scholarly journals An inquiry-based teaching tool for understanding arterial blood pressure regulation and cardiovascular function.

1999 ◽  
Vol 277 (6) ◽  
pp. S15 ◽  
Author(s):  
H L Collins ◽  
D W Rodenbaugh ◽  
T P Murphy ◽  
J M Kulics ◽  
C M Bailey ◽  
...  
Keyword(s):  
Active Learning ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Traditional Lecture ◽  
Inquiry Based Learning ◽  
Laboratory Exercise ◽  
Hemodynamic Variables ◽  
Arterial Blood ◽  
Level Of Understanding ◽  
Laboratory Experiences

Educators are placing a greater emphasis on the development of cooperative laboratory experiences that supplement the traditional lecture format. The new laboratory materials should encourage active learning, problem-solving, and inquiry-based approaches. To address these goals, we developed a laboratory exercise designed to introduce students to the hemodynamic variables (heart rate, stroke volume, total peripheral resistance, and compliance) that alter arterial pressure. For this experience, students are presented with "unknown" chart recordings illustrating pulsatile arterial pressure before and in response to several interventions. Students must analyze and interpret these unknown recordings and match each recording with the appropriate intervention. These active learning procedures help students understand and apply basic science concepts in a challenging and interactive format. Furthermore, laboratory experiences may enhance the students' level of understanding and ability to synthesize and apply information. In conducting this exercise, students are introduced to the joys and excitement of inquiry-based learning through experimentation.

Evidence for a vasodilatory effect of vasopressin in the conscious rat

1986 ◽  
Vol 251 (1) ◽  
pp. H34-H39 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Constant Infusion ◽  
Conscious Rat ◽  
Hemodynamic Variables ◽  
Arterial Blood ◽  
Vasodilatory Effect ◽  
Potent Vasoconstrictor ◽  
Circulating Levels ◽  
Final Group

Experiments were performed on conscious, chronically instrumented rats to determine the cardiovascular effects of intravenous arginine vasopressin (AVP) with and without V1-vasopressinergic antagonist administration. This design allowed the assessment of the cardiovascular effects of high circulating levels of AVP in the absence of the direct vasoconstrictor properties of the hormone. One group of rats (n = 10) were administered a constant infusion of AVP (2.5 mU/min iv) for 40 min and demonstrated increased mean arterial blood pressure (MABP) and total peripheral resistance (TPR), while heart rate (HR) and cardiac output (CO) fell. Another group of animals (n = 7) also received AVP for 40 min; however, at 25 min of the infusion, 10 micrograms/kg of d(CH2)5Tyr(Me)AVP was given intravenously. Administration of this V1-vasopressinergic antagonist caused MABP and TPR to fall below pre-infusion levels, although AVP infusion continued. HR and CO returned to control. Additional experiments showed no effect of the antagonist (n = 8) or AVP vehicle (n = 7) alone on the measured hemodynamic variables. In addition, pretreatment with the cyclooxygenase inhibitor meclofenamate did not affect the observed vasodilation in AVP-treated animals given the antagonist. A final group of animals (n = 6) was pretreated with d(CH2)5Tyr(Me)AVP prior to AVP infusion. On AVP administration, TPR fell in all animals. These data suggest that AVP exerts a vasodilatory effect unrelated to stimulation of V1-vasopressinergic receptors or arterial baroreceptors, which may partially offset the potent vasoconstrictor properties of this peptide.

LABORATORY DEMONSTRATION OF BAROREFLEX CONTROL OF HEART RATE IN CONSCIOUS RATS

2002 ◽  
Vol 26 (4) ◽  
pp. 309-316 ◽  
Author(s):  
Theresa L. O’Donaughy ◽  
Thomas C. Resta ◽  
Benjimen R. Walker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Peripheral Resistance ◽  
Baroreflex Control ◽  
Laboratory Exercise ◽  
Conscious Animal ◽  
Lecture Material ◽  
Arterial Blood ◽  
Lower Blood

We have developed a laboratory exercise that demonstrates arterial baroreflex control of heart rate (HR) in the conscious unrestrained rat, incorporating graduate level physiological topics as well as a hands-on exposure to conscious animal research. This demonstration utilizes rats chronically instrumented to measure cardiac output (CO), HR, and arterial blood pressure in response to agents that raise or lower blood pressure. The HR response to progressive increases or decreases in blood pressure is recorded, and a baroreflex curve is generated by plotting mean arterial blood pressure (MABP) vs. HR. Observation of altered CO allows for discussion of the relationship between MAP, CO, HR, stroke volume, and total peripheral resistance. Administration of arginine vasopressin demonstrates the ability of this hormone to alter the sensitivity of the baroreflex. Throughout the demonstration, students answer questions from a handout about general cardiovascular physiology, specific pathways of agonists, and the baroreflex system, encouraging group and individual critical analysis of the results. Interpretation of the data reemphasizes lecture material and allows students to observe the baroreflex response in a physiological setting.

scholarly journals Hemodynamic variables in piglets anesthetized with isoflurane or propofol, kept under spontaneous ventilation and FIO2 of 0.5

2019 ◽  
Vol 71 (6) ◽  
pp. 1846-1852
Author(s):  
C.K. Ido ◽  
P.E.S. Silva ◽  
H.R.A. Silva ◽  
E.G.F. Biteli ◽  
R.L. Carneiro ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Spontaneous Ventilation ◽  
Stroke Index ◽  
Hemodynamic Variables

ABSTRACT This study aimed to evaluate comparatively the effects of propofol or isoflurane on hemodynamic variables in piglets that received inspired oxygen fraction (FIO2) of 0.5 under spontaneous ventilation. Therefore, sixteen piglets weighing 16±1.1kg, were randomly divided into two groups: GI (Isoflurane and FIO2 of 0.5) and GP (Propofol and FIO2 of 0.5). Heart rate (HR), systolic, diastolic and mean arterial pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), mean pulmonary arterial pressure (mPAP) and mean capillary pulmonary pressure (mCPP) were assessed 40 minutes after anesthetic induction (T0), followed by 15 minutes intervals (from T15 to T60). The variables cardiac index (CI), stroke volume (SV), stroke index (SI), total peripheral resistance (TPR), total peripheral resistance index (TPRI), pulmonary vascular resistance (PVR), and pulmonary vascular resistance index (PVRI) were calculated. SAP and TPRI were significantly different between groups at T30 and T60 (P< 0.05) with higher GP values being recorded. There were no differences in the other variables, however, GP presented mean closer to normality on most of the analyzed variables. Therefore, we conclude that total intravenous anesthesia with propofol presented greater stability of the hemodynamic variables evaluated.

Hemodynamic similarities between the trigeminal and aortic vasodepressor responses

1978 ◽  
Vol 234 (1) ◽  
pp. H67-H73 ◽  
Author(s):  
M. Kumada ◽  
R. A. Dampney ◽  
M. H. Whitnall ◽  
D. J. Reis
Keyword(s):  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Regression Line ◽  
Peripheral Resistance ◽  
Hemodynamic Changes ◽  
Hemodynamic Variables ◽  
Significant Difference ◽  
Order Of Magnitude ◽  
Depressor Reflex ◽  
Percent Decrease

The hemodynamic changes associated with hypotension elicited by electrical stimulation of the spinal trigeminal complex (trigeminal depressor response, TDR) or the aortic nerve (aortic depressor reflex, ADR) were compared in rabbits anesthetized with urethan. The hypotension associated with each response was accompanied by bradycardia, a marked fall in total peripheral resistance, a small decrease in cardiac output, and a nonuniform decrease in regional vascular resistances, with the order of magnitude of the decrease being femoral greater than mesenteric greater than renal arterial resistance. In individual experiments the percent decrease in heart rate, total peripheral resistance, or regional resistances was plotted against the percent fall in arterial pressure to obtain a pair of regression lines during the TDR and ADR. There was no significant difference in the slope or y-intercept of the regression line between the TDR and ADR for all of the hemodynamic variables examined. In both responses, however, the slope of the femoral resistance/arterial pressure relationship was significantly greater than that of the renal resistance/arterial pressure relationship. We conclude that the TDR is characterized by a pattern of hemodynamic changes similar to that of the ADR.

Haemodynamic response to peripheral venous congestion in patients with unexplained recurrent syncope

2003 ◽  
Vol 105 (3) ◽  
pp. 331-337 ◽  
Author(s):  
Elisabeth BELLARD ◽  
Jacques-Olivier FORTRAT ◽  
Jean-Marc DUPUIS ◽  
Jacques VICTOR ◽  
Georges LEFTHÉRIOTIS
Keyword(s):  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Venous Occlusion ◽  
Venous Congestion ◽  
Haemodynamic Response ◽  
Volume Changes ◽  
Venous Pooling ◽  
Postural Tachycardia ◽  
Arterial Blood ◽  
Unexplained Syncope

In patients with recurrent unexplained syncope, exaggerated peripheral venous pooling and impaired circulatory adjustment is thought to contribute to the outcome of a head-up tilt (HUT) test. The present study investigated the role of leg volume changes during venous congestion in the haemodynamic response of patients with recurrent unexplained syncope and the ability to predict the outcome of a HUT test. Changes in calf volume (strain gauge plethysmography), heart rate and arterial blood pressure were recorded in 60 patients with history of unexplained syncope (without postural tachycardia symptom) during venous congestion provoked by pneumatic thigh cuffs while supine at rest and during the initial 10 min of a 45 min 70° HUT test. Twenty-seven patients [age (mean±S.D.), 39±16 years] exhibited symptoms [HUT(+)] and 33 patients (45±14 years) were asymptomatic [HUT(-)]. During venous congestion, mean±S.E.M. calf volume increased in both groups [HUT(-), 4.5±0.2; HUT(+), 4.8±0.4 ml·100 ml-1, not significant), but significantly less during head-upright tilt [HUT(-), 3.3±0.2, P<0.01; HUT(+), 2.6±0.3 ml·100 ml-1, P<0.001] without differences between the groups. During venous congestion, arterial pressure increased significantly in asymptomatic HUT(-) patients, but not in the HUT(+) patients. Calf volume changes did not correlate with a symptomatic outcome to a 70° HUT. The lack of exaggerated venous pooling during venous congestion and the inability of calf volume changes to predict a positive HUT suggest that excessive venous pooling does not contribute to the outcome of HUT. Attenuated changes in arterial pressure during venous congestion while supine suggest impaired adjustment of peripheral resistance to leg venous occlusion.

Graphic format for teaching long-term control of systemic arterial pressure.

1996 ◽  
Vol 270 (6) ◽  
pp. S40
Author(s):  
J J Faber
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Arterial Blood ◽  
Ventricular Filling Pressure ◽  
Ventricular Filling

Circulatory homeostasis is a difficult notion. The graphic format presented here facilitates the teaching of long-term control of systemic arterial blood pressure and cardiac output. It is based on the view that the following four "function curves" cooperate in long-term regulation: the relation between blood volume and ventricular filling pressure, the relation between ventricular filling pressure and cardiac output, the relation between cardiac output and peripheral resistance, and the relation between arterial pressure and natriuresis. Positioning the function curves in the format presented here clarifies their cooperativity. The distinction between a nonsteady state and a steady state deserves emphasis. Long-term pathophysiology of the circulation is most easily taught on the basis of the assumption that, generally, there will be a steady state. The format clarifies why some known physiological relations are almost impossible to demonstrate in the intact organism, and it discourages explanations of pathophysiology that are not firmly based on physiology.

scholarly journals Systemic and regional hemodynamic effects of leukotrienes D4 and E4 in the conscious rat

1986 ◽  
Vol 251 (4) ◽  
pp. H700-H709 ◽  
Author(s):  
J. Eimerl ◽  
A. L. Siren ◽  
G. Feuerstein
Keyword(s):  
Peripheral Resistance ◽  
Resistance Index ◽  
Low Doses ◽  
Hemodynamic Effects ◽  
Differential Distribution ◽  
Conscious Rat ◽  
Systemic Injection ◽  
Hemodynamic Variables ◽  
Arterial Blood ◽  
Series Of Experiments

The effect of leukotrienes (LTs) D4 and E4 on systemic and regional hemodynamic variables were studied in the conscious rat (n = 5-9). Renal (R), mesenteric (M), and hindquarter (HQ) blood flow (BF) were monitored by directional pulsed Doppler velocimetry, and mean arterial blood pressure (MAP) and heart rate were recorded through a catheter in the femoral artery. In a separate series of experiments, cardiac index (CI) was measured by the thermodilution method. Systemic injection of LTD4 or LTE4 (0.1-10 micrograms/kg) produced dose-dependent pressor responses; BF in the M, HQ, and R vessels declined, due to increased vascular resistance (VR) at the following order: M much greater than HQ greater than R. Low doses of LTD4 or LTE4 produced vasodilation in the HQ area. Infusion of LTD4 (3 micrograms X kg-1 X min-1) for 10 min produced progressive and pronounced vascular constriction in the M and HQ regions along with reduction in BF. The LTD4 infusion also markedly decreased CI with a concomitant rise in total peripheral resistance index (TPRI). Indomethacin (5 mg/kg iv) pretreatment did not modify any of the hemodynamic effects of LTD4 or LTE4. FPL 55712 (10 mg/kg iv) and LY 171883 (30 mg/kg iv), two different LT-receptor antagonists, partially blocked the constriction effects of these LTs. LY 171883, but not FPL 55172, blocked the HQ vasodilation produced by LTE4. LY 171883 alone increased HQ-BF and reduced HQ-VR. These data indicate that LTD4 and LTE4 are potent constrictors of the M vascular bed, but at low doses they also produce dilation of the HQ blood vessels. Furthermore, no escape from the effects of prolonged infusion of the LTs was demonstrated in this species. Finally, the hemodynamic responses to LTD4 and LTE4 in the conscious rat are independent of cyclooxygenase products of LTs and are only partially blocked by FPL 55712 or LY 171883. These studies taken together suggest a differential distribution of multiple LT receptors in the rat vasculature.

Arterial pressure control after chronic carotid sinus denervation

1988 ◽  
Vol 255 (4) ◽  
pp. H910-H916 ◽  
Author(s):  
D. S. O'Leary ◽  
A. M. Scher
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Pressure Control ◽  
Base Line ◽  
Baroreflex Control ◽  
Atrial Rate ◽  
Arterial Blood

This study examines the control of arterial blood pressure in conscious, instrumented dogs with atrioventricular block before and greater than or equal to 9 days after carotid sinus baroreceptor denervation. Strength of reflex control of blood pressure was quantitated by measuring the changes in peripheral resistance and atrial rate after square wave changes in cardiac output. Surprisingly, nine or more days after carotid denervation, the strength of baroreflex control of peripheral resistance and atrial rate were not different (P greater than 0.05) from the values before denervation. This was not due to a change in the base-line levels of arterial pressure, atrial rate, cardiac output, or peripheral resistance. Bilateral vagal block after carotid denervation removed reflex effects from remaining baroreceptors and virtually eliminated changes in peripheral resistance in response to changes in arterial pressure. Therefore, the compensatory responses observed after carotid denervation were mediated by the remaining baroreceptors. Thus, after chronic carotid sinus denervation, there is no decrease in the strength of baroreflex control of peripheral resistance or heart rate.

Hemodynamic effects of arginine vasopressin in conscious water-deprived rats

1985 ◽  
Vol 249 (1) ◽  
pp. H29-H33 ◽  
Author(s):  
W. Rascher ◽  
H. Meffle ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Total Peripheral Resistance ◽  
Water Deprivation ◽  
Peripheral Resistance ◽  
Conscious Rats ◽  
Arterial Blood

By means of a specific antagonist [d(CH2)5AVP] of the vasoconstrictor activity of arginine vasopressin (AVP), we studied whether the vasoconstrictor effect of AVP contributed to the blood pressure control during water deprivation in conscious rats. After 24 h of dehydration plasma AVP rose from 3.5 +/- 0.5 to 11.2 +/- 2.0 fmol/ml. Intravenous injection of 5 micrograms/kg d(CH2)5AVP reduced total peripheral resistance. Since cardiac output rose simultaneously, mean arterial blood pressure remained unchanged. In rats with sinoaortic deafferentation (SAD) 4 wk before water deprivation, d(CH2)5AVP caused a reduction of total peripheral resistance and of mean arterial pressure, whereas cardiac output remained unchanged. Consequently, mean arterial pressure fell. No hemodynamic changes were observed in hydrated control rats with and without SAD. It is concluded that the vasoconstrictor activity of AVP plays an important role in maintaining blood pressure during water deprivation in conscious rats. After AVP blockade, arterial pressure fell only in SAD rats as intact rats maintain arterial pressure via acute increase cardiac output.

scholarly journals On the Pathology of the dropsy produced by obstruction of the superior and inferior venœ and the portal vein.— Preliminary communication

1907 ◽  
Vol 79 (532) ◽  
pp. 267-283 ◽  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Mean Arterial Blood Pressure ◽  
Normal Limit ◽  
The Body ◽  
Diastolic Filling ◽  
Arterial Blood ◽  
Preliminary Communication ◽  
The Mean

In August, 1903, I published a paper in the ‘Journal of Pathology’(1) in which I demonstrated a method experimentally producing uncompensated hear disease in an animal, which was compatible with life. This method consisted in diminishing the size of the pericardial sac by stitches, so that the diastolic filling of the heart was impeded. The main symptoms of this condition were dropsy and diminution in the amount of urine excreted. As the immediate result of this interference with the action of the heart, there occurred a rise of pressure throughout the whole systemic venous system extending as far back as the capillaries, and a fall of the mean arterial blood-pressure. Further, I found that the pressure in all the veins fell to the normal limit again within the space of about one hour, and that subsequently when dropsy was being produced, the vanous pressure in all parts of the body was normal, and the arterial pressure had almost recovered itself.

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