Effect of arterial pulse pressure and hypoxia on myogenic responses in the gut

1978 ◽  
Vol 235 (2) ◽  
pp. H157-H161 ◽  
Author(s):  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Arterial Pressure ◽  
Vascular Smooth Muscle ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure ◽  
Circulatory Control ◽  
Myogenic Responses

In intestine, raising venous pressure (PV) elicits a precapillary vasconstriction that has been ascribed to a myogenic mechanism through which passive stretch elicits active contraction of vascular smooth muscle. A previous report from this laboratory indicated that myogenic responses in the gut were largely dependent on control conditions. The purpose of the present study was to determine whether control blood flow rates or the arterial pulse pressure affects the magnitude of myogenic responses. In isolated perfused canine small bowel arterial hypoxia was used to increase blood flow. Myogenic responses to elevated PV were not significantly different in the normoxic and hypoxic periods, indicating that blood flow per se does not greatly alter myogenic responses. When gut loops were perfused with pulsatile arterial pressure, myogenic responses occurred more than twice as frequently as during nonpulsatile pefusion and they had a greater magnitude. The results are consistent with the observation that vascular smooth muscle is stimulated not only by steady stretch but also by the rate of stretch. The results also suggest that the arterial pressure pulse should be considered in the design and interpretation of future studies of local circulatory control.

Arterial pulse pressure and vasopressin release in humans during lower body negative pressure

1993 ◽  
Vol 264 (5) ◽  
pp. R1024-R1030 ◽  
Author(s):  
P. Norsk ◽  
P. Ellegaard ◽  
R. Videbaek ◽  
C. Stadeager ◽  
F. Jessen ◽  
...  
Keyword(s):  
Pulse Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Arterial Pulse ◽  
Vasopressin Release ◽  
Arterial Pulse Pressure ◽  
Arterial Plasma

The hypothesis was tested that narrowing of arterial pulse pressure (PP) is a determinant of arginine vasopressin (AVP) release in humans. Six normal males completed a two-step lower body negative pressure (LBNP) protocol of -20 and -50 mmHg, respectively, for 10 min each. None of these subjects experienced presyncopal symptoms. Arterial plasma AVP and plasma renin activity (PRA) (at 2-min intervals) only increased subsequent to a decrease in PP (invasive brachial arterial measurements) and stroke volume (ultrasound Doppler technique, n = 4). Simultaneously, mean arterial pressure did not change. A selective decrease in central venous pressure and left atrial diameter (echocardiography, n = 4) at LBNP of -20 mmHg did not affect AVP or PRA, whereas arterial plasma norepinephrine increased (n = 4). During LBNP, significant (P < 0.05) intraindividual linear correlations were observed between log(AVP) and PP in four of the subjects with r values from -0.75 to -0.99 and between log(PRA) and PP in all six subjects with r values from -0.89 to -0.98. In conclusion, these results are in compliance with the hypothesis that narrowing of PP in humans during central hypovolemia is a determinant of AVP and renin release.

Mesenteric Blood Flow as Influenced by Progressive Hypercapnia

1956 ◽  
Vol 184 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Eugene W. Brickner ◽  
E. Grant Dowds ◽  
Bruce Willitts ◽  
Ewald E. Selkurt
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Oxygen Content ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Mesenteric Blood Flow ◽  
Initial Tendency ◽  
Elevated Heart Rate

The influence of hypercapnia on mesenteric blood flow was studied in dogs subjected to progressive increments in CO2 content of inspired air produced by rebreathing from a large spirometer. Oxygen content was maintained above 21 volumes %. Although some animals showed an initial tendency for mesenteric blood flow to decrease and arterial pressure to increase in the range 0–5 volumes % of CO2, the usual hemodynamic change in the range 5–16 volumes % was an increase in mesenteric blood flow resulting from decrease in intestinal vascular resistance, accompanied by a decline in arterial pressure. Portal venous pressure was progressively elevated. Heart rate slowed in association with an increase in pulse pressure. The observations suggest that in higher ranges of hypercapnia, CO2 has a direct dilating action on the mesenteric vasculature.

scholarly journals Positional circulatory control in the sleeping infant and toddler: role of the inner ear and arterial pulse pressure

2012 ◽  
Vol 590 (15) ◽  
pp. 3483-3493 ◽  
Author(s):  
Gary Cohen ◽  
Silvano Vella ◽  
Heather Jeffery ◽  
Hugo Lagercrantz ◽  
Miriam Katz-Salamon
Keyword(s):  
Inner Ear ◽  
Pulse Pressure ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure ◽  
Circulatory Control

Abstract 16747: The Artificial Pulse of the HeartMate3 LVAD Alters Mean Arterial Pressure Calculation, and the Relationship Between Arterial Pulse Pressure and Pulsatility Index

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Lorenzo Braghieri ◽  
Alberto Pinsino ◽  
Giulio Mondellini ◽  
Antonia Gaudig ◽  
Azka Javaid ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Pulsatility Index ◽  
Left Ventricular ◽  
Absolute Difference ◽  
Arterial Line ◽  
Arterial Pulse ◽  
Relative Contribution ◽  
Arterial Pulse Pressure

Introduction: The HeartMate (HM3) left ventricular assist device (LVAD) uniquely features an artificial pulse (AP) (designed to reduce blood stasis and simulate physiologic pulsatility) that alters arterial blood pressure (BP) tracings ( Fig. 1A ). Pulsatility Index (PI) corresponds to the magnitude of flow pulse through the LVAD and is used as a surrogate measure of arterial pulse pressure (PP). The effect of the AP on: i) relative contribution of systolic BP (SBP) and diastolic BP (DBP) to mean arterial pressure (MAP) calculation; and ii) association between PP and PI is presently unknown. Thus, we aimed to compare: i) MAP calculations; and ii) relation of PI with PP in HM3 vs HM II (LVAD with no AP) pts with arterial line (A-line) monitoring. Methods: A-line BP and LVAD PI data were prospectively collected in 48 HM3 and 29 HMII pts. MAP was calculated with the formula conventionally used in non LVAD pts (MAP = 2/3 DBP + 1/3 SBP) and compared to A-line MAP. Among HM3 pts, a multiple linear regression model was fit with A-line SBP and DBP as predictor variables, and A-line MAP as the dependent variable to derive the HM3 MAP Formula . The relation between arterial PP and PI in HM3 and HMII pts was assessed using Pearson’s correlation. Results: MAP calculated using the conventional formula accurately estimated A-line MAP in HMII pts, but overestimated A-line MAP in HM3 pts. The HM3 MAP Formula more closely approximated A-line MAP. Mean observed difference (MOD) and mean absolute difference (MAD) between calculated MAPs and A-line MAPs are reported in Fig. 1B . While median PP was similar in HM3 and HMII pts (16 vs 20 mmHg, p=0.11), median PI was significantly higher in HMII pts (3.45 vs 5.6, p<0.001). PI correlated with PP in HMII pts ( r 0.47, p=0.01). However, no significant correlation was found between PI and PP in HM3 pts ( r 0.24, p=0.1; Fig. 1C ). Conclusions: In HM3 pts, the AP significantly alters the relative contribution of SBP and DBP to MAP. Unlike in HM2 pts, PI does not relate to arterial PP in HM3 pts.

Pulsatile pulmonary microvascular pressure measured with vascular occlusion techniques

1991 ◽  
Vol 70 (3) ◽  
pp. 998-1005 ◽  
Author(s):  
J. M. Maarek ◽  
H. K. Chang
Keyword(s):  
Pulse Pressure ◽  
Venous Pressure ◽  
Arterial Occlusion ◽  
Vascular Occlusion ◽  
Arterial Pulse ◽  
Pump Frequency ◽  
Pressure Contour ◽  
Arterial Pulse Pressure ◽  
Pulmonary Arterial ◽  
Pulsatile Perfusion

The periodic variations of the pulmonary microvascular pressure during pulsatile perfusion were studied in isolated left lower lobes of canine lungs by the arterial occlusion (AO) and double occlusion (DO) techniques. Sixteen AO and eight DO maneuvers evenly distributed within the pump cycle were performed for each of four frequencies: 36, 54, 72, and 90 beats/min. Nearly identical microvascular pressure contours were reconstructed from the AO and DO maneuvers by relocating the measured occlusion pressures in time. These contours lagged behind the pulmonary arterial pressure waveform. Their amplitude decreased from 25 to 14% of the arterial pulse pressure as the pump frequency was increased from 36 to 90 beats/min. The modulus of the pressure transfer function at the site of arterial occlusion decreased as the frequency increased. The phase was negative for all frequencies and it approached -90 degrees for the higher frequencies. Vasoconstriction induced by serotonin resulted in an increase of the magnitude of the AO pressure contour that was nearly proportional to the increase of the pulmonary arterial pulse pressure. In contrast, elevation of the lobar venous pressure to 10 mmHg increased the amplitude of the AO pressure contour, whereas it slightly decreased the pulmonary arterial pulse pressure. These experiments demonstrate that the AO and DO pressures fluctuate markedly during pulsatile perfusion. Their oscillations would be indicative of the pulsatility in the pulmonary microvascular bed.

scholarly journals Adrenergic airway vascular smooth muscle responsiveness in healthy and asthmatic subjects

2001 ◽  
Vol 90 (2) ◽  
pp. 665-669 ◽  
Author(s):  
Jorge Brieva ◽  
Adam Wanner
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Dead Space ◽  
Healthy Subjects ◽  
Contractile Response ◽  
Mucosal Blood Flow ◽  
Forced Expiratory Volume ◽  
Baseline Values ◽  
The Mean

The purpose of the present study was to determine the responsiveness of airway vascular smooth muscle (AVSM) as assessed by airway mucosal blood flow (Q˙aw) to inhaled methoxamine (α1-agonist; 0.6–2.3 mg) and albuterol (β2-agonist; 0.2–1.2 mg) in healthy [ n = 11; forced expiratory volume in 1 s, 92 ± 4 (SE) % of predicted] and asthmatic ( n = 11, mean forced expiratory volume in 1 s, 81 ± 5%) adults. Mean baseline values for Q˙aw were 43.8 ± 0.7 and 54.3 ± 0.8 μl · min−1· ml−1of anatomic dead space in healthy and asthmatic subjects, respectively ( P < 0.05). After methoxamine inhalation, the maximal mean change in Q˙aw was −13.5 ± 1.0 μl · min−1· ml−1in asthmatic and −7.1 ± 2.1 μl · min−1· ml−1in healthy subjects ( P < 0.05). After albuterol, the mean maximal change in Q˙aw was 3.0 ± 0.8 μl · min−1· ml−1in asthmatic and 14.0 ± 1.1 μl · min−1· ml−1in healthy subjects ( P < 0.05). These results demonstrate that the contractile response of AVSM to α1-adrenoceptor activation is enhanced and the dilator response of AVSM to β2-adrenoceptor activation is blunted in asthmatic subjects.

Phenotype Dictates the Growth Response of Vascular Smooth Muscle Cells to Pulse Pressure in Vitro

1999 ◽  
Vol 250 (1) ◽  
pp. 174-186 ◽  
Author(s):  
Charles Cappadona ◽  
Eileen M. Redmond ◽  
Nicholas G. Theodorakis ◽  
Iain H. McKillop ◽  
Richard Hendrickson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Pulse Pressure ◽  
Growth Response ◽  
Muscle Cells

Splanchnic blood flow in the monkey during hemorrhagic shock

1965 ◽  
Vol 208 (2) ◽  
pp. 265-269 ◽  
Author(s):  
Francis L. Abel ◽  
John A. Waldhausen ◽  
Ewald E. Selkurt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Hemorrhagic Shock ◽  
Hepatic Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Mesenteric Arteries ◽  
Splanchnic Blood Flow

Blood flow in the celiac and superior mesenteric arteries was measured in nine Macaca monkeys during a standardized hemorrhagic shock procedure. Simultaneous pressures were obtained from the hepatic vein, portal vein, and aorta. Each animal was bled rapidly to an arterial pressure of 40 mm Hg and maintained at this level until 30% of the bled volume had spontaneously reinfused. The remaining blood was then rapidly reinfused and the animal observed until death. The results show a lack of overshoot of venous pressure on reinfusion, grossly pale intestines with some microscopic congestive changes, and a decrease in splanchnic conductance throughout the postinfusion period. Hepatic venous pressure exceeded portal pressure in six of the nine animals during the period of hemorrhage. The results are interpreted as indicative of insignificant splanchnic pooling during hemorrhagic shock in this animal.

scholarly journals SP284ARTERIAL STIFFNESS CALCULATED FROM PERIPHERAL ARTERIAL PULSE PRESSURE IS INDEPENDENTLY ASSOCIATED WITH ALL-CAUSE MORTALITY IN THE GENERAL POPULATION

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i183-i183
Author(s):  
Maarten A de Jong ◽  
Arie M van Roon ◽  
Jens T Bakker ◽  
Wernard Kersten ◽  
Pieter W. Kamphuisen ◽  
...  
Keyword(s):  
General Population ◽  
Pulse Pressure ◽  
Arterial Pulse ◽  
Arterial Pulse Pressure ◽  
All Cause Mortality ◽  
Peripheral Arterial
Sign in / Sign up

Export Citation Format

Share Document