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

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.

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Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

Clinical Science ◽

10.1042/cs0810727 ◽

1991 ◽

Vol 81 (6) ◽

pp. 727-732 ◽

Cited By ~ 18

Author(s):

Marohito Murakami ◽

Hiromichi Suzuki ◽

Atsuhiro Ichihara ◽

Mareo Naitoh ◽

Hidetomo Nakamoto ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Blood Flow ◽

Renal Blood Flow ◽

Arterial Blood Pressure ◽

Mean Arterial Blood Pressure ◽

Renal Haemodynamics ◽

Conscious Dogs ◽

Arginine Infusion ◽

Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

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Rhythmicity of urinary sodium excretion, mean arterial blood pressure, and heart rate in conscious dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.1.h149 ◽

1992 ◽

Vol 262 (1) ◽

pp. H149-H156 ◽

Cited By ~ 3

Author(s):

U. Palm ◽

W. Boemke ◽

H. W. Reinhardt

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Mean Arterial Blood Pressure ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Conscious Dogs ◽

Arterial Blood ◽

Infusion Regimen

The existence of urinary excretion rhythms in dogs, which is a matter of controversy, was investigated under strictly controlled intake and environmental conditions. In seven conscious dogs, 14.5 mmol Na, 3.55 mmol K, and 91 ml H2O.kg body wt-1.24 h-1 were either administered with food at 8:30 A.M. or were continuously infused at 2 consecutive days. During these 3 days, automatized 20-min urine collections, mean arterial blood pressure (MABP), and heart rate (HR) recordings were performed without disturbing the dogs. Fundamental and partial periodicities, the noise component of urinary sodium excretion (UNaV), MABP, and HR were analyzed using a method derived from Fourier and Cosinor analysis. Oral intake (OI) leads to powerful 24-h periodicities in all dogs and seems to synchronize UNaV. UNaV on OI peaked between 1 and 3 P.M. Under the infusion regimen, signs of nonstationary rhythms and desynchronization predominated. UNaV under the infusion regimen could be separated into two components: a rather constant component continuously excreted and superimposed to this an oscillating component. No direct coupling between UNaV and MABP periodicities could be demonstrated. On OI, an increase in HR seems to advance the peak UNaV in the postprandial period. HR and MABP signals were both superimposed with noise. We conclude that UNaV rhythms are present in dogs. They are considerably more pronounced on OI.

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THE EFFECTS OF INFUSIONS OF ADRENALINE AND NORADRENALINE ON THE HEART RATE AND ARTERIAL BLOOD PRESSURE OF CONSCIOUS DOGS

Quarterly Journal of Experimental Physiology and Cognate Medical Sciences ◽

10.1113/expphysiol.1958.sp001349 ◽

1958 ◽

Vol 43 (4) ◽

pp. 361-367

Author(s):

J. A. Holgate ◽

W. J. O'Connor

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Conscious Dogs ◽

Arterial Blood

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Ventilatory response to isocapnic hyperoxia

Journal of Applied Physiology ◽

10.1152/jappl.1995.78.2.696 ◽

1995 ◽

Vol 78 (2) ◽

pp. 696-701 ◽

Cited By ~ 39

Author(s):

H. Becker ◽

O. Polo ◽

S. G. McNamara ◽

M. Berthon-Jones ◽

C. E. Sullivan

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Minute Ventilation ◽

Normobaric Hyperoxia ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Blood Gas Analyses ◽

End Tidal ◽

Arterial Po2

Breathing O2 for up to 1 h has been shown to either not influence or slightly increase (6–13%) minute ventilation. However, end-tidal PCO2 was not kept constant in these experiments. In nine healthy men, we studied the ventilatory, blood pressure, and heart rate responses to 30 min of normobaric hyperoxia (50% O2) at isocapnic conditions. Hyperoxia led to a 60% increase in mean minute ventilation (P = 0.002), largely due to an increase in mean tidal volume from 0.66 +/- 0.04 (SE) to 0.88 +/- 0.05 liter (P = 0.007). Fifteen minutes after the termination of hyperoxia, minute ventilation was still increased (P = 0.02) compared with baseline, although it was reduced compared with hyperoxia (P = 0.02). Arterial blood gas analyses in six subjects before and during hyperoxia showed an increase in arterial PO2 and O2 saturation but no change in arterial PCO2 or pH. Hyperoxia induced no changes in arterial blood pressure or heart rate. We conclude that 1) isocapnic hyperoxia stimulates respiration markedly, an effect that is approximately five times higher than previously measured; 2) the increase in ventilation induced by hyperoxia does not affect arterial blood pressure and heart rate; and 3) in experiments using hyperoxia, its effect on breathing and subsequently on PCO2 has to be taken into account.

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Reflex inhibition of plasma renin activity by increased left ventricular pressure in conscious dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1989.256.6.r1299 ◽

1989 ◽

Vol 256 (6) ◽

pp. R1299-R1307

Author(s):

A. J. Gorman ◽

J. S. Chen

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Plasma Renin Activity ◽

Arterial Blood Pressure ◽

Left Atrial ◽

Plasma Renin ◽

Left Ventricular ◽

Renin Activity ◽

Conscious Dogs ◽

Arterial Blood

The purpose of the present study was to determine the effects of left ventricular (LV) outflow obstruction on plasma renin activity (PRA) and the contribution from afferent receptors located in the LV myocardium. In chronically instrumented, conscious dogs (n = 12), changes in PRA during a 15- to 20-mmHg decrease in arterial blood pressure were assessed during 1) intravenous infusions of nitroprusside (NP) alone and 2) infusions of NP while peak systolic LV pressure was elevated by acute ascending aortic occlusion (AAO + NP). Infusions of NP alone elicited significant increases in heart rate (24.9 +/- 5.1 beats/min; P less than 0.01) and in PRA [3.31 +/- 0.53 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.01]. These were accompanied by decreases in both LV pressure (-13.8 +/- 3.6 mmHg; P less than 0.05) and left atrial pressure (-3.0 +/- 0.7 mmHg; P less than 0.05). During AAO + NP, LV pressure was elevated to an absolute level of 169.2 +/- 4.6 mmHg (+53.3 +/- 4.2 mmHg; P less than 0.001), whereas left atrial pressure was not changed. Both the hypotension-induced rise in PRA and tachycardia were significantly inhibited during AAO + NP (+0.59 +/- 0.29 ng ANG I.ml-1.h-1 and +6.3 +/- 4.6 beats/min, respectively; NS). The topical application of a local anesthetic in the region of the main coronary artery, sufficient to block the heart rate and arterial blood pressure responses to selective LV receptor stimulation by intracoronary veratridine (0.1-0.4 microgram/kg), resulted in significant increases in PRA and heart rate during AAO + NP.(ABSTRACT TRUNCATED AT 250 WORDS)

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Acute hypoxemia stimulates atrial natriuretic factor secretion in vivo

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.2.h295 ◽

1988 ◽

Vol 255 (2) ◽

pp. H295-H300 ◽

Cited By ~ 4

Author(s):

A. J. Baertschi ◽

J. M. Adams ◽

M. P. Sullivan

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Mean Arterial Blood Pressure ◽

Atrial Natriuretic Factor ◽

Minute Ventilation ◽

Base Line ◽

Arterial Blood ◽

Natriuretic Factor ◽

Arterial Po2

The hypothesis was tested that acute hypoxemia may be a physiological stimulus for atrial natriuretic factor (ANF) secretion in anesthetized, spontaneously breathing rabbits. Base-line plasma ANF (range from 29.8 to 219 pg/ml; mean +/- SE = 87.0 +/- 14.1 pg/ml; n = 16 rabbits) was negatively correlated with base-line arterial PO2 (r = -0.759; P less than 0.01) but not with PCO2, pH, mean arterial blood pressure, central venous pressure (CVP), minute ventilation, heart rate, or type of anesthetics used. Acute hypoxemia (arterial PO2 22.3-44.3 mmHg) lasting 10 min increased plasma ANF levels over base line by 69.2 +/- 47.7 (SE) pg/ml at 6 min and 87.5 +/- 46.8 (SE) pg/ml at 9 min (P less than 0.01; n = 9). The increase in arterial pH and minute ventilation and the decrease of arterial PCO2 paralleled the changes in plasma ANF. Mean arterial blood pressure, CVP, and heart rate did not change significantly. ANF responses to hypoxemia (range from 4.4 to 423 pg/ml) correlated with base-line CVP (r = 0.761; P less than 0.01) and base-line ANF (r = 0.523; P less than 0.05) but with no other measured variable. Although the mediators of hypoxemia-induced release of ANF need to be explored further, this study raises the possibility that ANF might be involved in the adaptation to hypoxemia.

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