Cardiovascular responses of man during negative-pressure breathing

1960 ◽  
Vol 15 (4) ◽  
pp. 557-560 ◽  
Author(s):  
E. Y. Ting ◽  
S. K. Hong ◽  
H. Rahn

Blood pressures, heart rate and finger volumes were recorded while supine subjects submitted to various degrees of continuous negative-pressure breathing. The lowest pressure was –30 cm H2O. Systolic and diastolic arterial pressures as well as heart rate remained essentially unchanged. The peripheral venous pressure estimated by an indirect method was slightly lowered. Finger plethysmography indicated a peripheral vasoconstriction to the same degree as observed during positive-pressure breathing. Various considerations suggest that during negative-pressure breathing the veins entering the thoracic cavity collapse and effectively divide the circulation into the thoracic one which operates at a considerably reduced pressure, and the nonthoracic circulation which is maintained at normal pressures. The pressure difference between these two circulations is maintained by the left ventricle. Submitted on February 8, 1960

1967 ◽  
Vol 22 (6) ◽  
pp. 1053-1060 ◽  
Author(s):  
Maylene Wong ◽  
Edgardo E. Escobar ◽  
Gilberto Martinez ◽  
John Butler ◽  
Elliot Rapaport

We measured the end-diastolic volume (EDV) and stroke volume (SV) in the right ventricle of anesthetized dogs during continuous pressure breathing and compared them to measurements taken during breathing at atmospheric pressure. During intratracheal positive-pressure breathing, EDV, and SV decreased and end-diastolic pressure became more positive relative to atmospheric pressure. During intratracheal negative-pressure breathing, EDV enlarged and SV tended to increase; end-diastolic pressure became more negative. During extrathoracic negative-pressure breathing SV decreased, EDV fell, though not significantly, and end-diastolic pressure rose, but insignificantly. Changes in EDV observed during intratracheal positive-pressure breathing and intratracheal negative-pressure breathing were associated with minor shifts in transmural pressure (end-diastolic pressure minus intrapleural pressure) in the expected directions, but during extrathoracic negative-pressure breathing a large increase in transmural pressure took place with the nonsignificant reduction in EDV. We believe that intrathoracic pressure influences right ventricular filling by changing the peripheral-to-central venous pressure gradient. The cause of the alteration in diastolic ventricular distensibility demonstrated during extra-thoracic negative-pressure breathing remains unexplained. positive-pressure breathing; negative-pressure breathing; extrathoracic negative-pressure breathing Submitted on August 16, 1966


1965 ◽  
Vol 20 (4) ◽  
pp. 669-674 ◽  
Author(s):  
J. Salzano ◽  
F. G. Hall

Continuous pressure breathing was studied in hypothermic anesthetized dogs. Alveolar ventilation decreased during continuous positive-pressure breathing and increased during continuous negative-pressure breathing. The changes in alveolar ventilation were due to changes in respiratory rate as well as in respiratory dead space. Cardiac output fell significantly during continuous positive-pressure breathing due to a reduction in heart rate and stroke volume. During continuous negative-pressure breathing cardiac output was only slightly greater than during control as a result of a fall in heart rate and an increase in stroke volume. Oxygen consumption was reduced to 60% of control during continuous positive-pressure breathing of 16 cm H2O but was 25% greater than control during continuous negative-pressure breathing. Qualitatively, CO2 production changed as did O2 consumption but was different quantitatively during continuous negative-pressure breathing indicating hyperventilation due to increased respiratory rate. Mean pulmonary artery pressures and pulmonary resistance varied directly with the applied intratracheal pressure. The results indicate that the hypothermic animal can tolerate an imposed stress such as continuous pressure breathing and can increase its oxygen consumption during continuous negative-pressure breathing as does the normothermic animal. hypothermia; respiratory dead space; metabolic rate; cardiac output Submitted on December 8, 1964


1985 ◽  
Vol 59 (4) ◽  
pp. 1242-1248 ◽  
Author(s):  
J. D. Marks ◽  
J. M. Luce ◽  
N. M. Lazar ◽  
J. N. Wu ◽  
A. Lipavsky ◽  
...  

To study the effect of increases in lung volume on solute uptake, we measured clearance of 99mTc-diethylenetriaminepentaacetic acid (Tc-DTPA) at different lung volumes in 19 healthy humans. Seven subjects inhaled aerosol (1 micron activity median aerodynamic diam) at ambient pressure; clearance and functional residual capacity (FRC) were measured at ambient pressure (control) and at increased lung volume produced by positive pressure [12 cmH2O continuous positive airway pressure (CPAP)] or negative pressure (voluntary breathing). Six different subjects inhaled aerosol at ambient pressure; clearance and FRC were measured at ambient pressure and CPAP of 6, 12, and 18 cmH2O pressure. Six additional subjects inhaled aerosol at ambient pressure or at CPAP of 12 cmH2O; clearance and FRC were determined at CPAP of 12 cmH2O. According to the results, Tc-DTPA clearance from human lungs is accelerated exponentially by increases in lung volume, this effect occurs whether lung volume is increased by positive or negative pressure breathing, and the effect is the same whether lung volume is increased during or after aerosol administration. The effect of lung volume must be recognized when interpreting the results of this method.


1988 ◽  
Vol 255 (1) ◽  
pp. R149-R156 ◽  
Author(s):  
K. Sander-Jensen ◽  
J. Mehlsen ◽  
C. Stadeager ◽  
N. J. Christensen ◽  
J. Fahrenkrug ◽  
...  

Progressive central hypovolemia is characterized by a normotensive, tachycardic stage followed by a reversible, hypotensive stage with slowing of the heart rate (HR). We investigated circulatory changes and arterial hormone concentrations in response to lower-body negative pressure (LBNP) in six volunteers before and after atropine administration. LBNP of 55 mmHg initially resulted in an increase in HR from 55 +/- 4 to 90 +/- 5 beats/min and decreases in mean arterial pressure (MAP) from 94 +/- 4 to 81 +/- 5 mmHg, in central venous pressure from 7 +/- 1 to -3 +/- 1 mmHg, and in cardiac output from 6.1 +/- 0.5 to 3.7 +/- 0.11/min. Concomitantly, epinephrine and norepinephrine levels increased. After 8.2 +/- 2.3 min of LBNP, the MAP had decreased to 41 +/- 7 mmHg and HR had decreased to 57 +/- 3 beats/min. Vasopressin increased from 1.2 +/- 0.3 to 137 +/- 45 pg/ml and renin activity increased from 1.45 +/- 4.0 to 3.80 +/- 1.0 ng.ml-1.h-1 with no further changes in epinephrine, norepinephrine, and vasoactive intestinal polypeptide. A tardy rise in pancreatic polypeptide indicated increased vagal activity. After atropine. LBNP also caused an initial increase in HR, which, however, remained elevated during the subsequent decrease in MAP to 45 +/- 6 mmHg occurring after 8.1 +/- 2.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)


1981 ◽  
Author(s):  
G J Stewart ◽  
R G Schaub ◽  
R E Cartee

This study was done to correlate known cardiovascular responses to bradykinin (increased heart rate, lowered arterial blood pressure) with recently demonstrated endothelial damage and proposed venous dilation. Healthy dogs of mixed breed were used. Blood pressures and heart rate were monitored and recorded on a Narco physiograph. The diameter of a jugular vein was monitored with an ADR ultrasound machine using a 10 MHz probe with linear array of crystals and recorded on polaroid prints. Jugular veins and carotid arteries were removed and prepared for scanning electron microscopy after removal of blood and partial in situ fixation by whole body perfusion. The response of arterial pressure was dose dependent with no change at 6 ug/min, variable drop at 12 ug/min and 22-40% drop at 60 ug/min and above. Venous pressure increased in 1 dog but was unchanged in 4 others. The increase of heart rate paralled the drop in arterial blood pressure. The diameter of a jugular vein increased in 3 of 3 monitored dogs by 25, 33, 50% of baseline diameter (average increase 36%) with high (300 ug/min) bradykinin. Endothelial damage (microtears) occurred around 70-80% of branches, at some valves and on the main vessel occassionally. The tears were infiltrated with leukocytes and some red cells and platelets indicating that tearing occurred while blood was still circulating, i.e. before dissection for removal of vessels. Carotid arteries showed no tears. Dilation of arteries would be limited by their elastic layers (missing in veins). These observations show that venous dilation and endothelial tearing around side branches are part of the cardiovascular response to blood born bradykinin. They also show that venous dilation can be measured by ultrasound.


1992 ◽  
Vol 263 (6) ◽  
pp. R1303-R1308 ◽  
Author(s):  
T. J. Ebert ◽  
L. Groban ◽  
M. Muzi ◽  
M. Hanson ◽  
A. W. Cowley

Brief low-dose infusions of atrial natriuretic peptide (ANP) that emulate physiological plasma concentrations in humans have little if any effect on renal excretory function. This study explored the possibility that ANP-mediated reductions in cardiac filling pressures (through ANP's rapid effect on capillary dynamics) could attenuate its purported renal effects. Protocol A consisted of 16 healthy subjects (ages 19-27 yr old) who underwent three consecutive 45-min experimental sequences: 1) placebo, 2) ANP (10 ng.kg-1 x min-1), and 3) ANP alone (n = 8) or ANP with simultaneous lower body positive pressure (LBPP, n = 8). Electrocardiogram and direct measures of arterial and central venous pressures were continuously monitored. Blood was sampled at the end of each 45-min sequence before subjects stood to void. Compared with control (placebo), ANP produced a hemoconcentration and increased plasma norepinephrine, but did not change heart rate, blood pressure, plasma levels of renin, aldosterone, or vasopressin, or renal excretion of volume or sodium. In subjects receiving LBPP to maintain central venous pressure during the last 45 min of ANP infusion, norepinephrine did not increase and urine volume and sodium excretion increased (P < 0.05). In a second study (protocol B), five healthy subjects received a placebo infusion for 45 min followed by two consecutive 45-min infusions of ANP (10 ng.kg-1 x min-1). Central venous pressure was maintained (LBPP) at placebo baseline throughout the two ANP infusion periods. Urine volume and sodium excretion rates increased progressively and significantly during both ANP infusion periods (P < 0.05) without significant changes in creatinine clearance, blood pressure, or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)


2001 ◽  
Vol 281 (2) ◽  
pp. R468-R475 ◽  
Author(s):  
John S. Floras ◽  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
Steven C. Brooks ◽  
Michael J. Pollard ◽  
...  

Lower body negative pressure (LBNP; −5 and −15 mmHg) was applied to 14 men (mean age 44 yr) to test the hypothesis that reductions in preload without effect on stroke volume or blood pressure increase selectively muscle sympathetic nerve activity (MSNA), but not the ratio of low- to high-frequency harmonic component of spectral power (PL/PH), a coarse-graining power spectral estimate of sympathetic heart rate (HR) modulation. LBNP at −5 mmHg lowered central venous pressure and had no effect on stroke volume (Doppler) or systolic blood pressure but reduced vagal HR modulation. This latter finding, a manifestation of arterial baroreceptor unloading, refutes the concept that low levels of LBNP interrogate, selectively, cardiopulmonary reflexes. MSNA increased, whereas PL/PH and HR were unchanged. This discordance is consistent with selectivity of efferent sympathetic responses to nonhypotensive LBNP and with unloading of tonically active sympathoexcitatory atrial reflexes in some subjects. Hypotensive LBNP (−15 mmHg) increased MSNA and PL/PH, but there was no correlation between these changes within subjects. Therefore, HR variability has limited utility as an estimate of the magnitude of orthostatic changes in sympathetic discharge to muscle.


2006 ◽  
Vol 101 (3) ◽  
pp. 771-777 ◽  
Author(s):  
Adnan Cutuk ◽  
Eli R. Groppo ◽  
Edward J. Quigley ◽  
Klane W. White ◽  
Robert A. Pedowitz ◽  
...  

The purpose of this study is to assess cardiovascular responses to lower body positive pressure (LBPP) and to examine the effects of LBPP unloading on gait mechanics during treadmill ambulation. We hypothesized that LBPP allows comfortable unloading of the body with minimal impact on the cardiovascular system and gait parameters. Fifteen healthy male and female subjects (22–55 yr) volunteered for the study. Nine underwent noninvasive cardiovascular studies while standing and ambulating upright in LBPP, and six completed a gait analysis protocol. During stance, heart rate decreased significantly from 83 ± 3 beats/min in ambient pressure to 73 ± 3 beats/min at 50 mmHg LBPP ( P < 0.05). During ambulation in LBPP at 3 mph (1.34 m/s), heart rate decreased significantly from 99 ± 4 beats/min in ambient pressure to 84 ± 2 beats/min at 50 mmHg LBPP ( P < 0.009). Blood pressure, brain oxygenation, blood flow velocity through the middle cerebral artery, and head skin microvascular blood flow did not change significantly with LBPP. As allowed by LBPP, ambulating at 60 and 20% body weight decreased ground reaction force ( P < 0.05), whereas knee and ankle sagittal ranges of motion remained unaffected. In conclusion, ambulating in LBPP has no adverse impact on the systemic and head cardiovascular parameters while producing significant unweighting and minimal alterations in gait kinematics. Therefore, ambulating within LBPP is potentially a new and safe rehabilitation tool for patients to reduce loads on lower body musculoskeletal structures while preserving gait mechanics.


1988 ◽  
Vol 75 (2) ◽  
pp. 159-165 ◽  
Author(s):  
R. Hainsworth ◽  
Y. M. H. Al-Shamma

1. Carotid baroreceptors were stimulated by application of a subatmospheric pressure to a chamber fitted round the anterior and lateral aspects of the subject's neck (neck suction). Pulse interval and heart rate were determined from an electrocardiogram, cardiac output by a single-breath method and arterial blood pressure by an automatic sphygmomanometer. 2. The maximal prolongation of the pulse interval, determined during held expiration, occurred within 2–3 s from the onset of the neck suction. All the measured variables were in steady states between 2 and 3 min from the start of neck suction. 3. Neck suction at − 10 mmHg resulted only in an immediate change in pulse interval. All variables changed approximately linearly with the magnitude of the neck suction between − 10 and − 40 mmHg. 4. The reproducibilities of the responses to neck suction at − 30 mmHg, expressed as two standard deviations of the differences between responses on two occasions, were (mean responses in parentheses): immediate pulse interval, ± 32 (+ 236) ms; steady-state heart rate, ± 2.5 (− 6.5) beats/min; cardiac output ± 0.14 (− 0.59) 1/min; systolic and diastolic blood pressures, ± 10.0 (− 16.9) and ± 5.4 (− 10.1) mmHg, respectively. 5. Control values and responses to neck suction at − 30 mmHg were compared in subjects grouped in four age bands between 19 and 80 years. With increasing age, the control value of cardiac index (cardiac output divided by calculated body surface area) decreased, systolic and diastolic pressures increased, and the responses of all the measured variables to neck suction decreased. These results, obtained from a healthy population, provide reference values for comparison with those of individuals who may have abnormal baroreceptor reflexes.


2013 ◽  
pp. 653-662 ◽  
Author(s):  
T. SOTA ◽  
S. MATSUO ◽  
Y. UCHIDA ◽  
H. HAGINO ◽  
Y. KAWAI

This study was undertaken to investigate the effects of lower body positive pressure (LBPP) on cardiovascular responses during a 15-min walking trial in young (22.1±0.4 years) and elderly women (67.8±1.1 years). The application of 20 mm Hg LBPP reduced ground reaction forces by 31.2±0.5 kgw in both groups. We hypothesized that cardiovascular responses to LBPP during walking were different between the young and elderly subjects. Applying 20 mm Hg of LBPP increased diastolic and mean blood pressure but not systolic blood pressure in both groups. LBPP-induced reduction in heart rate (HR) occurred more quickly in the young group compared to the elderly group (p<0.05). Applying LBPP also decreased double product (systolic blood pressure x HR) in both groups, suggesting that LBPP reduces myocardial oxygen consumption during exercise. These results suggest that heart rate responses to LBPP during exercise vary with increasing age.


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