Roles of cardiac output and peripheral resistance in mediating blood pressure response to stress in rats

1998 ◽  
Vol 274 (4) ◽  
pp. R1065-R1069 ◽  
Author(s):  
Sheng-Gang Li ◽  
David C. Randall ◽  
David R. Brown
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Unconditioned Response ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Behavioral Stress

The change in arterial blood pressure (BP) in response to presentation of an acute behavioral stress (i.e., classical conditioning) in rat includes an initial rapid rise (C1) followed by a delayed, but more sustained, pressor response (C2). The purpose of this experiment is to determine the patterns of change in cardiac output (CO) and total peripheral vascular resistance (TPR) that are associated with the behaviorally induced pressor response. A blood flow probe was implanted around the ascending aorta, and a catheter was implanted in a femoral artery in 10 male Sprague-Dawley rats. The rats were trained by a 15-s tone (CS+) followed by a 0.5-s tail shock; another tone (CS−), never followed by shock, served as a behavioral control. BP responded to the stressful stimulus (CS+) by a rapid C1 increase (8 ± 1 mmHg; mean ± SE) followed by the delayed C2 response (2 ± 0.3 mmHg); the unconditioned response to shock was a 9 ± 2 mmHg increase in BP. The C1 BP increase produced a significant increase in TPR (10 ± 1 dyn ⋅ s/cm5); CO was not significantly changed. TPR decreased during C2 (−4 ± 2 dyn ⋅ s/cm5), whereas CO was significantly increased (2 ± 1 ml/min). These data contribute to our understanding of how the autonomic nervous system organizes the cardiovascular response to a suddenly perceived behavioral stress.

Effects of vasopressin on arterial blood pressure and cardiac output in male and female rats

1991 ◽  
Vol 261 (5) ◽  
pp. R1118-R1125 ◽  
Author(s):  
K. Toba ◽  
J. T. Crofton ◽  
M. Inoue ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Arterial Blood ◽  
Male And Female Rats ◽  
Cycle Dependent

This study was performed to investigate further the mechanisms underlying the sexual dimorphism of the pressor responses to vasopressin. We have confirmed our earlier findings that the pressor response to graded infusions of vasopressin in conscious unrestrained male rats is similar to that in estrous females and greater than in diestrus, proestrus, and metestrus. This difference was due primarily to greater increases in total peripheral resistance (TPR) in males and estrous females, since there were no sex- or cycle-related differences in the vasopressin-induced reductions in cardiac output. Gonadectomy was without effect in males but, in females, increased blood pressure responses to vasopressin to levels found in males. Chronic treatment of ovariectomized rats with estradiol reduced pressor responsiveness to vasopressin; treatment with progesterone was without effect. These differences were also due to differences in TPR. It is concluded that the sex- and cycle-dependent differences in vasopressin-induced increases in blood pressure are due largely to attenuation of increases in TPR by estrogen.

Augmentation of the exercise pressor reflex in prehypertension: roles of the muscle metaboreflex and mechanoreflex

2013 ◽  
Vol 38 (2) ◽  
pp. 209-215 ◽  
Author(s):  
Hyun-Min Choi ◽  
Charles L. Stebbins ◽  
Og-Taeg Lee ◽  
Hosung Nho ◽  
Joon-Hee Lee ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Percentage Increase ◽  
Muscle Metaboreflex ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Static Contraction ◽  
Pressor Reflex

This study investigated the hemodynamic mechanisms underlying the exaggerated blood pressure response to muscle contraction in prehypertensive humans and the potential role of skeletal muscle metabo- and mechanoreceptors in this response. To accomplish this, changes in peak mean arterial blood pressure (ΔMAP), cardiac output, and total peripheral resistance (ΔTPR) were compared between prehypertensive (n = 23) and normotensive (n = 19) male subjects during 2 min of static contraction (at 50% of maximal tension), 2 min of postexercise muscle ischemia (metaboreflex), and 1 min of passive dorsiflexion of the foot (tendon stretch, mechanoreceptor reflex). These variables were assessed before and during the interventions. Percentage increases from baseline in MAP and TPR in response to the exercise pressor reflex were augmented in the prehypertensives, compared with the normotensives (44% ± 5% vs. 33% ± 4% and 34% ± 15% vs. 2% ± 8%, respectively) (p < 0.05). Metaboreflex-induced increases in MAP and TPR were also augmented in the prehypertensives (28% ± 5% vs. 14% ± 4% and 36% ± 12% vs. 14% ± 9%, respectively) (p < 0.05). In response to the mechanoreflex, no differences in the percentage increase in MAP or TPR were seen between groups. The results indicate that the reflex pressor response to static contraction is augmented in prehypertension and suggest that this phenomenon is due, at least in part, to enhanced activation of metaboreceptors.

Cardiovascular response to submaximal exercise in sustained microgravity

1996 ◽  
Vol 81 (1) ◽  
pp. 26-32 ◽  
Author(s):  
B. E. Shykoff ◽  
L. E. Farhi ◽  
A. J. Olszowka ◽  
D. R. Pendergast ◽  
M. A. Rokitka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Life Sciences ◽  
Submaximal Exercise ◽  
Arterial Blood ◽  
Response To Exercise

Cardiac output (Q), heart rate (HR), blood pressure, and oxygen consumption (VO2) were measured repeatedly both at rest and at two levels of exercise in six subjects during microgravity exposure. Exercise was at 30 and 60% of the workload producing the individual's maximal VO2 in 1 G. Three of the subjects were on a 9-day flight, Spacelab Life Sciences-1, and three were on a 15-day flight, Spacelab Life Sciences-2. We found no temporal differences during the flights. Thus we have combined all microgravity measurements to compare in-flight values with erect or supine control values. At rest, Q in flight was 126% of Q erect (P < 0.01) but was not different from Q supine, and HR in flight was 81% of HR erect (P < 0.01) and 91% of HR supine (P < 0.05). Thus resting stroke volume (SV) in flight was 155% of SV erect (P < 0.01) and 109% SV supine (P < 0.05). Resting mean arterial blood pressure and diastolic pressure were lower in flight than erect (P < 0.05). Exercise values were considered as functions of VO2. The increase in Q with VO2 in flight was less than that at 1 G (slope 3.5 vs. 6.1 x min-1.l-1.min-1). SV in flight fell with increasing VO2, whereas SV erect rose and SV supine remained constant. The blood pressure response to exercise was not different in flight from erect or supine. We conclude that true microgravity causes a cardiovascular response different from that seen during any of its putative simulations.

scholarly journals Factors mediating the pressor response to isometric muscle contraction: An experimental study in healthy volunteers during lower body negative pressure

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0243627
Author(s):  
Niels A. Stens ◽  
Jonny Hisdal ◽  
Espen F. Bakke ◽  
Narinder Kaur ◽  
Archana Sharma ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Isometric Exercise ◽  
Peripheral Resistance ◽  
Relative Importance ◽  
Lower Body ◽  
Arterial Blood

Whilst both cardiac output (CO) and total peripheral resistance (TPR) determine mean arterial blood pressure (MAP), their relative importance in the pressor response to isometric exercise remains unclear. This study aimed to elucidate the relative importance of these two different factors by examining pressor responses during cardiopulmonary unloading leading to step-wise reductions in CO. Hemodynamics were investigated in 11 healthy individuals before, during and after two-minute isometric exercise during lower body negative pressure (LBNP; -20mmHg and -40mmHg). The blood pressure response to isometric exercise was similar during normal and reduced preload, despite a step-wise reduction in CO during LBNP (-20mmHg and -40mmHg). During -20mmHg LBNP, the decreased stroke volume, and consequently CO, was counteracted by an increased TPR, while heart rate (HR) was unaffected. HR was increased during -40 mmHg LBNP, although insufficient to maintain CO; the drop in CO was perfectly compensated by an increased TPR to maintain MAP. Likewise, transient application of LBNP (-20mmHg and -40mmHg) resulted in a short transient drop in MAP, caused by a decrease in CO, which was compensated by an increase in TPR. This study suggests that, in case of reductions of CO, changes in TPR are primarily responsible for maintaining the pressor response during isometric exercise. This highlights the relative importance of TPR compared to CO in mediating the pressor response during isometric exercise.

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.

Comparison of cardiovascular response to passive tilt in young and elderly men

1988 ◽  
Vol 66 (11) ◽  
pp. 1425-1432 ◽  
Author(s):  
D. A. Cunningham ◽  
R. J. Petrella ◽  
D. H. Paterson ◽  
P. M. Nichol
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Age Effects ◽  
Hemodynamic Responses ◽  
Arterial Blood ◽  
Postural Changes

To test the hypothesis that altered hemodynamic responses to postural changes are associated with aging, cardiovascular responses to head-up tilt (HUT) and head-down tilt (HDT) were examined in 12 healthy young (average age, 24.6 ± 1.7 years) and 12 healthy elderly (average age, 68.6 ± 2.2 years) men. Subjects were passively tilted from supine to 30°, 60°, and 90° HUT and HDT. Responses to these perturbations were determined 5 min after tilting with measures of heart rate (HR), blood pressure (SBP, DBP), and echocardiographically determined left ventricular diameter in systole and diastole (LVIDs, LVIDd). In HUT there were no significant age effects. In both young and elderly, SBP decreased significantly (p < 0.05), and DBP and HR increased significantly. Ejection fraction (EF), mean arterial blood pressure (MABP), and rate-pressure product (RPP) were unchanged in both groups. In HDT, the hemodynamic responses of the young and elderly were in opposite directions and significant age effects were found for SBP, DBP, HR, LVIDs, EF, MABP, and RPP. In HDT, the young appear to increase cardiac output primarily due to an increase in EF and end-diastolic volume (LVIDd), while HR is unchanged and SBP is decreased. MABP is unchanged, suggesting a small decrease in total peripheral resistance. The elderly may increase cardiac output slightly, owing to an increase in LVIDd with no change in EF, and a large increase in HR. Afterload increased markedly, therefore attenuating any increase in cardiac output. These results suggest that in healthy men, the cardiovascular response to HUT is not age related, while conversely there appear to be significant differences between young and elderly in response to HDT.

Changes in cardiac output and vascular resistance during behavioral stress in the rat

1986 ◽  
Vol 251 (1) ◽  
pp. R82-R90 ◽  
Author(s):  
J. W. Hubbard ◽  
R. H. Cox ◽  
B. J. Sanders ◽  
J. E. Lawler
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Plasma Norepinephrine ◽  
Wky Rats ◽  
Arterial Blood ◽  
Behavioral Stress

Normotensive Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHR) were exposed to aversive classical conditioning procedures and chronically instrumented with arterial catheters and electromagnetic flow probes around the ascending aorta. After postoperative recovery, hemodynamic measurements and blood samples were obtained from conscious animals at rest and during aversive conditioning. The cardiovascular response to the behavioral stress consisted of a significant increase in mean arterial blood pressure, total peripheral resistance index, cardiac index, heart rate, and aortic dP/dt for both strains. However, the elevated vascular resistance seen in the BHR resulted in a significantly greater increase in mean arterial blood pressure (21 mmHg) compared with the WKY rats (14 mmHg). In addition, the BHR showed a significantly (P less than 0.05) greater plasma norepinephrine concentration (760 +/- 99 pg/ml) in response to the stress than did the WKY rats (559 +/- 53 pg/ml). These data suggest that an increase in cardiac output, elevated vascular resistance, and increased sympathetic drive may contribute to the development of stress-induced hypertension in this animal model.

Abstract 119: Influence of Anesthetics on the Hemodynamic Response in a Rat Model of Hemorrhagic Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Claudius Balzer ◽  
Franz J Baudenbacher ◽  
Susan S Eagle ◽  
Michele M Salzman ◽  
William J Cleveland ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Rat Model ◽  
Cardiovascular Response ◽  
Femoral Vein ◽  
Blood Pressure Measurement ◽  
Experimental Models ◽  
Sprague Dawley ◽  
Compensatory Mechanisms ◽  
Arterial Blood

Introduction: Experimental models of hemorrhagic shock (HS) in rats are important to test new treatments that may improve outcomes in humans, and general anesthesia is required during these experiments. The volatile anesthetic Isoflurane is known for its beneficial effects in rat HS models. Focusing on cardiovascular compensatory mechanisms, we wanted to evaluate Isoflurane versus the injectable anesthetic Pentobarbital in our rat model of mild HS (class 2). We hypothesize that Isoflurane during development of HS improves hemodynamics compared to Pentobarbital. Methods: Twelve Sprague-Dawley rats were initially anesthetized with an intraperitoneal (IP) injection of Pentobarbital (45 mg/kg) and intubated (1 L/min, FiO 2 0.25); heart rate (HR) was monitored by subcutaneous ECG needles. Femoral artery and vein were cannulated for continuous blood pressure measurement and delivery of fluids, respectively. In one group (n=7), anesthesia was continued with repeated IP injections of Pentobarbital (dose mg/kg), the other group (n=5) received continuous Isoflurane (1%). After 30 min of stabilization and administration of Heparin (100 IU/kg), HS was induced by removal of 1 ml of blood over 1 min via the femoral vein, repeated every 3 min until a volume of 5 ml of blood was removed. Mean arterial blood pressure (MAP) and HR were recorded and analyzed in LabChart. Results: During baseline, rats showed no significant differences in HR and MAP between both groups. After 5 ml of hemorrhage, both groups showed significant changes compared to baseline, with significantly higher MAP and HR in rats given only Pentobarbital. Conclusions: In our rat model of HS, Isoflurane dampens the physiologic response to compensate for mild hemorrhage. The cardiovascular response of rats in the Isoflurane group was a decrease of HR and MAP to every ml of hemorrhage, while rats given only Pentobarbital were able to maintain their MAP by raising their HR until decompensation.

Role of vasopressin in acutely altered baroreflex sensitivity during hemorrhage in rats

1991 ◽  
Vol 261 (3) ◽  
pp. R677-R685 ◽  
Author(s):  
B. L. Brizzee ◽  
R. D. Russ ◽  
B. R. Walker
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Blood Loss ◽  
Baroreflex Sensitivity ◽  
Peripheral Resistance ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Arterial Hemorrhage ◽  
Moderate Elevation

Experiments were performed to examine the potential role of circulating arginine vasopressin (AVP) on baroreflex sensitivity during hypotensive and nonhypotensive hemorrhage in the conscious rat. Animals were chronically instrumented for measurement of cardiac output, blood pressure, and heart rate (HR). Three potential stimuli for release of AVP were utilized: 1) rapid 20% arterial hemorrhage that resulted in hypotension, 2) nonhypovolemic hypotension induced by intravenous infusion of nitroprusside, and 3) nonhypotensive hemorrhage (rapid 10% arterial blood withdrawal). Hypotensive hemorrhage was associated with significant reductions in blood pressure, cardiac output, HR, and calculated total peripheral resistance, an increase in baroreflex (BRR) bradycardia in response to pressor infusions of phenylephrine, and a moderate elevation in circulating AVP. Prior intravenous administration of a specific V1-vasopressinergic antagonist augmented the hypotensive response to hemorrhage; however, neither V1- nor V2-blockade affected hemorrhage-induced augmentation of the BRR. Inducement of hypotension by infusion of nitroprusside did not alter subsequent BRR sensitivity. Finally, nonhypotensive hemorrhage was associated with an increase in resting HR and augmented BRR sensitivity. However, in contrast to hypotensive hemorrhage, either V1- or V2-antagonism attenuated the increase in BRR sensitivity seen with 10% hemorrhage. These data suggest that, although AVP may play a role in blood pressure maintenance via its direct vasoconstrictor actions during hypotensive hemorrhage, the observed augmentation of BRR sensitivity associated with severe blood loss is not attributable to a vasopressinergic mechanism activated by circulating AVP. However, blood-borne AVP may contribute to BRR sensitivity alterations in response to mild blood loss.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

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