Integrating behavior and cardiovascular responses: posture and locomotion. I. Static analysis

1993 ◽  
Vol 265 (6) ◽  
pp. R1458-R1468 ◽  
Author(s):  
O. A. Smith ◽  
C. A. Astley ◽  
F. A. Spelman ◽  
E. V. Golanov ◽  
V. G. Chalyan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Computer Control ◽  
Cardiovascular Responses ◽  
Papio Hamadryas ◽  
Code Generator ◽  
Frequency Distributions ◽  
Arterial Blood ◽  
Free Ranging

Heart rate, arterial blood pressure, and renal and mesenteric or femoral blood flow were telemetered from 11 Papio hamadryas in an untethered free-ranging situation. The animals' behavior was recorded on videotape, and the cardiovascular (CV) data were recorded on the audio channels of the tape. The behavior was coded, and the codes were linked to the CV data via a time-code generator and computer control. The CV data were digitized into 1-s intervals, and the static relations between CV measures and the postures/locomotions (P/Ls) associated with the behavior were analyzed. The total frequency distributions for heart rate, blood pressure, and renal conductance approximated Gaussian distributions, whereas femoral conductance was positively skewed. The distribution for renal conductance suggested that during normal waking conditions the kidney is not maximally dilated and may increase or decrease its blood flow. All distributions were highly influenced by the Sit category, which occupied 80% of the total time. The CV measures for all P/Ls had wide ranges, and the CV values associated with each P/L overlapped those for the other P/Ls. The heart rate and renal conductance associated with the various P/Ls showed the largest deviations from the grand means and therefore contributed the most to the ability to discriminate one P/L from another. Blood pressure varied little from one P/L to another. The patterns of CV variables served to distinguish particular P/Ls very effectively. The frequency distributions were separated best when they were parceled on the basis of the intensity of behavior associated with a particular P/L. These variations in intensity were the major cause of the overlaps in the frequency distributions associated with P/Ls.

Effect of intravenous infusion of adrenaline on the cardiovascular responses to distal body subatmospheric pressure in man

1988 ◽  
Vol 75 (4) ◽  
pp. 389-394 ◽  
Author(s):  
I. W. Fellows ◽  
I. A. MacDonald ◽  
T. Bennett ◽  
D. P. O'Donoghue
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Forearm Blood Flow ◽  
Cardiovascular Responses ◽  
Saline Infusion ◽  
Subatmospheric Pressure ◽  
Arterial Blood ◽  
Adrenaline Infusion

1. On two separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline [0.27 nmol (50 ng) min−1 kg−1] or saline (154 mmol/l NaCl), plus ascorbic acid (5.68 mmol/l), over 30 min. 2. On each occasion, the subjects were exposed to distal body subatmospheric pressure (DBSP), 0 to 50 mmHg (0 to 6.65 kPa) in 10 mmHg (1.33 kPa) steps, before infusion, during the final 15 min of the infusion, and at 15 min and 30 min after the cessation of the infusion. 3. Venous adrenaline concentrations of 2.85 ±0.22 nmol/l were achieved during the adrenaline infusion, compared with 0.49 ± 0.07 nmol/l during the saline infusion (P < 0.001). At 15 min and at 30 min after cessation of the adrenaline infusion, venous adrenaline concentrations had fallen to levels similar to those achieved after the cessation of the saline infusion. 4. Heart rate rose significantly from 58 ±4 beats/min to 67 ±4 beats/min during the adrenaline infusion (P < 0.05), but there was no further significant change in response to 50 mmHg (6.65 kPa) DBSP. At 30 min after the cessation of the adrenaline infusion, heart rate rose from 60 ± 4 beats/min to 78 ± 7 beats/min in response to 50 mmHg DBSP. This increase was significantly greater than that observed before the adrenaline infusion [58 ± 4 beats/min to 69 ±7 beats/min during 50 mmHg (6.65 kPa) DBSP; P < 0.01]. 5. During the infusion of adrenaline, systolic arterial blood pressure rose and diastolic arterial blood pressure fell, but the blood pressure responses to DBSP were unaffected. 6. Forearm blood flow increased significantly during adrenaline infusion but there was no significant difference in the fall in forearm blood flow during DBSP compared with the values before infusion. At 15 min after the cessation of the adrenaline infusion, forearm vascular resistance rose proportionately more in response to DBSP than it had before the adrenaline infusion (P < 0.05). 7. These results are consistent with adrenaline-mediated facilitation of sympathetic neuronal release of noradrenaline in the heart and in the forearm vascular bed.

scholarly journals Effects of Vibration, Noise and Restraint on Heart Rate, Blood Pressure and Renal Blood Flow in the Pig

1983 ◽  
Vol 76 (10) ◽  
pp. 841-847 ◽  
Author(s):  
D B Stephens ◽  
R D Rader
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Cardiovascular Responses ◽  
Experimental Manipulation ◽  
Farm Animals ◽  
Arterial Blood ◽  
Ultrasonic Techniques ◽  
Vibration Noise

Pigs and other farm animals are usually transported at least once during their lives; for example, all meat animals are finally taken to the abattoir for slaughter. The vibration, noise and handling associated with such transportation is usually novel to the animals, and therefore constitutes a potential ‘stressor’. Such adverse stimuli may trigger physiological and psychological changes which rapidly produce profound changes in blood flow to peripheral organs, particularly the kidney, whose blood vessels are richly supplied with sympathetic nerve fibres. In the present study, ultrasonic techniques have been used with chronically implanted flow sensors for measuring heart rate (HR) and changes in renal blood flow (RBF) in conscious, freestanding and unanaesthetized pigs to monitor their cardiovascular responses to vibration, noise and various handling procedures. In addition, arterial blood pressure (BP) was measured via a catheter placed in the carotid artery. To ensure that vibration and noise could be accurately reproduced, a transport simulator (TS) was constructed in the laboratory. A small decrease of approximately 5% was observed in RBF during the first few minutes of exposure to vibration and noise, but this returned to the control levels monitored in undisturbed animals within a few minutes. Thereafter, RBF became significantly elevated for the remaining period of exposure to vibration and noise. In contrast, HR remained significantly increased throughout. BP was not significantly changed as a result of the experimental manipulation. Restraint and handling of the animals appeared to cause maximal disturbance. HR and BP were more than doubled compared with the resting value, but there was a concomitant marked decrease in RBF. For example, in one pig, the normal renal blood flow of 5 ml/s was reduced to nearly half during the handling procedure. This, however, returned to normal levels within 4 min of release.

Cardiovascular responses to head-stand posture

1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
High Pressure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Skin Temperature ◽  
Cardiovascular Responses ◽  
Posterior Tibial Artery ◽  
Nervous Control ◽  
Posterior Tibial

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963

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

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
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.

Ascending pathways mediating somatoautonomic reflexes in exercising dogs

1987 ◽  
Vol 62 (3) ◽  
pp. 1186-1191 ◽  
Author(s):  
J. W. Kozelka ◽  
G. W. Christy ◽  
R. D. Wurster
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Surgical Techniques ◽  
Arterial Occlusion ◽  
Cardiovascular Responses ◽  
Spinal Pathways ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Dorsolateral Funiculus ◽  
Carotid Arterial

The ascending spinal pathways mediating somatocardiovascular reflexes during exercise were studied in unanesthetized dogs by placing lesions in the lumbar spinal cord. After training to run on a treadmill with hindlimbs only, 20 dogs were anesthetized and instrumented using sterile surgical techniques. To chronically record heart rate and arterial blood pressure, the aorta was cannulated via the omocervical artery. To test the intactness of descending spinal sympathetic pathways, reflex pressor responses to baroreceptor hypotension were produced by bilateral carotid arterial occlusion using pneumatic vessel occluders placed around the common carotid arteries. To generate transient ischemic exercise (120 s), a pneumatic occluder was placed around the left iliac artery. Eight to 10 days after instrumentation, blood pressure and heart rate were monitored at rest and during hindlimb running with and without simultaneous iliac arterial occlusion. The modest pressor response and tachycardia elicited by hindlimb exercise were markedly augmented by simultaneous hindlimb ischemia (i.e., iliac arterial occlusion). Lesion placement in the dorsolateral sulcus area and the dorsolateral funiculus at L2 significantly reduced the blood pressure and heart rate responses to simultaneous exercise occlusion. The cardiovascular responses to nonischemic exercise and bilateral carotid arterial occlusion were not altered by such spinal sections. It is concluded that in the dog the ascending spinal pathways mediating cardiovascular responses to ischemic exercise are located in the lateral funiculus, including the dorsolateral sulcus area and dorsolateral funiculus.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

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.

Patterned cardiovascular responses to sleep and nonrespiratory arousals in a porcine model

1998 ◽  
Vol 85 (4) ◽  
pp. 1285-1291 ◽  
Author(s):  
Sandrine H. Launois ◽  
Joseph H. Abraham ◽  
J. Woodrow Weiss ◽  
Debra A. Kirby
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Eye Movement ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Arterial Blood

Patients with obstructive sleep apnea experience marked cardiovascular changes with apnea termination. Based on this observation, we hypothesized that sudden sleep disruption is accompanied by a specific, patterned hemodynamic response, similar to the cardiovascular defense reaction. To test this hypothesis, we recorded mean arterial blood pressure, heart rate, iliac blood flow and vascular resistance, and renal blood flow and vascular resistance in five pigs instrumented with chronic sleep electrodes. Cardiovascular parameters were recorded during quiet wakefulness, during non-rapid-eye-movement and rapid-eye-movement sleep, and during spontaneous and induced arousals. Iliac vasodilation (iliac vascular resistance decreased by −29.6 ± 4.1% of baseline) associated with renal vasoconstriction (renal vascular resistance increased by 10.3 ± 4.0%), tachycardia (heart rate increase: +23.8 ± 3.1%), and minimal changes in mean arterial blood pressure were the most common pattern of arousal response, but other hemodynamic patterns were observed. Similar findings were obtained in rapid-eye-movement sleep and for acoustic and tactile arousals. In conclusion, spontaneous and induced arousals from sleep may be associated with simultaneous visceral vasoconstriction and hindlimb vasodilation, but the response is variable.

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