Direct measurement of flow from the posterior lymph hearts of hydrated and dehydrated toads (Bufo marinus).

1997 ◽  
Vol 200 (11) ◽  
pp. 1695-1702 ◽  
Author(s):  
J M Jones ◽  
A K Gamperl ◽  
A P Farrell ◽  
D P Toews
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Systolic Pressure ◽  
Lymph Flow ◽  
Bufo Marinus ◽  
Experimental Chamber ◽  
Doppler Flow ◽  
Simultaneous Measurements ◽  
Pressure Development ◽  
Lymph Heart

Flow from the posterior lymph hearts of Bufo marinus was measured using Doppler flow probes. These probes were placed on the posterior vertebral vein and recorded flow as lymph was ejected from the heart. In resting, hydrated toads, mean lymph flow from one of the paired posterior lymph hearts was 25.9 +/- 4.9 ml kg-1 h-1, stroke volume was 8.9 +/- 1.4 microL kg-1 and lymph heart rate was 47.5 +/- 3.7 beats min-1. We estimate that, together, the paired posterior lymph hearts are capable of generating flows that are approximately one-sixtieth of the resting cardiac output. Mean peak systolic pressure developed by the posterior lymph hearts was 1.62 +/- 0.08 kPa. Simultaneous measurements of lymph heart pressure development and flow revealed that the outflow pore of the heart opened at a pressure of 0.71 +/- 0.04 kPa, approximately 113 +/- 5 ms into systole. When toads were moderately disturbed, stroke volume increased by as much as fourfold with little change in lymph heart rate (< 5 beats min-1). When toads were dehydrated, lymph flow decreased by 70% at 12h and by 80% and 24h. Since there was only a modest non-significant decrease in lymph heart rate (30%), this reduction in flow was attributed to decreases in stroke volume (approximately 80%). Lymph heart flow and stroke volume returned to control values 30 min after adding water back into the experimental chamber. Stroke volume was clearly more important in regulating lymph flow than lymph heart rate under these conditions in Bufo marinus.

scholarly journals Posterior lymph heart pressure and rate and lymph flow in the toad Bufo marinus in response to hydrated and dehydrated conditions

1992 ◽  
Vol 169 (1) ◽  
pp. 207-220 ◽  
Author(s):  
J. M. Jones ◽  
L. A. Wentzell ◽  
D. P. Toews
Keyword(s):  
Heart Rate ◽  
Systolic Pressure ◽  
Lymph Flow ◽  
Bufo Marinus ◽  
Lymph Drainage ◽  
Constant Measurement ◽  
Lymph Heart ◽  
The Mean ◽  
Toad Bufo ◽  
New Surgical Technique

Posterior lymph heart pressure, rate and flow were measured in chronically cannulated Bufo marinus during normal hydrated and dehydrated conditions. A new surgical technique was developed which allowed direct and constant measurement of the functioning of the posterior lymph hearts with minimal disruption to normal lymph drainage. The mean intra-lymph-heart systolic pressure was 2.29 +/− 0.12 kPa for hydrated animals at rest, decreasing to 1.01 +/− 0.10 kPa after 24 h of dehydration. Similarly, lymph heart rate, which was 48.2 +/− 1.7 beats min-1 under hydrated conditions, decreased to 31.8 +/− 4.6 beats min-1 after 18 h of dehydration. Lymph flow decreased almost to zero during dehydration from a hydrated rate of 1.11 +/− 0.04 ml h-1 100 g-1. This is the first study to measure directly and to correlate these variables in an amphibian and to show specifically that pressure, rate and lymph flow are significantly reduced during periods of dehydration.

Rhythm effects on contractility of the beating isovolumic left ventricle

1960 ◽  
Vol 199 (6) ◽  
pp. 1115-1120 ◽  
Author(s):  
B. Lendrum ◽  
H. Feinberg ◽  
E. Boyd ◽  
L. N. Katz
Keyword(s):  
Heart Rate ◽  
Left Ventricle ◽  
Systolic Pressure ◽  
Ventricular Volume ◽  
Contractile Force ◽  
Postextrasystolic Potentiation ◽  
Pressure Development ◽  
Induced Changes ◽  
Electrical Alternans

Variation in contractile force of the isovolumic contracting left ventricle of the dog was studied in open-chested in situ hearts. The electrocardiogram and intraventricular pressures were recorded at various heart volumes. Spontaneous changes in heart rate and rhythm occurred at all volumes. Isovolumic systolic pressure development (contractile force) varied with rate and rhythm. Contractile force increased with heart rate (treppe) regardless of pacemaker origin. When a premature beat was followed by a compensatory pause, the premature beat showed a decrease and the next beat an increase in contractile force (postextrasystolic potentiation). The magnitude of the changes varied directly with the prematurity of the beat. Mechanical alternans was observed with electrical alternans, despite the absence of significant volume change. Rate-induced changes, postextrasystolic potentiation and mechanical alternans were additive when they occurred simultaneously. For practical purposes, ventricular volume (filling), hence muscle fiber length, remained constant during these rate and rhythm change, therefore could not affect the strength of contraction. Contractile force changes directly attributable to rate and rhythm changes do, therefore, occur in the intact mammalian heart.

Experimental hypothermia and rewarming: changes in mechanical function and metabolism of rat hearts

1996 ◽  
Vol 80 (1) ◽  
pp. 291-297 ◽  
Author(s):  
T. Tveita ◽  
M. Skandfer ◽  
H. Refsum ◽  
K. Ytrehus
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Maximum Rate ◽  
Energy Charge ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Mechanical Function ◽  
Control Value

Rewarming from accidental hypothermia is associated with fatal circulatory derangements. To investigate potential pathophysiological mechanisms involved, we examined heart function and metabolism in a rat model rewarmed after 4 h at 15-13 degrees C. Hypothermia resulted in a significant reduction of left ventricular (LV) systolic pressure, cardiac output, and heart rate, whereas stroke volume increased. The maximum rate of LV pressure rise decreased to 191 +/- 28 mmHg/s from a control value of 9,060 +/- 500 mmHg/s. Myocardial tissue content of ATP, ADP, and glycogen was significantly reduced, whereas lactate content remained unchanged. After rewarming, heart rate returned to control value, whereas LV systolic pressure, cardiac output, and stroke volume all remained significantly depressed. The posthypothermic maximum rate of LV pressure rise was 5,966 +/- 1.643 mmHg/s. The posthypothermic myocardial lactate content was significantly increased (to 13.3 +/- 3.2 nmol/mg from control value of 5.7 +/- 1.9 nmol/mg), and ATP and glycogen remained significantly lowered. Creatine phosphate or energy charge did not change significantly during the experiment. The finding of deteriorated myocardial mechanical function and a shift in energy metabolism shows that the heart could be an important target during hypothermia and rewarming in vivo, thus contributing to the development of a posthypothermic circulatory collapse.

CARDIOVASCULAR EFFECTS OF PRONETHALOL IN THE DOG

1965 ◽  
Vol 43 (3) ◽  
pp. 411-420 ◽  
Author(s):  
M. A. Chiong ◽  
P. F. Binnion ◽  
J. D. Hatcher
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Cardiovascular Effects ◽  
Stroke Work ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure

The cardiovascular effects of an intravenous injection of pronethalol (2.5 mg/kg) and the effect of this agent on the cardiovascular changes induced by an infusion of adrenaline (0.2 μg/kg per minute) were investigated in intact anaesthetized dogs. Fifteen minutes after the administration of pronethalol, significant increases were observed in oxygen consumption, right ventricular systolic pressure, and haematocrit, and decreases in arterial blood pressure and total peripheral resistance. Arterial hypotension and a fall in stroke work were the only changes noted at 30 minutes. There was considerable variability in cardiac output, stroke volume, and heart rate but, on the average, no significant change was observed. Pretreatment with pronethalol abolished or significantly reduced the adrenaline-induced rises in cardiac output, heart rate, stroke volume, stroke work, oxygen consumption, right ventricular systolic pressure, and arterial haematocrit, and reversed the changes in diastolic arterial pressure and peripheral resistance. It is concluded that pronethalol is not devoid of sympathomimetic activity and that it effectively blocks the adrenaline responses mediated by β-receptors.

3071Peptidomimetic targeting of CavBeta2 improves contractility in models of senescence- or genetically (MYBPC3 KI)-induced heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
B El-Mathari ◽  
P Briand ◽  
A Corbier ◽  
B Poirier ◽  
S Le-Claire ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Dilated Cardiomyopathy ◽  
Diastolic Function ◽  
Myocardial Contractility ◽  
Calcium Release ◽  
Applied Pressure ◽  
Systolic Pressure

Abstract Background L-type calcium channel (LTCC) trafficking controls LTCC density at T-tubule levels for optimal Excitation-Coupling (EC) and resultant adaptive heart work. In some forms of heart failure (HF), abnormalities in calcium-induced calcium-release have been proposed to arise from alteration of T-tubular dyad architecture (LTCC-RyRs) associated with impaired LTCC density. Recently, the R7W-MP peptide, working as a binder of the LTCC Cavβ2 chaperone, was shown to restore the altered density of LTCC current by both promoting forward and reducing reverse trafficking, which consequently improved cellular calcium homeostasis. Accordingly, R7W-MP improved the impaired cardiomyocyte calcium current density and the reduced Ejection Fraction (EF%) in a pharmacologically-induced diabetes model (STZ mice). We aimed to investigate further the benefit to improve LTCC trafficking pathway with R7W-MP in a more physiological model of HF (senescent mice) and in a Dilated Cardiomyopathy (DCM) model (HO MYBPC3 targeted KI mutant). Methods Senescent male C57Bl/6J mice (26 months) or HO MYBPC3 KI male mice (2 months) were treated with R7W-MP (3 mg/kg/d IP for 3 days). Echocardiographies (echo) were conducted before treatment and 4-hours after the last injection. When applied, Pressure-Volume (PV)-loop investigations were conducted one day post-echo 4 hours following an additional R7W-MP injection. Results In senescent mice population, HF was characterized by a midrange ejection fraction (EF%= 43±2 vs 55±1 for young adult mice) associated with enlarged ventricles and decreased cardiac contractility. In contrast to a scrambled peptide (scrP), R7W-MP markedly increased EF% monitored by echo (+38%, 63±3 vs 45±1 for scrP, p≤0.001, n=6–7) without modification of heart rate. EF% improvement was confirmed by PV-loop analysis (78±3 vs 51±4 for scrP (+54%), p≤0.001, n=5), associated with a marked, although not significant, 2.5-fold increase in myocardial contractility [end systolic pressure volume relationship (ESPVR) = 12.1±3.6 vs 4.9±1.3 for scrP, p=0.10, n=4]. Stroke volume, cardiac output and end diastolic volume tended to decrease suggesting an impaired LV filling at this dose regimen. In the DCM model, HF was more severe with a dramatically low EF% (26±1, n=8), impaired myocardial contractility and a pronounced left ventricle enlargement. R7W-MP significantly increased EF% (+17%, reaching 31±1, p≤0.01, n=8) without altering heart rate. Stroke volume was significantly increased by 36% (32±3 vs 24±3 mL at baseline, p≤0.01), without any impairment of diastolic function. All parameters returned to baseline after a 2 week-washout period. Conclusions R7W-MP displays potent positive inotrope properties in senescent or DCM mice models. Although further asses tsments of diastolic function are needed (different dosing and duration), these data underline the potential benefit brought by LTCC trafficking modulation to treat severe dilated cardiomyopathy.

Left ventricular function during chronic endotoxemia in swine

1988 ◽  
Vol 254 (2) ◽  
pp. H324-H330 ◽  
Author(s):  
K. Lee ◽  
H. van der Zee ◽  
S. W. Dziuban ◽  
K. Luhmann ◽  
R. D. Goldfarb
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Salmonella Enteritidis ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Inotropic State ◽  
Pressure Development ◽  
Hyperdynamic Sepsis

Cardiac performance was studied in 15 chronically instrumented awake pigs during chronic endotoxemia (CET) induced by intravenous infusion of low doses of endotoxin. We sought to test the hypothesis that left ventricular inotropic state was depressed during the stage of chronic endotoxemia when cardiac output, heart rate, and left ventricular systolic pressures are elevated, termed "hyperdynamic sepsis". Left ventricular pressure, internal short axis diameter (SAX), pulmonary artery blood flow, and electrocardiogram were recorded. After initial surgical preparation, each pig was observed for 7-10 days to measure representative basal values. Each pig was then reoperated on day 10 to implant an endotoxin-loaded osmotic pump whose output, infused Salmonella enteritidis endotoxin at a rate calculated to be 10 micrograms.kg-1.h-1 for up to 7 days. Cardiac performance was monitored by measuring dP/dt, heart rate, stroke volume, end-diastolic diameter, percent change in diameter, and the slope of the end-systolic pressure diameter relationship (ESPDR). Data from the basal days were pooled and compared with the data obtained each day of CET by two-way analysis of variance. Ten of 15 pigs survived more than 2 days of CET; 5 died before the morning of the second CET day. The surviving pigs demonstrated elevated systolic pressures, left ventricular maximum rate of pressure development (+dP/dtmax and -dP/dtmax), heart rates, and cardiac output. However, both ESPDR and percent SAX shortening were significantly depressed during both CET days. We conclude that cardiac inotropic state is depressed during hyperdynamic sepsis as indicated by the load-independent parameter ESPDR and confirmed by depressed percent SAX shortening.

Hemodynamic responses to acute carboxyhemoglobinemia in the rat

1983 ◽  
Vol 244 (3) ◽  
pp. H320-H327 ◽  
Author(s):  
W. E. Kanten ◽  
D. G. Penney ◽  
K. Francisco ◽  
J. E. Thill
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Cardiac Index ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work

The effects of carbon monoxide on the hemodynamics of the adult rat were investigated. A number of parameters were measured using an open-chest, chloralose-urethan anesthetized preparation. Our experiments showed this anesthetic agent to have several advantages over pentobarbital sodium. One group inhaled 150 ppm CO for 0.5-2 h, carboxyhemoglobin (HbCO) reaching 16%. Heart rate, cardiac output, cardiac index, dF/dtmax (aortic), and stroke volume rose significantly; mean arterial pressure, total peripheral resistance, and left ventricular systolic pressure fell, whereas stroke work, left ventricular dP/dtmax, and stroke power changed little. These effects were evident at a HbCO saturation as low as 7.5% (0.5 h). A second group inhaled 500 ppm CO for 5-48 h, HbCO reaching 35-38%. The same parameters changed in the same direction as in the first group, with mean arterial pressure and peripheral resistance remaining depressed, while heart rate, cardiac output, cardiac index, and stroke volume remained elevated. Heart rate and arterial systolic pressure were also monitored in conscious rats; rats in one group inhaled 500 ppm CO for 24 h, and rats in a second group were injected with a bubble of pure CO ip. In both cases heart rate was sharply elevated and blood pressure depressed as HbCO saturation increased. Both parameters recovered on CO washout. There was no significant difference between the response to inhaled vs. injected CO.

Hemodynamic effects of epinephrine: concentration-effect study in humans

1985 ◽  
Vol 58 (4) ◽  
pp. 1199-1206 ◽  
Author(s):  
J. R. Stratton ◽  
M. A. Pfeifer ◽  
J. L. Ritchie ◽  
J. B. Halter
Keyword(s):  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Hemodynamic Effects ◽  
Plasma Epinephrine ◽  
Ventricular Performance

The hemodynamic effects of three different infusion rates of epinephrine (25, 50, or 100 ng X kg-1 X min-1 for 14 min) were examined in 10 normal human subjects. Ejection fraction and changes in cardiac volumes were assessed by radionuclide ventriculography. Plasma epinephrine was increased to levels that spanned the normal physiological range (178 +/- 15, 259 +/- 24, and 484 +/- 69 pg/ml, respectively). Epinephrine infusions resulted in dose-dependent increases in heart rate (8 +/- 3, 12 +/- 2, and 17 +/- 1 beats/min, mean +/- SE) and systolic pressure (8 +/- 1, 18 +/- 2, and 30 +/- 6 mmHg). Although epinephrine infusions had minimal effects on end-diastolic volume, there were significant increases in stroke volume (+26 +/- 2, 31 +/- 4, and 40 +/- 4%), ejection fraction (+0.10 +/- 0.01, 0.14 +/- 0.02 and 0.16 +/- 0.03 ejection fraction units), and cardiac output (+41 +/- 4, 58 +/- 5, and 74 +/- 1%). These increases in left ventricular performance were associated with a decreased systemic vascular resistance (-31 +/- 3, -42 +/- 2, and -48 +/- 8%). Supine bicycle exercise resulted in similar plasma epinephrine levels (417 +/- 109 pg/ml) and similar changes in stroke volume, ejection fraction, and systemic vascular resistance but greater increases in heart rate and systolic blood pressure. Since infusion-associated hemodynamic changes occurred at plasma epinephrine levels commonly achieved during many types of physical and emotional stress, epinephrine release may have an important role in regulating systemic vascular resistance, stroke volume, and ejection fraction responses to stress in man.

Relationship between Invasive and Non-Invasive Hemodynamic Measures in Experimental Pulmonary Hypertension

2020 ◽  
Vol 16 (1) ◽  
pp. 47-53
Author(s):  
Vicente Benavides-Córdoba ◽  
Mauricio Palacios Gómez
Keyword(s):  
Heart Rate ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Right Ventricle ◽  
Correlation Coefficient ◽  
Pearson Correlation ◽  
Systolic Pressure ◽  
Control Group ◽  
Pearson Correlation Coefficient ◽  
Non Invasive

Introduction: Animal models have been used to understand the pathophysiology of pulmonary hypertension, to describe the mechanisms of action and to evaluate promising active ingredients. The monocrotaline-induced pulmonary hypertension model is the most used animal model. In this model, invasive and non-invasive hemodynamic variables that resemble human measurements have been used. Aim: To define if non-invasive variables can predict hemodynamic measures in the monocrotaline-induced pulmonary hypertension model. Materials and Methods: Twenty 6-week old male Wistar rats weighing between 250-300g from the bioterium of the Universidad del Valle (Cali - Colombia) were used in order to establish that the relationships between invasive and non-invasive variables are sustained in different conditions (healthy, hypertrophy and treated). The animals were organized into three groups, a control group who was given 0.9% saline solution subcutaneously (sc), a group with pulmonary hypertension induced with a single subcutaneous dose of Monocrotaline 30 mg/kg, and a group with pulmonary hypertension with 30 mg/kg of monocrotaline treated with Sildenafil. Right ventricle ejection fraction, heart rate, right ventricle systolic pressure and the extent of hypertrophy were measured. The functional relation between any two variables was evaluated by the Pearson correlation coefficient. Results: It was found that all correlations were statistically significant (p <0.01). The strongest correlation was the inverse one between the RVEF and the Fulton index (r = -0.82). The Fulton index also had a strong correlation with the RVSP (r = 0.79). The Pearson correlation coefficient between the RVEF and the RVSP was -0.81, meaning that the higher the systolic pressure in the right ventricle, the lower the ejection fraction value. Heart rate was significantly correlated to the other three variables studied, although with relatively low correlation. Conclusion: The correlations obtained in this study indicate that the parameters evaluated in the research related to experimental pulmonary hypertension correlate adequately and that the measurements that are currently made are adequate and consistent with each other, that is, they have good predictive capacity.

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