhinoceros. This study was designed to develop a technique to improve safety for field-anaesthetised white rhinoceros by tracheal intubation and oxygen insufflation. Twenty-five free-ranging white rhinoceros were anaesthetised with an etorphine and azaperone combination for translocation or placing microchips in their horns. Once anaesthetised the rhinoceros were monitored prior to crating for transportation or during microchip placement. Physiological measurements included heart and respiratory rate, blood pressure and arterial blood gas samples. Eighteen rhinoceros were intubated using an equine nasogastric tube passed nasally into the trachea and monitored before and after tracheal insufflation with oxygen. Seven rhinoceros were not intubated or insufflated with oxygen and served as controls. All anaesthetised rhinoceros were initially hypoxaemic (percentage arterial haemoglobin oxygen saturation (% O2Sa) = 49 % + 16 (mean + SD) and PaO2 = 4.666 + 1.200 kPa (35 + 9 mm Hg)), hypercapnic (PaCO2 = 8.265 + 1.600 kPa (62 + 12 mm Hg)) and acidaemic (pHa = 7.171 + 0.073 ). Base excess was -6.7 + 3.9 mmol/ℓ, indicating a mild to moderate metabolic acidosis. The rhinoceros were also hypertensive (systolic blood pressure = 21.861 + 5.465 kPa (164 + 41 mm Hg)) and tachycardic (HR = 107 + 31/min). Following nasal tracheal intubation and insufflation, the % O2Sa and PaO2 increased while blood pHa and PaCO2 remained unchanged.Tracheal intubation via the nose is not difficult, and when oxygen is insufflated, the PaO2 and the % O2Sa increases, markedly improving the safety of anaesthesia, but this technique does not correct the hypercapnoea or acidosis. After regaining their feet following reversal of the anaesthesia, the animals' blood gas values return towards normality.

Augmentation of respiratory sinus arrhythmia in response to progressive hypercapnia in conscious dogs

2001 ◽  
Vol 280 (5) ◽  
pp. H2336-H2341 ◽  
Author(s):  
Fumihiko Yasuma ◽  
Jun-Ichiro Hayano
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Respiratory Sinus Arrhythmia ◽  
Physiological Response ◽  
Minute Ventilation ◽  
Control Level ◽  
Conscious Dogs ◽  
Sinus Arrhythmia ◽  
Arterial Blood

Respiratory sinus arrhythmia (RSA) may serve to enhance pulmonary gas exchange efficiency by matching pulmonary blood flow with lung volume within each respiratory cycle. We examined the hypothesis that RSA is augmented as an active physiological response to hypercapnia. We measured electrocardiograms and arterial blood pressure during progressive hypercapnia in conscious dogs that were prepared with a permanent tracheostomy and an implanted blood pressure telemetry unit. The intensity of RSA was assessed continuously as the amplitude of respiratory fluctuation of heart rate using complex demodulation. In a total of 39 runs of hypercapnia in 3 dogs, RSA increased by 38 and 43% of the control level when minute ventilation reached 10 and 15 l/min, respectively ( P < 0.0001 for both), and heart rate and mean arterial pressure showed no significant change. The increases in RSA were significant even after adjustment for the effects of increased tidal volume, respiratory rate, and respiratory fluctuation of arterial blood pressure ( P < 0.001). These observations indicate that increased RSA during hypercapnia is not the consequence of altered autonomic balance or respiratory patterns and support the hypothesis that RSA is augmented as an active physiological response to hypercapnia.

Ventilatory responses to cardiac output changes in patients with pacemakers

1981 ◽  
Vol 51 (5) ◽  
pp. 1103-1107 ◽  
Author(s):  
P. W. Jones ◽  
W. French ◽  
M. L. Weissman ◽  
K. Wasserman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Blood Gas ◽  
Cardiac Pacemakers ◽  
Ventilatory Responses ◽  
Mean Delay ◽  
Arterial Blood ◽  
End Tidal

Cardiac output changes were induced by step changes of heart rate (HR) in six patients with cardiac pacemakers during monitoring of ventilation and gas exchange, breath-by-breath. Mean low HR was 48 beats/min; mean high HR was 82 beats/min. The change of oxygen uptake immediately after the HR change was used as an index of altered cardiac output. After HR increase, oxygen uptake (V02) rose by 34 +/- 20% (SD), and after HR decrease, Vo2 fell by 24 +/- 11%. There was no change in arterial blood pressure. After HR increase, ventilation increased, after a mean delay of 19 +/- 4 s; after HR reduction, ventilation fell, after a mean delay of 29 +/- 7 s. In the period between HR increase and the resulting increase in ventilation, end-tidal PCO2 (PETCO2) rose by 2.6 +/- 2.0 Torr, and in the period between HR decreases and the fall in ventilation, PETCO2 dropped by 2.9 +/- 2.2 Torr. The response time and end-tidal gas tension changes implicate the chemoreceptors in the reflex correction of blood gas disturbances that may result from imbalances between cardiac output and ventilation.

Cardioaccelerator action of angiotensin

1962 ◽  
Vol 202 (2) ◽  
pp. 237-240 ◽  
Author(s):  
S. D. Nishith ◽  
L. D. Davis ◽  
W. B. Youmans
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Abdominal Aorta ◽  
Intravenous Infusion ◽  
Control Level ◽  
Arterial Blood ◽  
Initial Decrease ◽  
Slow Intravenous Infusion

Effects of synthetic angiotensin II on heart rate and blood pressure were determined in dogs under the influence of morphine (3 mg/kg) and chloralose (90 mg/kg). Angiotensin in total doses of 2.5–20 µg, rapidly injected intravenously in intact dogs, caused an initial decrease in heart rate followed by a rise above the control level, despite the continued elevation of arterial blood pressure. When the degree of rise in arterial pressure was buffered by a mechanical compensator connected with the abdominal aorta, rapid intravenous angiotensin injection produced no initial cardioinhibitory phase, and the magnitude of the accleration of heart rate was much greater than in the unbuffered animal. Slow intravenous infusion of angiotensin in some cases caused only a rise in heart rate. In sinoaortic denervated animals both blood pressure and heart rate were greatly increased when a total dose of 10 µg angiotensin was rapidly injected intravenously. Thus, it is demonstrated that the cardioinhibitory response to angiotensin depends largely or exclusively on reflex effects from sinoaortic pressoreceptors, and that angiotensin has a strong cardioaccelerator action which is exerted through the efferent nerves to the heart.

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