Altered hormonal regulation and blood flow distribution with cardiovascular deconditioning after short-duration head down bed rest

2007 ◽  
Vol 103 (6) ◽  
pp. 2018-2025 ◽  
Author(s):  
D. Fischer ◽  
P. Arbeille ◽  
J. K. Shoemaker ◽  
D. D. O'Leary ◽  
R. L. Hughson
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Stroke Volume ◽  
Vascular Resistance ◽  
Hormonal Regulation ◽  
Venous Pressure ◽  
Plasma Concentrations ◽  
Bed Rest ◽  
Arterial Blood

This study tested the hypothesis that cardiovascular and hormonal responses to lower body negative pressure (LBNP) would be altered by 4-h head down bed rest (HDBR) in 11 healthy young men. In post-HDBR testing, three subjects failed to finish the protocol due to presyncopal symptoms, heart rate was increased during LBNP compared with pre-HDBR, mean arterial blood pressure was elevated at 0, −10, and −20 mmHg and reduced at −40 mmHg, central venous pressure (CVP) and cardiac stroke volume were reduced at all levels of LBNP. Plasma concentrations of renin, angiotensin II, and aldosterone were significantly lower after HDBR. Renin and angiotensin II increased in response to LBNP only post-HDBR. There was no effect of HDBR or LBNP on norepinephrine while epinephrine tended to increase at −40 mmHg post-HDBR ( P = 0.07). Total blood volume was not significantly reduced. Splanchnic blood flow taken from ultrasound measurement of the portal vein was higher at each level of LBNP post-compared with pre-HDBR. The gain of the cardiopulmonary baroreflex relating changes in total peripheral resistance to CVP was increased after HDBR, but splanchnic vascular resistance was actually reduced. These results are consistent with our hypothesis and suggest that cardiovascular instability following only 4-h HDBR might be related to altered hormonal and/or neural control of regional vascular resistance. Impaired ability to distribute blood away from the splanchnic region was associated with reduced stroke volume, elevated heart rate, and the inability to protect mean arterial pressure.

Effects on intravascular pressures of vasopressin and angiotensin II in dogs

1983 ◽  
Vol 245 (6) ◽  
pp. R906-R914 ◽  
Author(s):  
P. Bie ◽  
J. Warberg
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Cardiovascular Response ◽  
Venous Pressure ◽  
Plasma Concentrations ◽  
Ang Ii ◽  
Central Venous ◽  
Arterial Blood ◽  
Blood Pressures ◽  
Pressor Activity

The effects of 30-min intravenous infusions of 8-arginine vasopressin (AVP) and angiotensin-(1,8)-octapeptide (ANG II) to conscious dogs were studied by measurements of systolic (SABP), mean (MABP), and diastolic arterial blood pressures, central venous pressure (CVP), heart rate (HR), and plasma concentrations of vasopressin (pAVP). Infusion of AVP at six rates (0.4-12.8 ng X min-1 X kg-1) raised mean pAVP by 5-490 pg/ml and increased CVP by 2-10 cmH2O. HR decreased and arterial pressures increased with infusion rates of 1.6-12.8 ng X min-1 X kg-1. However, the increase in SABP was only transient. ANG II increased all arterial pressures; however, it barely changed CVP and did not change HR or pAVP. It is concluded that 1) AVP can elevate MABP without changes in SABP, 2) the effects of AVP on arterial pressures are buffered within 5-15 min, 3) CVP can be increased by doses of AVP that do not affect arterial pressures, and 4) the pressor activity is independent of the presence of ANG II. The results confirm that the cardiovascular response to vasopressin is qualitatively different from that elicited by ANG II.

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.

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.

Leukotriene end organ antagonists increase pulmonary blood flow in fetal lambs

1985 ◽  
Vol 249 (3) ◽  
pp. H570-H576 ◽  
Author(s):  
S. J. Soifer ◽  
R. D. Loitz ◽  
C. Roman ◽  
M. A. Heymann
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Blood Gases ◽  
Physiological Control ◽  
Arterial Blood ◽  
High Pulmonary Vascular Resistance

The factors responsible for maintaining the normally low pulmonary blood flow and high pulmonary vascular resistance in the fetus are not well understood. Since leukotrienes are potent pulmonary vasoconstrictors in many adult animal species, we determined whether leukotrienes were perhaps involved in the control of the fetal pulmonary circulation by studying the effects of putative leukotriene end organ antagonists in two groups of fetal lambs. In six fetal lambs studied at 130-134 days gestation, FPL 55712 increased pulmonary blood flow by 61% (P less than 0.05) and reduced pulmonary vascular resistance by 45% (P less than 0.05). There was a small increase in heart rate but no changes in pulmonary and systemic arterial pressures and systemic arterial blood gases. In six other fetal lambs studied at 130-140 days gestation, FPL 57231 increased pulmonary blood flow by 580% (P less than 0.05) and decreased pulmonary vascular resistance by 87% (P less than 0.05). Pulmonary and systemic arterial pressures decreased (P less than 0.05), and heart rate increased (P less than 0.05). Leukotriene end organ antagonism significantly increases fetal pulmonary blood flow and decreases pulmonary vascular resistance. Leukotrienes may play a role in the physiological control of the fetal pulmonary circulation.

Systemic and uterine responses to chronic infusion of estradiol-17 beta

1993 ◽  
Vol 265 (5) ◽  
pp. E690-E698 ◽  
Author(s):  
R. R. Magness ◽  
C. R. Parker ◽  
C. R. Rosenfeld
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Stroke Volume ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Pressor Responses ◽  
Chronic Infusion

Human and ovine pregnancies are associated with increases in plasma levels of estrogens and angiotensin II (ANG II), cardiac output (CO), blood volume (BV), and uterine blood flow (UBF), as well as attenuated ANG II pressor responses. We hypothesized that, in nonpregnant animals, prolonged estradiol-17 beta (E2 beta) treatment would reproduce these endocrine and hemodynamic alterations. Nonpregnant ovariectomized ewes (n = 5) received 5 microgram E2 beta/kg iv followed by 220 micrograms/day for 14 days. Plasma E2 beta increased from 36 +/- 6 to 269 +/- 79 (SE) pg/ml (P < 0.05) during E2 beta treatment, returning to control values 4 days posttreatment. By 3 days of E2 beta, mean arterial pressure (MAP) and systemic vascular resistance (SVR) fell 9 +/- 1 and 29 +/- 1%, whereas heart rate (HR) and CO increased 20 +/- 5 and 26 +/- 1% (P < 0.05). Stroke volume (SV), BV, and plasma volume were unchanged until 7 days of E2 beta, with values rising 17 +/- 5, 13 +/- 3, and 14 +/- 4, respectively (P < 0.05). Although MAP remained similarly depressed (-11 +/- 1%) during week 2 of E2 beta, SVR decreased further (-37 +/- 3%) and was associated with additional increases (P < 0.05) in CO to 44 +/- 5%, reflecting rises in SV (21 +/- 2%) but not HR. Increases in BV correlated with rises in CO (r = 0.55) and SV (r = 0.64) but not HR (r = -0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Haemodynamic effects of physiological concentrations of circulating noradrenaline in man

1988 ◽  
Vol 75 (5) ◽  
pp. 469-475 ◽  
Author(s):  
Peter C. Chang ◽  
Eugene Kriek ◽  
Jacques A. Van Der Krogt ◽  
Gerard-Jan Blauw ◽  
Peter Van Brummelen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Haemodynamic Effects ◽  
Plasma Noradrenaline ◽  
Arterial Blood ◽  
Forearm Vascular Resistance ◽  
Venous Plasma

1. To define the role of circulating noradrenaline in cardiovascular regulation, threshold concentrations for haemodynamic effects were determined in arterial and venous plasma of eight healthy volunteers. 2. Five doses of noradrenaline, 0–54 ng min−1 kg−1, were infused intravenously in random order and single-blind for 15 min per dose. Changes in intra-arterial blood pressure, heart rate, forearm blood flow and forearm vascular resistance were determined, and plasma noradrenaline was measured in arterial and venous blood samples. 3. Significant increases in systolic and diastolic blood pressure were found at arterial and venous plasma noradrenaline concentrations (means ±sem) of 3.00 ± 0.23 and 1.35 ±0.12 nmol/l, respectively. A significant decrease in heart rate was found at arterial and venous plasma noradrenaline concentrations of 8.99 ± 0.69 and 3.09 ± 0.60 nmol/l, respectively. The lower doses of noradrenaline tended to increase forearm blood flow and to decrease forearm vascular resistance, whereas the higher doses had no consistent effect on forearm haemodynamics. 4. During the noradrenaline infusions 73 ± 5% of the increase in arterial plasma noradrenaline concentration was extracted in the forearm. 5. The venous plasma noradrenaline threshold concentration was found to be much lower than previously reported. It is concluded that arterial and venous plasma noradrenaline concentrations which are readily encountered in physiological circumstances elicit haemodynamic effects.

Sympathetic discharge and vascular resistance after bed rest

1998 ◽  
Vol 84 (2) ◽  
pp. 612-617 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Cynthia S. Hogeman ◽  
Urs A. Leuenberger ◽  
Michael D. Herr ◽  
Kristen Gray ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Peripheral Resistance ◽  
Bed Rest ◽  
Burst Frequency ◽  
Sympathetic Discharge ◽  
Stroke Distance

Shoemaker, J. Kevin, Cynthia S. Hogeman, Urs A. Leuenberger, Michael D. Herr, Kristen Gray, David H. Silber, and Lawrence I. Sinoway. Sympathetic discharge and vascular resistance after bed rest. J. Appl. Physiol. 84(2): 612–617, 1998.—The effect of −6° head-down-tilt bed rest (HDBR) for 14 days on supine sympathetic discharge and cardiovascular hemodynamics at rest was assessed. Mean arterial pressure, heart rate ( n = 25), muscle sympathetic nerve activity (MSNA; n = 16) burst frequency, and forearm blood flow ( n = 14) were measured, and forearm vascular resistance (FVR) was calculated. Stroke distance, our index of stroke volume, was derived from measurements of aortic mean blood velocity (Doppler) and R-R interval ( n = 7). With these data, an index of total peripheral resistance was determined. Heart rate at rest was greater in the post (71 ± 2 beats/min)- compared with the pre-HDBR test (66 ± 2 beats/min; P < 0.003), but mean arterial pressure was unchanged. Aortic stroke distance during post-HDBR (15.5 ± 1.1 cm/beat) was reduced from pre-HDBR levels (20.0 ± 1.5 cm/beat) ( P < 0.03). Also, MSNA burst frequency was reduced in the post (16.7 ± 2.8 beats/min)- compared with the pre (25.2 ± 2.6 beats/min)-HDBR condition ( P < 0.01). Bed rest did not alter forearm blood flow, FVR, or total peripheral resistance. Thus reductions in MSNA with HDBR were not associated with a decrease in FVR.

scholarly journals Systemic evaluation on ischemia and reperfusion injury of splanchnic organs in rats

2009 ◽  
Vol 24 (4) ◽  
pp. 290-295 ◽  
Author(s):  
Nereide Freire Cerqueira ◽  
Carlos Alberto Hussni ◽  
Winston Bonetti Yoshida ◽  
Carlos Roberto Padovani
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mesenteric Artery ◽  
Venous Pressure ◽  
Aortic Blood Flow ◽  
Ischemia And Reperfusion ◽  
Esophageal Temperature ◽  
Ischemia And Reperfusion Injury ◽  
Arterial Blood ◽  
Group I

PURPOSE: To evaluate hemodynamic and systemic changes during and after splanchnic ischemia and reperfusion (I/R). METHODS: Rats were divided into two groups: a) control: animals submitted to surgery, but not to I/R, treated with saline (5 ml/kg/h) for 150 min; b) group I/R: animals continuously infused with saline, and submitted to occlusion of the celiac trunk, superior mesenteric artery (SMA), and inferior mesenteric artery for 30 min, followed by a 120-min reperfusion. Mean arterial blood pressure (MABP), venous pressure, aortic and SMA blood flow, heart rate, esophageal temperature and hematocrit were evaluated. RESULTS: During reperfusion in I/R groups, there was a progressive decrease in MABP, aortic blood flow, SMA blood flow, heart rate and esophageal temperature; vein pressure and hematocrit remained unchanged during the experiment. CONCLUSION: The model of ischemia used causes systemic changes, which are evidenced by hypotension, decrease in mesenteric blood flow, heart rate and esophageal temperature.

Regulation of arterial blood pressure in the common green iguana

1975 ◽  
Vol 228 (2) ◽  
pp. 386-391 ◽  
Author(s):  
LA Hohnke
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Carotid Arterial

Arterial blood pressure (ABP) responses to graded hemorrhage and passive head-up tilt were studied in restrained, anesthetized, and unanesthetized iguanas. The ABP fell slowly in response to hemorrhage up to a critical deficit of 35 plus or minus 19% of the estimated blood volume; the rate of ABP fall then increased nearly 40-fold to continued hemorrhage. Increased heart rate and decreased femoral arterial blood flow accompanied progressive hemorrhage. Propranolol (2-3 mug/kg) did not appreciably alter arterial pressure-hemorrhage curves but hemorrhage-induced increases in heart rate were diminished nearly 50%. Atropine had little effect on either the blood pressure or heart rate changes induced by hemorrhage. During passive tilts of 0-90 degrees carotid arterial pressure fell 33% before returning to control levels (2 min). Heart rate increased and femoral arterial blood flow and central venous pressure fell in response to head-up tilts. It is concluded that hemorrhage and passive head-up tilting can induce reflex cardiovascular changes that assist ABP regulation in iguanas.

Differential responses of uterine and umbilical vasculatures to angiotensin II and norepinephrine

1990 ◽  
Vol 259 (1) ◽  
pp. H197-H203 ◽  
Author(s):  
K. E. Clark ◽  
G. L. Irion ◽  
C. E. Mack
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Base Line ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Umbilical Blood ◽  
Arterial Blood ◽  
Pregnant Sheep

Although the uterine vascular responses to endogenous vasoactive substances have been extensively investigated in pregnant sheep, the fetal umbilical responses to angiotensin II (ANG II) and norepinephrine (NE) have not been well characterized. Twenty-five pregnant ewes between 105 and 115 days of gestation were anesthetized and instrumented for hemodynamic measurements, systemic fetal and maternal intravenous infusions, and local maternal uterine arterial infusions of ANG II and NE. Fetal and maternal arterial pressure and heart rate, maternal uterine blood flow (total of left and right middle uterine arteries), and fetoplacental blood flow (common umbilical artery) were measured during continuous infusions of ANG II or NE. Fetal infusions of ANG II (0.03–1.0 micrograms.min-1.kg estimated fetal body wt-1) increased fetal arterial blood pressure by as much as 44% over base-line values, decreased umbilical blood flow by as much as 63%, and increased umbilical vascular resistance by up to 345%. Fetal infusions of NE (0.1–3 micrograms.min-1.kg-1) increased fetal arterial pressure 42% and increased umbilical vascular resistance by up to 38% but did not significantly alter fetoplacental blood flow. No significant maternal changes were observed during fetal infusions. Maternal infusion of ANG II increased maternal arterial pressure by as much as 59% and significantly increased uterine vascular resistance at the two highest doses but significantly decreased uterine blood flow only at the highest dose (17%; P less than 0.05). Maternal infusions of NE increased arterial pressure by as much as 113%, decreased uterine blood flow by as much as 76%, and increased uterine vascular resistance 3- to 10-fold over the base-line value.(ABSTRACT TRUNCATED AT 250 WORDS)

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