Effect of regular voluntary exercise on resting cardiovascular responses in SHR and WKY pregnant rats

1992 ◽  
Vol 73 (2) ◽  
pp. 713-720 ◽  
Author(s):  
M. T. Jones ◽  
K. I. Norton ◽  
D. M. Black ◽  
R. E. Graham ◽  
R. B. Armstrong
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Cytochrome C ◽  
Arterial Pressure ◽  
Vastus Lateralis ◽  
Cardiovascular Responses ◽  
Voluntary Exercise ◽  
Uterine Blood Flow ◽  
Pregnant Rats ◽  
Significant Difference

The purpose of this study was to assess the influence of regular voluntary exercise in pregnant normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats on 1) uteroplacental perfusion and mean arterial pressure in the resting conscious condition and 2) fetal number, fetal weight, and number of fetal resorptions. WKYs and SHRs were randomly assigned to standard cages [CWKY (n = 10); CSHR (n = 6)] or cages with activity wheels [EWKY (n = 7); ESHR (n = 8)]. EWKYs and ESHRs exercised for 12 wk, and then all rats were bred and experiments were conducted on gestational day 17. Resting blood flow (microspheres), heart rate (HR), and mean arterial pressure (Pa) were measured. No significant difference was found in Pa, HR, uterine blood flow (ESHRs 52 +/- 8 ml.min-1.100 g-1; CSHRs 28 +/- 6 ml.min-1.100 g-1), or maternal placental blood flow (ESHRs, 122 +/- 31 ml.min-1.100 g-1; CSHRs 78 +/- 21 ml.min-1.100 g-1) among the groups. Exercise altered the relationship between maternal placental and uterine blood flow and Pa in the SHR; SHRs with lower Pa maintained higher placental and uterine blood flow after training. Before gestation ESHRs ran on average more kilometers per week than EWKYs (43 +/- 3 vs. 34 +/- 4), but during gestation ESHRs averaged fewer kilometers per week than EWKYs (16 +/- 4 vs. 22 +/- 4). Succinate dehydrogenase activity was higher in the white vastus lateralis (1.02 +/- 0.2 mumol cytochrome c reduced.min-1.g wet wt-1) and vastus intermedius (3.1 +/- 0.5 mumol cytochrome c reduced.min-1.g wet wt-1) muscles of ESHRs.(ABSTRACT TRUNCATED AT 250 WORDS)

Maternal responses to long-term hypoxemia in sheep

1989 ◽  
Vol 256 (6) ◽  
pp. R1340-R1347 ◽  
Author(s):  
T. Kitanaka ◽  
R. D. Gilbert ◽  
L. D. Longo
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Cardiovascular Responses ◽  
Uterine Blood Flow ◽  
O2 Uptake ◽  
Arterial Po2

To determine the maternal cardiovascular responses to long-term hypoxemia, we studied three groups of animals: 1) pregnant ewes (n = 20) at 110-115 days gestation subjected to hypoxia for up to 28 days; 2) pregnant ewes (n = 4) that served as normoxic controls; and 3) nonpregnant ewes (n = 6) subjected to hypoxemia for up to 28 days. We measured mean arterial pressure, heart rate, uterine blood flow, and uterine vascular resistance continuously for 1 h/day while the ewe was exposed to an inspired O2 fraction of 12-13% for at least 17 days. Arterial PO2, O2 saturation, hemoglobin, arteriovenous O2 difference, and uterine O2 uptake were measured daily while blood volume and erythropoietin concentration were measured weekly. In the pregnant hypoxic group arterial PO2 decreased from a control value of 101.5 +/- 5.1 to 59.2 +/- 5.1 Torr within a few minutes, where it remained throughout the study. The hemoglobin concentration increased from 8.9 +/- 0.5 to 10.0 +/- 0.5 g/dl within 24 h where it remained, whereas erythropoietin concentration increased from 16.6 +/- 2.1 to 39.1 +/- 7.8 mU/ml at 24 h but then returned to near-control levels. Arterial glucose concentration, mean arterial pressure, and cardiac output decreased slightly but insignificantly. In contrast, body weight, heart rate, blood volume, uterine blood flow, uterine O2 flow, uteroplacental O2 uptake, and the concentrations of catecholamines and cortisol remained relatively constant. Thus both pregnant and nonpregnant sheep experience relatively minor cardiovascular and hematologic responses in response to long-term hypoxemia of moderate severity.

scholarly journals Losartan does not decrease renal oxygenation and norepinephrine effects in rats after resuscitated hemorrhage

2018 ◽  
Vol 315 (2) ◽  
pp. F241-F246
Author(s):  
Sofia Jönsson ◽  
Jacqueline M. Melville ◽  
Mediha Becirovic-Agic ◽  
Michael Hultström
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Oxygen Tension ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Oxygen Consumption ◽  
Significant Difference ◽  
Renal Vascular

Renin-angiotensin-system blockers are thought to increase the risk of acute kidney injury after surgery and hemorrhage. We found that losartan does not cause renal cortical hypoxia after hemorrhage in rats because of decreased renal vascular resistance, but we did not evaluate resuscitation. We aimed to study losartan’s effect on renal cortical and medullary oxygenation, as well as norepinephrine’s vasopressor effect in a model of resuscitated hemorrhage. After 7 days of losartan (60 mg·kg−1·day−1) or control treatment, male Wistar rats were hemorrhaged 20% of their blood volume and resuscitated with Ringerʼs acetate. Mean arterial pressure, renal blood flow, and kidney tissue oxygenation were measured at baseline and after resuscitation. Finally, the effect of norepinephrine on mean arterial pressure and renal blood flow was investigated. As expected, losartan lowered mean arterial pressure but not renal blood flow. Losartan did not affect renal oxygen consumption and oxygen tension. Mean arterial pressure and renal blood flow were lower after resuscitated hemorrhage. A smaller increase of renal vascular resistance in the losartan group translated to a smaller decrease in cortical oxygen tension, but no significant difference was seen in medullary oxygen tension, either between groups or after hemorrhage. The effect of norepinephrine on mean arterial pressure and renal blood flow was similar in control- and losartan-treated rats. Losartan does not decrease renal oxygenation after resuscitated hemorrhage because of a smaller increase in renal vascular resistance. Further, losartan does not decrease the efficiency of norepinephrine as a vasopressor, indicating that blood pressure may be managed effectively during losartan treatment.

Chemical activation of thin-fiber phrenic afferents. 2. Cardiovascular responses

1991 ◽  
Vol 70 (1) ◽  
pp. 77-86 ◽  
Author(s):  
S. N. Hussain ◽  
A. Chatillon ◽  
A. Comtois ◽  
C. Roussos ◽  
S. Magder
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Chemical Activation ◽  
Cardiovascular Responses ◽  
Arterial Flow ◽  
Aortic Blood Flow ◽  
Thin Fiber ◽  
The Right

To assess the effects of groups III and IV (thin-fiber) phrenic afferents on arterial pressure, heart rate, and distribution of cardiac output, we injected capsaicin into phrenic arteries of in situ isolated and innervated left diaphragms of dogs anesthetized with chloralose, vagotomized, and mechanically ventilated. Blood flow in the ascending aorta, common carotid, renal, superior mesenteric, and femoral arteries was measured by electromagnetic and Doppler flow probes. Injection of 1 mg capsaicin into the left phrenic artery produced congruent to 15% increase in mean arterial pressure and congruent to 7% increase in heart rate with no change in aortic flow. Phrenic arterial flow decreased by 64%, renal arterial flow by 16%, and superior mesenteric arterial flow by 10%, whereas carotid flow increased by 13% and flow to the right gastrocnemius muscle did not change. Mean arterial pressure, heart rate, and blood flow distribution (with the exception of the decline in phrenic blood flow) returned to baseline within 60 s of the injection. Injection of 1.5 mg capsaicin into the right isolated and innervated gastrocnemius produced congruent to 35% increase in mean arterial pressure, 17% rise in heart rate, and no change in aortic blood flow. Phrenic and carotid arterial flow rose by 240 and 41%, respectively, whereas renal and superior mesenteric flow declined by 50 and 20%, respectively. In conclusion, thin-fiber phrenic afferents have an excitatory effect on arterial pressure and heart rate. They redistribute blood flow away from the renal and intestinal vascular beds and toward the carotid vascular bed. On the other hand, the cardiovascular reflex from thin-fiber phrenic afferents seems less potent than that from limb muscle afferents.

scholarly journals Influence of passive stretch on muscle blood flow, oxygenation and central cardiovascular responses in healthy young males

2016 ◽  
Vol 310 (9) ◽  
pp. H1210-H1221 ◽  
Author(s):  
Nicholas T. Kruse ◽  
Christopher R. Silette ◽  
Barry W. Scheuermann
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Moderate Intensity ◽  
Dependent Manner ◽  
Muscle Stretching ◽  
Retrograde Blood Flow ◽  
Passive Stretch

The aim of this study was to examine the effect of skeletal muscle stretching on peripheral, central, and autonomic cardiovascular responses in humans. Twelve healthy males completed a controlled passive stretch of the plantar flexors for 4 min at three different intensities. Doppler ultrasound velocimetry and imaging techniques assessed mean leg blood flow (MLBF), antegrade blood flow, and retrograde blood flow of the popliteal artery. Near-infrared spectroscopy assessed the concentration of deoxygenated hemoglobin + myoglobin ([HHb]) and the sum of its deoxygenated and oxygenated forms [i.e., blood volume ([Hbtot])]. Heart rate (HR) and mean arterial pressure were measured simultaneously to peripheral hemodynamic responses. During stretch there was an increase ( P < 0.05) in antegrade and retrograde blood flow along with [HHb] and [Hbtot] relative to baseline, whereas MLBF was not altered. HR increased ( P < 0.01) in a stretch intensity- and time-dependent manner, suggesting a threshold tension must be met that results in a mechanoreflex-mediated increase in HR. After stretch there was an increase ( P < 0.05) in [Hbtot] and MLBF in each condition, suggesting that stretch creates a poststretch hyperemic response. Furthermore, retrograde blood flow was decreased ( P < 0.05) after stretch in each stretch condition. Mean arterial pressure was decreased ( P < 0.05) after moderate-intensity stretching. Collectively, our data provide novel mechanistic evidence on cardiovascular responses to skeletal muscle stretching in humans. Moreover, the reductions in MAP and retrograde blood flow suggest that stretch transiently reduces myogenic vascular tone in a poststretch resting period.

Influence of muscle length and force on endurance and pressor responses to isometric exercise

1994 ◽  
Vol 76 (6) ◽  
pp. 2561-2569 ◽  
Author(s):  
A. V. Ng ◽  
J. C. Agre ◽  
P. Hanson ◽  
M. S. Harrington ◽  
F. J. Nagle
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Length ◽  
Cardiovascular Responses ◽  
Knee Extension ◽  
Endurance Time ◽  
External Torque ◽  
Significant Difference ◽  
Isometric Knee Extension

Experiments were performed to determine whether endurance time, mean arterial pressure, or heart rate was related to either muscle length or external torque production in humans during isometric knee extension. Eight men and nine women performed isometric knee extension to the endurance limit at each of three muscle lengths, determined by knee angles of 40 degrees (0.698 rad, shortest), 60 degrees (1.047 rad, intermediate), and 90 degrees (1.571 rad, longest), and at intensities of 30 and 50% maximal voluntary contraction (MVC). Knee extension forms an ascending-descending length-torque curve, and lengths were chosen to result in different external torques. MVC was greatest at a knee angle of 60 degrees (P < 0.05 vs. 40 degrees, 90 degrees), with no significant difference between 90 degrees and 40 degrees. Endurance time was inversely related to muscle length, independent of torque production, at 30% MVC [40 degrees, 395 +/- 139 (SE); 60 degrees, 237 +/- 60; 90 degrees, 165 +/- 51 s; P < 0.05 vs. each other] and 50% MVC (40 degrees, 176 +/- 64; 60 degrees, 137 +/- 40; 90 degrees, 85 +/- 23 s; P < 0.05 vs. each other). Evidence is presented that endurance is a function of internal muscle force and not resultant external torque. The experimental design allowed the relationship of external torque and cardiovascular responses to be examined independent of exercise intensity. Muscle mass was also controlled in that the same muscle group was involved in all contractions. There were no differences in mean arterial pressure, heart rate, or rating of perceived exertion at any percentage of endurance time under any condition.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Plasma hyperosmolality and arterial pressure regulation during heating in dehydrated and awake rats

1998 ◽  
Vol 275 (5) ◽  
pp. R1703-R1711 ◽  
Author(s):  
Yasufumi Nakajima ◽  
Hiroshi Nose ◽  
Akira Takamata
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Skin Blood Flow ◽  
Plasma Osmolality ◽  
Cardiovascular Responses ◽  
Pressure Regulation ◽  
Highly Correlated ◽  
Arterial Pressure Regulation

To gain better insights into the effect of dehydration on thermal and cardiovascular regulation during hyperthermia, we examined these regulatory responses during body heating in rats under isosmotic hypovolemia and hyperosmotic hypovolemia. Rats were divided into four groups: normovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma volume loss (ΔPV) = −20% of control], hypovolemic and less hyperosmotic [HL1, increase in plasma osmolality (ΔPosm) = 23 mosmol/kgH2O, ΔPV = −16%], and hypovolemic and more hyperosmotic (HL2, ΔPosm = 52 mosmol/kgH2O, ΔPV = −17%). Hyperosmolality was attained by subcutaneous injection of hypertonic saline and hypovolemia by intra-arterial injection of furosemide before heating. Then rats were placed in a thermocontrolled box (35°C air temperature, ∼20% relative humidity) for 1–2 h until rectal temperatures (Tre) reached 40.0°C. Mean arterial pressure in L decreased with rise in Tre( P < 0.001), whereas mean arterial pressure remained constant in the other groups. Maximal tail skin blood flow in L, HL1, and HL2 was decreased to ∼30% of that in C ( P < 0.001). Tre threshold for tail skin vasodilation (TVD) was not changed in L, whereas the threshold shifted higher in the HL groups. Trethreshold for TVD was highly correlated with Posm( r = 0.94, P < 0.001). Heart rate in the HL groups increased with rise in Tre( P < 0.001), whereas it remained unchanged in C and L. Cardiovascular responses to heating were not influenced by V1 antagonist in C, L, and HL2. Thus isotonic hypovolemia attenuates maximal tail skin blood flow, whereas hypertonic hypovolemia causes an upward shift of Tre threshold for TVD and an increase in heart rate during hyperthermia. These results suggest that plasma hyperosmolality stimulates pressor responses in the hypovolemic condition that subsequently contribute to arterial pressure regulation during heat stress.

scholarly journals Anesthetic Techniques for Fetal Surgery

2013 ◽  
Vol 118 (4) ◽  
pp. 796-808 ◽  
Author(s):  
Pornswan Ngamprasertwong ◽  
Erik C. Michelfelder ◽  
Shahriar Arbabi ◽  
Yun Suk Choi ◽  
Christopher Statile ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Function ◽  
Fetal Surgery ◽  
Left Ventricular ◽  
High Dose ◽  
Anesthetic Techniques ◽  
Uterine Blood Flow ◽  
Fetal Cardiac Function ◽  
Significant Difference ◽  
Fetal Acidosis

Abstract Background: Use of high-dose inhalational anesthesia during open fetal surgery may induce maternal–fetal hemodynamic instability and fetal myocardial depression. The authors’ preliminary human retrospective study demonstrated less fetal bradycardia and left ventricular systolic dysfunction with lower dose desflurane supplemented with propofol and remifentanil IV anesthesia (SIVA). In this animal study, the authors compare maternal–fetal effects of high-dose desflurane anesthesia (HD-DES) and SIVA. Methods: Of 26 instrumented midgestational ewes, data from 11 animals exposed to both SIVA and HD-DES in random sequences and six animals exposed to HD-DES while maternal normotension was maintained were analyzed. Maternal electroencephalography was used to guide comparable depths of anesthesia in both techniques. Hemodynamic parameters, blood gas, and fetal cardiac function from echocardiography were recorded. Results: Compared with SIVA, HD-DES resulted in significant maternal hypotension (mean arterial pressure difference, 19.53 mmHg; 95% CI, 17.6–21.4; P &lt; 0.0001), fetal acidosis (pH 7.11 vs. 7.24 at 150 min, P &lt; 0.001), and decreased uterine blood flow. In the HD-DES group with maternal normotension, uterine blood flow still declined and fetal acidosis persisted, with no statistically significant difference from the group exposed to HD-DES that had maternal hypotension. There was no statistically significant difference in fetal cardiac function. Conclusion: In sheep, SIVA affects maternal hemodynamics less and provides better fetal acid/base status than high-dose desflurane. Fetal echocardiography did not reflect myocardial dysfunction in this model.

Cardiovascular and Valsalva responses during parabolic flight

1998 ◽  
Vol 85 (5) ◽  
pp. 1957-1965 ◽  
Author(s):  
Todd T. Schlegel ◽  
Edgar W. Benavides ◽  
Donald C. Barker ◽  
Troy E. Brown ◽  
Deborah L. Harm ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Human Subjects ◽  
Parabolic Flight ◽  
Cardiovascular Responses ◽  
Systematic Evaluation ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Flight Measurements

We investigated the integrated cardiovascular responses of 15 human subjects to the acute gravitational changes (micro- and hypergravity portions) of parabolic flight. Measurements were made with subjects quietly seated and while subjects performed controlled Valsalva maneuvers. During quiet, seated, parabolic flight, mean arterial pressure increased during the transition into microgravity but decreased as microgravity was sustained. The decrease in mean arterial pressure was accompanied by immediate reflexive increases in heart rate but by absent (or later-than-expected) reflexive increases in total vascular resistance. Mean arterial pressure responses in Valsalva phases IIl, III, and IV were accentuated in hypergravity relative to microgravity ( P < 0.01, P < 0.01, and P < 0.05, respectively), but accentuations differed qualitatively and quantitatively from those induced by a supine-to-seated postural change in 1 G. This study is the first systematic evaluation of temporal and Valsalva-related changes in cardiovascular parameters during parabolic flight. Results suggest that arterial baroreflex control of vascular resistance may be modified by alterations of cardiopulmonary, vestibular, and/or other receptor activity.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

Cardiovascular responses to head-stand posture

1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
High Pressure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Skin Temperature ◽  
Cardiovascular Responses ◽  
Posterior Tibial Artery ◽  
Nervous Control ◽  
Posterior Tibial

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963

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