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.

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.

Primary vagally mediated decelerations in heart rate during tonic rapid eye movement sleep in cats

1998 ◽  
Vol 274 (4) ◽  
pp. R1136-R1141 ◽  
Author(s):  
Richard L. Verrier ◽  
T. Rern Lau ◽  
Umesha Wallooppillai ◽  
James Quattrochi ◽  
Bruce D. Nearing ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Eye Movement ◽  
Arterial Blood Pressure ◽  
Rem Sleep ◽  
Blocking Agent ◽  
Rapid Eye Movement ◽  
Arterial Blood ◽  
State Dependent ◽  
Hippocampal Theta

Rapid eye movement (REM) sleep results in profound state-dependent alterations in heart rate. The present study describes a novel phenomenon of a primary deceleration in heart rate that is not preceded or followed by increases in heart rate or arterial blood pressure and occurs primarily during tonic REM sleep. The goals were to characterize the primary decelerations and to provide insights on the underlying central and peripheral autonomic mechanisms. Cats were chronically implanted with electrodes to record electroencephalogram, pontogeniculooccipital wave activity in lateral geniculate nucleus, hippocampal theta rhythm, electromyogram, electrooculogram, respiration (diaphragm), and electrocardiogram. Arterial blood pressure was monitored from a carotid artery catheter. R-R interval fluctuations were continuously tracked using customized software. The muscarinic blocking agent glycopyrrolate (0.1 mg/kg iv) and the β-adrenergic blocking agent atenolol (0.3 mg/kg iv) were administered in alternating sequence with a 90- to 120-min interval. Glycopyrrolate immediately eliminated the decelerations during REM sleep. Atenolol alone had no effect on their frequency. These findings suggest that a change in the centrally induced pattern of autonomic activity to the heart is responsible for the primary decelerations, namely, a bursting of cardiac vagal efferent fiber activity.

Nocturnal variations in peripheral blood flow, systemic blood pressure, and heart rate in humans

1991 ◽  
Vol 261 (4) ◽  
pp. H982-H988
Author(s):  
J. H. Sindrup ◽  
J. Kastrup ◽  
H. Christensen ◽  
B. Jorgensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Flow Rate ◽  
Mean Arterial Blood Pressure ◽  
Blood Flow Rate ◽  
Tissue Blood Flow ◽  
Peripheral Blood Flow ◽  
Arterial Blood

Subcutaneous adipose tissue blood flow rate, together with systemic arterial blood pressure and heart rate under ambulatory conditions, was measured in the lower legs of 15 normal human subjects for 12-20 h. The 133Xe-washout technique, portable CdTe(Cl) detectors, and a portable data storage unit were used for measurement of blood flow rates. An automatic portable blood pressure recorder and processor unit was used for measurement of systolic blood pressure, diastolic blood pressure, and heart rate every 15 min. The change from upright to supine position at the beginning of the night period was associated with a 30-40% increase in blood flow rate and a highly significant decrease in mean arterial blood pressure and heart rate (P less than 0.001 for all). Approximately 100 min after the subjects went to sleep an additional blood flow rate increment (mean 56%) and a simultaneous significant decrease in mean arterial blood pressure (P less than 0.001) were observed. The duration of this hyperemic phase was 116 min. A highly significant reduction of the subcutaneous vascular resistance (50%) was demonstrated during the hyperemic blood flow rate phase compared with the surrounding phases (P less than 0.0001). The synchronism of the nocturnal subcutaneous hyperemia and the decrease in systemic mean arterial blood pressure point to a common, possibly central nervous or humoral, eliciting mechanism.

Renal vascular effects of epinephrine infusion in the halothane-anesthetized piglet

1994 ◽  
Vol 72 (4) ◽  
pp. 394-396 ◽  
Author(s):  
Keith J. Harrington ◽  
Robert G. Allen ◽  
Jay W. Dewald
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Renal Vascular Resistance ◽  
Epinephrine Infusion ◽  
Arterial Blood ◽  
Renal Vascular

The objective of this study was to determine the dose–response effects of epinephrine, given by systemic intravenous infusion to the halothane-anesthetized newborn piglet, on renal blood flow, mean arterial blood pressure, and renal vascular resistance. Seven newborn piglets were acutely instrumented. A transit-time ultrasound flow probe was placed around the renal artery and a femoral arterial catheter was placed for blood pressure monitoring. Epinephrine was infused in doubling doses from 0.2 to 3.2 μg∙kg−1∙min−1. Mean arterial blood pressure increased from 54 mmHg (1 mmHg = 133.3 Pa) to an average of 96 mmHg at 3.2 μg∙kg−1∙min−1 of epinephrine. Renal blood flow increased from 165 mL∙min−1∙100 g−1 at baseline to 185 mL∙min−1∙100 g−1 at a dose of 0.2 μg∙kg−1∙min−1 and increased further at 0.4 and 0.8 μg∙kg−1∙min−1 to reach 261 mL∙min−1∙100 g−1. Renal blood flow began to fall at a dose of 3.2 μg∙kg−1∙min−1, remaining however, significantly above baseline (211 mL∙min−1∙100 g−1). Consequently, calculated renal vascular resistance fell as the dose was increased from 0.2 to 0.8 μg∙kg−1∙min−1 and then rose again at 1.6 and 3.2 μg∙kg−1∙min−1, being significantly above baseline at 3.2 μg∙kg−1∙min−1. These results demonstrate that epinephrine when given by systemic infusion to the halothane-anesthetized newborn pig is a renal vasodilator at low doses and causes renal vasoconstriction at moderate to high doses. Renal blood flow remained above baseline at all doses tested, and thus, within the dosage range tested, epinephrine infusion should not cause renal ischemia.Key words: epinephrine, kidney blood flow, piglet, renal vascular resistance.

Central and regional hemodynamic effects during infusion of Big endothelin-1 in healthy humans

1996 ◽  
Vol 80 (6) ◽  
pp. 1921-1927 ◽  
Author(s):  
G. Ahlborg ◽  
A. Ottosson-Seeberger ◽  
A. Hemsen ◽  
J. M. Lundberg
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Endothelin 1 ◽  
Healthy Humans ◽  
Arterial Blood

Big endothelin-1 (Big ET-1) was given intravenously to six healthy men to study uptakes and vascular effects. Blood samples were taken from systemic and pulmonary arterial and internal jugular and deep forearm venous catheters. Arterial Big ET-1-like immunoreactivity (Big ET-1-LI) increased from 5.43 +/- 0.60 to 756 +/- 27 pmol/l, and ET-1-LI increased from 4.67 +/- 0.08 to 6.67 +/- 0.52 pmol/l (P < 0.001). Skeletal muscle fractional extraction of Big ET-1-LI was 15 +/- 4%. ET-1-LI release did not increase in the studied vascular beds. Heart rate fell by 17% (P < 0.001), cardiac output fell by 26% (P < 0.001), and stroke volume fell by 11% (P < 0.05). Mean arterial blood pressure increased 18%, systemic vascular resistance increased 65%, and pulmonary vascular resistance increased 57% (P < 0.01-0.001). Pulmonary blood pressures, forearm blood flow, arterial pH, arterial PCO2, and systemic arterial-internal jugular venous O2 difference remained unchanged. No specific Big ET-1 receptors were found in human pulmonary membranes. The half-maximal inhibitory concentration for the receptor antagonist bosentan was 181 nM. In summary, circulating Big ET-1 elicits greater increases in mean arterial blood pressure and systemic vascular resistance and decreases in heart rate and cardiac output compared with an equimolar ET-1 infusion (26).

scholarly journals Neurovascular responses to mental stress in the supine and upright postures

2008 ◽  
Vol 104 (4) ◽  
pp. 1129-1136 ◽  
Author(s):  
Nathan T. Kuipers ◽  
Charity L. Sauder ◽  
Jason R. Carter ◽  
Chester A. Ray
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Doppler Ultrasound ◽  
Mean Arterial Blood Pressure ◽  
Mental Stress ◽  
Upright Posture ◽  
Vascular Responses ◽  
Arterial Blood

The purpose of this study was to determine neurovascular responses to mental stress (MS) in the supine and upright postures. MS was elicited in 23 subjects (26 ± 1 yr) by 5 min of mental arithmetic. In study 1 ( n = 9), Doppler ultrasound was used to measure mean blood flow velocity in the renal (RBFV) and superior mesenteric arteries (SMBFV), and venous occlusion plethysmography was used to measure forearm blood flow (FBF). In study 2 ( n = 14), leg blood flow (LBF; n = 9) was measured by Doppler ultrasound, and muscle sympathetic nerve activity (MSNA; n = 5) was measured by microneurography. At rest, upright posture increased heart rate and MSNA and decreased LBF, FBF, RBFV, and SMBFV and their respective conductances. MS elicited similar increases in mean arterial blood pressure (∼12 mmHg) and heart rate (∼17 beats/min), regardless of posture. MS in both postures elicited a decrease in RBFV, SMBFV, and their conductances and an increase in LBF, FBF, and their conductances. Changes in blood flow were blunted in the upright posture in all vascular beds examined, but the pattern of the vascular response was the same as the supine posture. MS did not change MSNA in either posture (change: ∼1 ± 3 and ∼3 ± 3 bursts/min, respectively). In conclusion, the augmented sympathetic activity of the upright posture does not alter heart rate, mean arterial blood pressure, or MSNA responses to MS. MS elicits divergent vascular responses in the visceral and peripheral vasculature. These results indicate that, although the upright posture attenuates vascular responses to MS, the pattern of neurovascular responses does not differ between postures.

Cardiovascular responses to V1-vasopressinergic antagonism in conscious versus anesthetized rats

1988 ◽  
Vol 66 (11) ◽  
pp. 1437-1441 ◽  
Author(s):  
Barbara L. Brizzee ◽  
Benjimen R. Walker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Arginine Vasopressin ◽  
Surgical Stress ◽  
Arterial Blood ◽  
Anesthetized Rats

Experiments were performed to compare the possible effect of endogenous arginine vasopressin on renal hemodynamics between anesthetized, surgically stressed rats and conscious rats. Animals were instrumented with arterial and venous catheters as well as with a pulsed Doppler flow probe on the left renal artery. The rats were studied under the following conditions: (1) conscious and unrestrained; (2) anesthetized only; (3) anesthetized with minor surgical stress; and (4) anesthetized with major surgical stress. Two anesthetic agents were also compared, a mixture of ketamine (110 mg/kg i.m.) and acepromazine (1 mg/kg i.m.), and sodium pentobarbital (50 mg/kg i.p.). Baseline mean arterial blood pressure was significantly higher in pentobarbital-anesthetized rats following surgical stress compared with conscious animals, but blood pressure was not affected by ketamine–acepromazine anesthesia. After baseline measurements of blood pressure, heart rate, and renal blood flow, a specific V1-vasopressinergic antagonist (d(CH2)5Tyr(Me) arginine vasopressin, 10 mg/kg i.v.) was administered to each group. Mean arterial blood pressure, heart rate, and renal blood flow were monitored for an additional 15 min. Mean arterial blood pressure and renal blood flow decreased after V1 antagonism in ketamine–acepromazine-anesthetized rats with major surgical stress, but were not affected in pentobarbital-anesthetized animals. Heart rate and renal vascular resistance were not affected following V1 blockade with either anesthetic agent. These data suggest that arginine vasopressin plays a role in maintaining blood pressure and renal perfusion in ketamine–acepromazine-anesthetized rats following surgical stress, but does not have a significant effect on renal hemodynamics under pentobarbital anesthesia.

Sympathetic vascular transduction is augmented in young normotensive blacks

2002 ◽  
Vol 92 (2) ◽  
pp. 651-656 ◽  
Author(s):  
Chester A. Ray ◽  
Kevin D. Monahan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Blacks And Whites

The purpose of the present study was to determine sympathetic vascular transduction in young normotensive black and white adults. We hypothesized that blacks would demonstrate augmented transduction of muscle sympathetic nerve activity (MSNA) into vascular resistance. To test this hypothesis, MSNA, forearm blood flow, heart rate, and arterial blood pressure were measured during lower body negative pressure (LBNP). At rest, no differences existed in arterial blood pressure, heart rate, forearm blood flow, and forearm vascular resistance (FVR). Likewise, LBNP elicited comparable responses of these variables for blacks and whites. Baseline MSNA did not differ between blacks and whites, but whites demonstrated greater increases during LBNP (28 ± 7 vs. 55 ± 18%, 81 ± 21 vs. 137 ± 42%, 174 ± 81 vs. 556 ± 98% for −5, −15, and −40 mmHg LBNP, respectively; P < 0.001). Consistent with smaller increases in MSNA but similar FVR responses during LBNP, blacks demonstrated greater sympathetic vascular transduction (%FVR/%MSNA) than whites (0.95 ± 0.07 vs. 0.82 ± 0.07 U; 0.82 ± 0.11 vs. 0.64 ± 0.09 U; 0.95 ± 0.37 vs. 0.35 ± 0.09 U; P < 0.01). In summary, young whites demonstrate greater increases in MSNA during baroreceptor unloading than age-matched normotensive blacks. However, more importantly, for a given increase in MSNA, blacks demonstrate greater forearm vasoconstriction than whites. This finding may contribute to augmented blood pressure reactivity in blacks.

Effect of sleep/wake state on arterial blood pressure in genetically identical mice

1998 ◽  
Vol 85 (1) ◽  
pp. 366-371 ◽  
Author(s):  
C. D. Schaub ◽  
C. Tankersley ◽  
A. R. Schwartz ◽  
P. L. Smith ◽  
J. L. Robotham ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Eye Movement ◽  
Arterial Blood Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Large Variability ◽  
Arterial Blood ◽  
Blood Pressure Responses ◽  
Wake State

Genetic determinants may contribute to the large variability in arterial blood pressure responses to changes in sleep/wake state in humans. In this study, we developed techniques to examine the relationship between sleep/wake state and mean arterial pressure (MAP) in unrestrained, genetically identical mice (C57BL/6J; n = 9). The left common carotid artery was catheterized, and arterial blood gases were analyzed 24–48 h postsurgery to verify normal respiratory and metabolic function. The animals were then allowed to cycle naturally through sleep/wake states over a 3- to 4-h period while continuous polysomnography and arterial pressure measurements were made. The MAP decreased from quiet wakefulness to non-rapid-eye-movement sleep (9.8 ± 1.3 mmHg; P < 0.001) and further decreased from non-rapid-eye-movement to rapid-eye-movement sleep (9.7 ± 1.8 mmHg; P < 0.001). We conclude that the inbred strain of C57BL/6J mice exhibits significant and consistent changes in MAP related to sleep/wake state. Future studies can compare responses in this strain of mice with those in other inbred or transgenic mice to determine whether specific genes regulate arterial blood pressure responses to sleep/wake state.

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