scholarly journals Hemodynamic effects of pressures applied to the upper airway during sleep

2000 ◽  
Vol 89 (2) ◽  
pp. 537-548 ◽  
Author(s):  
P. R. Eastwood ◽  
A. K. Curran ◽  
C. A. Smith ◽  
J. A. Dempsey
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Upper Airway ◽  
Intrathoracic Pressure ◽  
Nrem Sleep ◽  
Pressure Response ◽  
Central Apnea ◽  
Tracheal Occlusion ◽  
Negative Pressures

The increase in systemic blood pressure after an obstructive apnea is due, in part, to sympathetically mediated vasoconstriction. We questioned whether upper airway (UA) receptors could contribute reflexly to this vasoconstriction. Four unanesthetized dogs were studied during wakefulness and non-rapid-eye-movement (NREM) sleep. The dogs breathed via a fenestrated tracheostomy tube sealed around the tracheal stoma. The snout was sealed with an airtight mask, thereby isolating the UA when the fenestration was closed and exposing the UA to negative inspiratory intrathoracic pressure when it was open. The blood pressure response to three UA perturbations was studied: 1) square-wave negative pressures sufficient to cause UA collapse with the fenestration closed during a mechanical hyperventilation-induced central apnea; 2) tracheal occlusion with the fenestration open vs. closed; and 3) high-frequency pressure oscillations (HFPO) with the fenestration closed. During NREM sleep, 1) blood pressure response to tracheal occlusion was similar with the fenestration open or closed; 2) collapsing the UA with negative pressures failed to alter blood pressure during a central apnea; and 3) application of HFPO to the UA during eupnea and resistive-loaded breaths increased heart rate and blood pressure. However, these changes were likely to be secondary to the effects of HFPO-induced reflex changes on prolonging expiratory time. These findings suggest that activation of UA pressure-sensitive receptors does not contribute directly to the pressor response associated with sleep-disordered breathing events.

scholarly journals Arterial blood pressure response to heavy resistance exercise

1985 ◽  
Vol 58 (3) ◽  
pp. 785-790 ◽  
Author(s):  
J. D. MacDougall ◽  
D. Tuxen ◽  
D. G. Sale ◽  
J. R. Moroz ◽  
J. R. Sutton
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Valsalva Maneuver ◽  
Pressor Response ◽  
Intrathoracic Pressure ◽  
Pressure Response ◽  
Weight Lifting ◽  
Capacitance Transducer ◽  
Arterial Blood ◽  
Peak Pressures

The purpose of this study was to record the blood pressure response to heavy weight-lifting exercise in five experienced body builders. Blood pressure was directly recorded by means of a capacitance transducer connected to a catheter in the brachial artery. Intrathoracic pressure with the Valsalva maneuver was recorded as mouth pressure by having the subject maintain an open glottis while expiring against a column of Hg during the lifts. Exercises included single-arm curls, overhead presses, and both double- and single-leg presses performed to failure at 80, 90, 95, and 100% of maximum. Systolic and diastolic blood pressures rose rapidly to extremely high values during the concentric contraction phase for each lift and declined with the eccentric contraction. The greatest peak pressures occurred during the double-leg press where the mean value for the group was 320/250 mmHg, with pressures in one subject exceeding 480/350 mmHg. Peak pressures with the single-arm curl exercise reached a mean group value of 255/190 mmHg when repetitions were continued to failure. Mouth pressures of 30–50 Torr during a single maximum lift, or as subjects approached failure with a submaximal weight, indicate that a portion of the observed increase in blood pressure was caused by a Valsalva maneuver. It was concluded that when healthy young subjects perform weight-lifting exercises the mechanical compression of blood vessels combines with a potent pressor response and a Valsalva response to produce extreme elevations in blood pressure. Pressures are extreme even when exercise is performed with a relatively small muscle mass.

scholarly journals Modulation of cardiac contractility by muscle metaboreflex following efforts of different intensities in humans

2006 ◽  
Vol 291 (6) ◽  
pp. H3035-H3042 ◽  
Author(s):  
Antonio Crisafulli ◽  
Enrico Salis ◽  
Gianluigi Pittau ◽  
Luigi Lorrai ◽  
Filippo Tocco ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Myocardial Contractility ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Cardiac Contractility ◽  
Preliminary Test ◽  
Knee Extension ◽  
Pressure Response ◽  
Sensory Nerves

Accumulation of metabolic end products within skeletal muscle stimulates sensory nerves, thus evoking a pressor response termed “metaboreflex.” The aim of this study was to evaluate changes in hemodynamics occurring during metaboreflex activation obtained by postexercise muscle ischemia (PEMI) after two different exercise intensities. In twelve healthy subjects, the metaboreflex was studied with the PEMI method at the start of recovery from one leg-dynamic knee extension performed at intensities of 30% (PEMI 30%) and 70% (PEMI 70%) of the maximum workload achieved in a preliminary test. Control exercise recovery tests at the same intensities were also conducted. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were that 1) during metaboreflex, exercise conducted against the higher workload caused a more pronounced blood pressure increase than the strain conducted against the lower workload; and 2) during PEMI 70%, this blood pressure response was mainly achieved through enhancement of myocardial contractility that increased stroke volume and, in turn, cardiac output, whereas during PEMI 30%, the blood pressure response was reached predominantly by means of vasoconstriction. Thus a substantial enhancement of myocardial contractility was reached only in the PEMI 70% test. These results suggest that hemodynamic regulation during metaboreflex engagement caused by PEMI in humans is dependent on the intensity of the previous effort. Moreover, the cardiovascular response during metaboreflex is not merely achieved by vasoconstriction alone, but it appears that there is a complex interplay between peripheral vasoconstriction and heart contractility recruitment.

Blunted blood pressure response to exercise and isolated muscle metaboreflex activation in patients with cirrhosis

2020 ◽  
Author(s):  
Pedro Augusto Carvalho Mira ◽  
Maria Fernanda Almeida Falci ◽  
Janaína Becari Moreira ◽  
Rosa Virginia Diaz Guerrero ◽  
Tarsila Campanha da Rocha Ribeiro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Pressure Response ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Cirrhotic Patients ◽  
Response To Exercise

We sought to test the hypothesis that the cardiovascular responses to isolated muscle metaboreflex activation would be blunted in patients with cirrhosis. Eleven patients with cirrhosis and 15 healthy controls were evaluated. Blood pressure (BP, oscillometric method), contralateral forearm blood flow (FBF, venous occlusion plethysmography) and heart rate (HR, electrocardiogram) were measured during baseline, isometric handgrip at 30% of maximal voluntary contraction followed by post-exercise ischemia (PEI). Forearm vascular conductance (FVC) was calculated as follows: (FBF/mean BP) x 100. Changes in HR during handgrip were similar between groups, but tended to be different during PEI (controls: ∆0.5 ± 1.1 bpm vs. cirrhotic patients: ∆3.6 ± 1.0 bpm, P = 0.057). Mean BP response to handgrip (controls: ∆20.9 ± 2.7 mmHg vs. cirrhotic patients: ∆10.6 ± 1.5 mmHg, P = 0.006) and PEI was attenuated in cirrhotic patients (controls: ∆16.1 ± 1.9 mmHg vs. cirrhotic patients: ∆7.2 ± 1.4 mmHg, P = 0.001). In contrast, FBF and FVC increased during handgrip and decreased during PEI similarly between groups. These results indicate that an abnormal muscle metaboreflex activation explained, at least partially, the blunted pressor response to exercise exhibited by cirrhotic patients. Novelty bullets: • Patients with cirrhosis present abnormal muscle metaboreflex activation • Blood pressure response was blunted, but forearm vascular response was preserved • Heart rate response was slightly elevated

Cardiovascular consequences of microinjection of vasopressin and angiotensin II in the area postrema

1993 ◽  
Vol 265 (3) ◽  
pp. R625-R631 ◽  
Author(s):  
V. L. Lowes ◽  
L. E. McLean ◽  
N. W. Kasting ◽  
A. V. Ferguson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Area Postrema ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Systemic Administration ◽  
Pressure Response ◽  
Arterial Blood ◽  
At1 Antagonist

Microinjection of angiotensin II (ANG II) into the area postrema (AP) of urethan-anesthetized male Sprague-Dawley rats elicited statistically significant increases in mean arterial blood pressure at doses ranging from 10 pg to 500 ng (10 pg, mean +/- SE, 10.8 +/- 1.1 mmHg, P < 0.001; 250 ng, 15.2 +/- 2.6 mmHg, P < 0.001). Heart rate was also significantly increased at doses > 10 pg, although these increases were not dose dependent. Systemic administration of losartan (Dup-753), an AT1 antagonist, was able to significantly reduce the pressor response to 250 ng ANG (post-losartan: 81.9 +/- 9.5% reduction in blood pressure response, P < 0.0001), whereas PD123319, an AT2 antagonist, was without significant effect (P > 0.1). Microinjection of vasopressin (VP) (10 pg-500 ng) into the AP also resulted in statistically significant increases in blood pressure at doses ranging from 10 to 100 pg (10 pg, 7.0 +/- 1.5 mmHg, P < 0.05) and 100-500 ng (250 ng, 12.2 +/- 1.8 mmHg, P < 0.0001). Small but significant changes in heart rate were observed only at 100 pg and 100 ng. Systemic administration of a V1 antagonist significantly attenuated the increases in blood pressure in response to 50, 100, and 250 ng VP (250 ng, post-V1 antagonist: 66.4 +/- 8.6% reduction in blood pressure response, P < 0.001), whereas [desamino,D-Arg8]vasopressin (DDAVP), a V2 agonist, had a depressor effect when microinjected directly into the AP (250 ng, -9.9 +/- 1.6 mmHg, P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial Blood Pressure Response to Transient Arousals From NREM Sleep in Nonapneic Snorers With Sleep Fragmentation

CHEST Journal ◽  
1998 ◽  
Vol 113 (4) ◽  
pp. 985-991 ◽  
Author(s):  
Frédéric Lofaso ◽  
Françoise Goldenberg ◽  
Marie Pia d'Ortho ◽  
André Coste ◽  
Alain Harf
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Nrem Sleep ◽  
Pressure Response ◽  
Sleep Fragmentation ◽  
Arterial Blood

A model of dynamic exercise: the decerebrate rat locomotor preparation

1992 ◽  
Vol 72 (1) ◽  
pp. 121-127 ◽  
Author(s):  
T. G. Bedford ◽  
P. K. Loi ◽  
C. C. Crandall
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Pressure Response ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Decerebrate Rat ◽  
Stimulation Of

The purpose of this study was to develop a dynamic exercise model in the rat that could be used to study central nervous system control of the cardiovascular system. Rats of both sexes were decerebrated under halothane anesthesia and prepared for induced locomotion on a freely turning wheel. Electrical stimulation of the mesencephalic locomotor region (MLR) elicited locomotion at different speeds and gait patterns and increased heart rate and blood pressure. Two maneuvers were performed to illustrate the potential use of the preparation. The first maneuver consisted of muscular paralysis, which prevents excitation of muscle mechanoreceptors and chemoreceptors resulting from exercise. MLR stimulation still increased blood pressure. The second maneuver was performed to determine whether the blood pressure response obtained during paralysis was an artifact of electrical stimulation of the MLR. After microinjection of gamma-aminobutyric acid into the MLR, electrical current thresholds for blood pressure and locomotion increased in parallel. gamma-Aminobutyric acid injection also reduced the pressor response to suprathreshold electrical stimulation by 76%. The injection results suggest that electrical stimulation of the MLR activates cells rather than fibers of passage. The blood pressure response of the exercise model is probably not an artifact of stimulation. The decerebrate rat locomotor preparation should offer another approach to investigate difficult problems in exercise physiology.

Effects of nicotine and dietary salt on a learned blood pressure response in Dahl-S rats

2003 ◽  
Vol 284 (5) ◽  
pp. H1793-H1799 ◽  
Author(s):  
Justin H. Kuo ◽  
Richard O. Speakman ◽  
Aletia G. Sprinkle ◽  
Sheng-Gang Li ◽  
David R. Brown ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Pressure Response ◽  
High Salt ◽  
Dietary Salt ◽  
Arterial Blood ◽  
Behavioral Stress ◽  
Low Salt ◽  
External Stimuli

We examined the effects of chronic nicotine exposure and dietary salt on the arterial blood pressure (BP) changes learned in response to an acute behavioral stress in the Dahl salt-sensitive rat. Four groups were tested: low salt + vehicle; low salt + nicotine; high salt + vehicle; and high salt + nicotine. Rats were fed a low-salt (0.08% NaCl) or a high-salt (8% NaCl) diet for 4 wk; 2.4 mg · kg−1 · day−1nicotine or vehicle was given via an implanted osmotic minipump for the last 2 wk. All rats were conditioned by following one tone (CS+) with a 0.5-s tail shock; another tone (CS−) was never followed by shock. CS+ in low salt + vehicle and high salt + vehicle-treated rats evoked an initial arterial BP increase (C1), a component of the startle response, and an ensuing, smaller, but more sustained, pressor response (C2), which is acquired with training. In these rats, both C1 and C2 evoked by CS− were significantly smaller than those to CS+, demonstrating that these groups discriminated between the two tests. Conversely, although the low salt + nicotine-treated rats had both the C1 and C2 components of the conditional arterial pressure response, they did not discriminate between CS+ and CS−. Finally, the high salt + nicotine group failed to both discriminate between tones and acquire (i.e., learn) the C2 response. The unconditional response to shock did not differ between groups. We conclude that combined exposure to high salt and to nicotine inhibits the salt-sensitive animal's acquisition of a learned conditional BP response, perhaps because nicotine acts preferentially on those central processes required for associative learning versus those involved in orientating to external stimuli.

scholarly journals Central and peripheral modulation of exercise pressor reflex sensitivity after nonfatiguing work

2020 ◽  
Vol 319 (5) ◽  
pp. R575-R583
Author(s):  
Jon Stavres ◽  
J. Carter Luck ◽  
Guillaume P. Ducrocq ◽  
Aimee E. Cauffman ◽  
Samuel Pai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Plantar Flexion ◽  
Pressure Response ◽  
Peak Oxygen Consumption ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Leg Cycling ◽  
Pressor Reflex

Autonomic blood pressure control is fundamentally altered during a single bout of exercise, as evidenced by the downward resetting of the baroreflex following exercise (postexercise hypotension). However, it is unclear if an acute bout of exercise is also associated with a change in the sensitivity of the exercise pressor response to a controlled stimulus, such as a static contraction. This study tested the hypothesis that the blood pressure response to a controlled static contraction would be attenuated after unilateral cycling of the contralateral (opposite) leg, but preserved after cycling of the ipsilateral (same) leg. To test this, the blood pressure response to 90 s of isometric plantar flexion [50% maximal voluntary contraction (MVC)] was compared before and after 20 min of contralateral and ipsilateral single-leg cycling at 20% peak oxygen consumption and rest (control) in 10 healthy subjects (three males and seven females). The mean arterial pressure response was significantly attenuated after contralateral single-leg cycling (+9.8 ± 7.5% ∆mmHg vs. +6.7 ± 6.6% ∆mmHg pre and postexercise, respectively, P = 0.04) and rest (+9.0 ± 7.5% ∆mmHg vs. +6.6 ± 5.2% ∆mmHg pre and postexercise, respectively, P = 0.03). In contrast, the pressor response nonsignificantly increased following ipsilateral single-leg cycling (+5.5 ± 5.2% ∆mmHg vs. +8.9 ± 7.2% ∆mmHg pre and postexercise, respectively, P = 0.08). The heart rate, leg blood flow, and leg conductance responses to plantar flexion were not affected by any condition ( P ≥ 0.12). These results are consistent with the notion that peripheral, but not central mechanisms promote exercise pressor reflex sensitivity after exercise.

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