Influence of CO2 on cardiovascular response to hypoxia in conscious dogs

1980 ◽  
Vol 239 (4) ◽  
pp. H545-H545 ◽  
Author(s):  
Raymond C. Koehler ◽  
Brian W. McDonald ◽  
John A. Krasney
Keyword(s):  
Cardiovascular Response ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Coronary Vasodilation ◽  
Circulatory Response ◽  
Wide Range ◽  
Before And After ◽  
Tension Time ◽  
Arterial Chemoreceptor

The modulating effect of CO2 on the circulatory response to hypoxia in chronically instrumented conscious dogs was examined over a wide range of arterial partial pressure of O2 [PaO2 (from 80 to 25 Torr)] during a 41-min rebreathing period at three CO2 levels: hypocapnia (from PaCO2 of 32 to 18 Torr), eucapnia (32 Torr), and mild hypercapnia (40 Torr). Eucapnic and hypercapnic hypoxic responses were also measured after sinoaortic denervation (SAD) to assess the arterial chemoreceptor and baroreceptor reflex contributions. Elevating PaCO2 attenuated the tachycardia during hypoxia and produced progressively greater systemic, renal, and splanchnic vasoconstriction before but not after SAD. Vagal block converted the rises in renal and splanchnic flows observed during hypocapnic hypoxia to declines. The increase in left ventricular dP/d tmax was not affected by varying PaCO2 either before or after SAD. Coronary flow increased an additional onefold during hypoxia when PaCO2 was elevated both before and after SAD, but the tension-time indices did not differ significantly. These results indicate that: a) cardiopulmonary vagal afferents effectively counteract chemoreflex-induced vasoconstriction during hypocapnic hypoxia; b) chemoreflex vasoconstriction predominates in the renal and splanchnic beds when PaCO2 is elevated; c) the sinoaortic reflexes restrain the heart rate, but not the contractility response to hypoxia when PaCO2 is increased; and d) the augmented coronary vasodilation produced by CO2 is probably mediated by local CO2-hypoxic interactions.

Left ventricular-arterial coupling in conscious dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H70-H76 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Inotropic State ◽  
End Diastolic Volume ◽  
Wide Range

We investigated the criteria for the coupling of the left ventricle (LV) and the arterial system to maximize LV stroke work (SW) and the transformation of LV pressure-volume area (PVA) to SW. We studied eight conscious dogs that were instrumented to measure LV pressure and determine LV volume from three ultrasonically determined dimensions. The LV end-systolic pressure (PES)-volume (VES) relation was determined by caval occlusion. Its slope (EES) was compared with the arterial elastance (EA) and determined as PES per stroke volume. At rest, with intact reflexes, EES/EA was 0.96 +/- 0.20 EES/EA was varied over a wide range (0.18-2.59) by the infusion of graded doses of phenylephrine and nitroprusside before and during administration of dobutamine. Maximum LV SW, at constant inotropic state and end-diastolic volume (VED), occurred when EES/EA equaled 0.99 +/- 0.15. At constant VED and contractile state, SW was within 20% of its maximum value when EES/EA was between 0.56 and 2.29. The conversion of LV PVA to SW increased as EES/EA increased. The shape of the observed relations of the SW to EES/EA and SW/PVA to EES/EA was similar to that predicted by the theoretical consideration of LV PES-VES and arterial PES-stroke volume relations. We conclude that the LV and arterial system produce maximum SW at constant VED when EES and EA are equal; however, the relation of SW to EES/EA has a broad plateau. Only when EA greatly exceeds EES does the SW fall substantially. However, the conversion of PVA to SW increases as EES/EA increases. These observations support the utility of analyzing LV-arterial coupling in the pressure-volume plane.

scholarly journals P342 Left atrial contraction longitudinal strain is a volume-independet parameter

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Unlu ◽  
B Sezenoz ◽  
A Sahinarslan ◽  
T Arinsoy ◽  
A Cengel
Keyword(s):  
Speckle Tracking ◽  
Longitudinal Strain ◽  
Heart Diseases ◽  
Left Ventricular ◽  
Reference Points ◽  
Volume Index ◽  
Valvular Heart Diseases ◽  
Wide Range ◽  
Before And After ◽  
2D Speckle Tracking

Abstract Background The left atrium (LA) is the main contributor of left ventricular (LV) filling. LA volume and volume index are routinely evaluated during echocardiographic assessment as having prognostic value in a wide range of cardiovascular pathologies. Yet, LA volume is easily affected by volume status. Thus, a non-invasive novel parameter such as indices of LA longitudinal strain (LS) have been proposed as alternative measurements. LA strain was shown to be associated with LV filling pressures and it has been suggested to provide prognostic information in patients with heart failure, atrial fibrillation, ischemic and valvular heart diseases. Nevertheless the acute effect of hemodynamic changes on LA LS indices is not well-established due to lack of evidence in healthy subjects and patient populations. The aim of this study is to evaluate the LA mechanics and change in echocardiographic methods used for assessment of LA by examining the end stage kidney patients before and after the hemodialysis (HD). Methods Patients between 18 and 85 years of age, receiving HD for at least 6 months were included. The echocardiographic images were obtained before and after HD. 2D speckle tracking strain analysis was performed for LA in 45 patients. Reference points for analysis are set on the "P" waves. LA reservoir, conduit and contraction phase LS were calculated. The changes in echocardiographic methods before and after hemodialysis were examined. Correlation between volume depletion and change in echocardiographic parameters were calculated. Results 45 patients (47.7 ± 14.7 years of age, 19 women) were included in study. The mean volume of ultrafiltration was 2755.12 ± 845.5 ml . The chamber sizes of LA are decreased after hemodialysis (LA diameter; 4.9 ± 0.8 cm vs. 4.4 ± 0.5 cm p < 0.001, LA area; 27.8 ± 4.0 cm2 vs. 19.6 ± 3.8 cm2 p < 0.001). LA reservoir phase LS measurements (% 44.6 ± 10.8 vs. % 38.15 ± 8.11 p < 0.001) showed significant changes after HD. In contrast LA contraction LS measurements (% -16.6 ± 7.0 vs. % -16.4 ± 7.1 p:0.893) did not differ after HD. The relative change in LA reservoir phase LS (r = 0.74, p:0.001) showed correlation with the ultrafiltrated volume. Conclusion LA contraction LS is a volume independent measurement obtained by 2D speckle tracking. Assessment of LA mechanics with echocardiography would be an easy and repeatable assessment which can guide to describe the cardiac pathophysiology and hemodynamics better. Moreover defining novel volume independent parameters for evaluation of LA would contribute to clinical perspectives of the patients.

Prostacyclin reduces "preload" in conscious dogs via a vagal reflex mechanism

1987 ◽  
Vol 253 (6) ◽  
pp. H1477-H1483
Author(s):  
D. M. Nganele ◽  
T. H. Hintze
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Reflex Mechanism ◽  
Capacitance Vessels ◽  
Preload Reduction ◽  
Cardiopulmonary Receptors ◽  
Electrical Pacing

The purpose of this study was to determine the effects of prostacyclin on left ventricular (LV) preload in conscious dogs. LV end-diastolic diameter (LV EDD) was used as an index of preload. Because prostacyclin reduces arterial pressure, data were sampled when mean arterial pressure, heart rate, and first derivative of LV pressure (dP/dt) had returned to control levels. There was no dose-response relationship in the preload reduction to prostacyclin, the threshold dose being 0.1 microgram/kg. Intravenous prostacyclin (2.0 micrograms/kg) reduced LV EDD 2.9 +/- 0.5% from 36 +/- 2.2 mm, (P less than 0.01). With heart rate held constant (146 +/- 2.5 beats/min) by electrical pacing, prostacyclin still reduced LV EDD by 4.0 +/- 1.0% from 32 +/- 2.5 mm (P less than 0.05). Intravenous administration of arachidonic acid (500 micrograms/kg) gave similar results. The magnitude of the preload response to prostacyclin was similar to that of nitroglycerin (25 micrograms/kg). Prazosin (1 mg/kg) or bilateral cervical vagal section completely abolished the preload response to prostacyclin but not to nitroglycerin. We, therefore, propose a mechanism where prostacyclin activates cardiopulmonary receptors with vagal afferents that results in a withdrawal of peripheral sympathetic tone to capacitance vessels to reduce preload, in contrast to nitroglycerin, whose mechanism of action is most probably a direct effect on capacitance vessels.

Mechanisms of desensitization to a PDE inhibitor (milrinone) in conscious dogs with heart failure

1999 ◽  
Vol 276 (5) ◽  
pp. H1699-H1705 ◽  
Author(s):  
Naoki Sato ◽  
Kuniya Asai ◽  
Satoshi Okumura ◽  
Gen Takagi ◽  
Richard P. Shannon ◽  
...  
Keyword(s):  
Heart Failure ◽  
Wall Stress ◽  
Major Effect ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Internal Diameter ◽  
Compensatory Mechanism ◽  
Before And After ◽  
Rapid Ventricular Pacing ◽  
Camp Levels

The goal of this study was to determine the extent to which the effects of milrinone were desensitized in heart failure (HF) and to determine the mechanisms, i.e., whether these effects could be ascribed to changes in cAMP or phosphodiesterase (PDE) activity in HF. Accordingly, we examined the effects of milrinone in seven conscious dogs before and after HF was induced by rapid ventricular pacing at 240 beats/min. The dogs were chronically instrumented for measurements of left ventricular (LV) pressure and first derivative of LV pressure (dP/d t), arterial pressure, LV internal diameter, and wall thickness. Milrinone (10 μg ⋅ kg−1 ⋅ min−1iv) increased LV dP/d t by 1,854 ± 157 from 2,701 ± 105 mmHg/s ( P < 0.05) before HF. After HF the increase in LV dP/d t in response to milrinone was attenuated significantly ( P < 0.05); it increased by 615 ± 67 from 1,550 ± 107 mmHg/s, indicating marked desensitization. In the presence of ganglionic blockade the increases in LV dP/d t (+445 ± 65 mmHg/s) in response to milrinone were markedly less ( P < 0.01), and milrinone increased LV dP/d t even less in HF (+240 ± 65 mmHg/s). cAMP and PDE activity were measured in endocardial and epicardial layers in normal and failing myocardium. cAMP was decreased significantly ( P < 0.05) in LV endocardium (−26%) but not significantly in LV epicardium (−14%). PDE activity was also decreased significantly ( P < 0.05) in LV endocardium (−18%) but not in LV epicardium (−4%). Thus significant desensitization to milrinone was observed in conscious dogs with HF. The major effect was autonomically mediated. The biochemical mechanism appears to be due in part to the modest reductions in PDE activity in failing myocardium, which, in turn, may be a compensatory mechanism to maintain cAMP levels in HF. Reductions in cAMP and PDE levels were restricted to the subendocardium, suggesting that the increased wall stress and reduced coronary reserve play a role in mediating these changes.

Sodium channel enhancer restores baroreflex sensitivity in conscious dogs with heart failure

2005 ◽  
Vol 288 (4) ◽  
pp. H1508-H1514 ◽  
Author(s):  
Weiqun Shen ◽  
Robert M. Gill ◽  
Jian-Ping Zhang ◽  
Bonita D. Jones ◽  
Angela K. Corbly ◽  
...  
Keyword(s):  
Heart Failure ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Vena Cava ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Inotropic Effect ◽  
Pulse Interval ◽  
Adrenergic Blockade ◽  
Before And After

We compared the cardiac inotropic, lusitropic, and chronotropic responses to the Na+ channel enhancer LY-368052 in conscious dogs before and after development of congestive heart failure (CHF). We also examined the effect of LY-368052 on baroreflex sensitivity and the efferent neural mechanisms of the bradycardic response in heart failure. Dogs were chronically instrumented, and heart failure was induced by right ventricular pacing at 240 beats/min for 3–4 wk. LY-368052 dose-dependently increased left ventricular contractile performance before and after the development of CHF to a similar extent. The inotropic effect of LY-368052 in heart failure was not altered by either ganglionic or β-adrenergic receptor blockade. LY-368052 improved cardiac relaxation and induced bradycardia in dogs with heart failure but not in normal dogs. The negative chronotropic effect of LY-368052 was eliminated by ganglionic blockade but not β-adrenergic blockade, suggesting that the bradycardia was mediated by the autonomic nervous system via enhanced parasympathetic tone. Baroreflex sensitivity was assessed as the pulse interval-mean arterial pressure slope in response to temporary pharmacological (nitroglycerin or phenylephrine) and mechanical (brief occlusion of inferior vena cava) alterations of arterial pressure in conscious dogs before and after development of heart failure. Baroreflex sensitivity was significantly depressed in heart failure and restored completely by acute treatment with LY-368052. Thus the Na+ channel enhancer LY-368052 maintains its β-receptor-independent inotropic effect in chronic CHF and specifically improves ventricular relaxation and depressed baroreflex function.

Enhanced left ventricular shortening during chronic volume overload in conscious dogs

1980 ◽  
Vol 238 (2) ◽  
pp. H126-H133 ◽  
Author(s):  
M. M. LeWinter ◽  
R. L. Engler ◽  
J. S. Karliner
Keyword(s):  
Volume Overload ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Stimulation ◽  
Ventricular Performance ◽  
Blood Pressure Elevation ◽  
Chronic Volume Overload ◽  
Before And After ◽  
Ejection Phase

Prior work with the arteriovenous fistula model indicates that left ventricular performance is at least normal and may be enhanced during chronic volume overload. The present study was undertaken in conscious dogs to determine whether ejection-phase indices of ventricular function are enhanced after 1 mo of volume overload, using an experimental design in which loading conditions could be accounted for and animals were used as their own controls before and after volume overload. We also examined the response of the volume-overloaded left ventricle to an afterload stress and the role of adrenergic stimulation in maintenance of function. Both at rest and during hemodynamically matched conditions, percent shortening (ultrasonic dimension gauges) and mean shortening rates were increased during volume overload. This difference was maintained during phenylephrine-induced blood pressure elevation, although diastolic dimensions increased more in control studies during phenylephrine. Propranolol produced significantly larger reductions in these indices during volume overload than in the control state. Thus, ejection-phase function is enhanced during volume overload, at least in part due to increased adrenergic stimulation.

Influence of pericardium on left atrial compliance and pulmonary venous flow

1993 ◽  
Vol 264 (6) ◽  
pp. H1781-H1787 ◽  
Author(s):  
B. D. Hoit ◽  
Y. Shao ◽  
M. Gabel ◽  
R. A. Walsh
Keyword(s):  
Left Atrial ◽  
Diastolic Pressure ◽  
Dynamic Stiffness ◽  
Left Ventricular ◽  
Venous Flow ◽  
Stiffness Constant ◽  
Wide Range ◽  
Before And After ◽  
Volume Relation ◽  
Conduit Function

We studied seven open-chest anesthetized dogs to test the hypothesis that left atrial (LA) compliance is increased after pericardiectomy and to determine the effect of pericardiectomy on left atrial reservoir and conduit function. Two orthogonal sonomicrometer crystal pairs were used to estimate LA volume, and LA filling was assessed with a pulmonary vein (PV) flow probe. The left ventricular (LV) systolic (JFTI) and diastolic (KFTI) PV flow integrals were used as indexes of LA reservoir and conduit function, respectively. Diastolic LV transmitral flow was assessed with transesophageal Doppler echocardiography. Data were acquired over a wide range of intracardiac pressures and volumes obtained by intravenous hetastarch infusion both before and after pericardiectomy. The mean dynamic stiffness constant of the LA diastolic pressure-volume relation was significantly greater before pericardiectomy than afterwards (0.15 +/- 0.04 vs. 0.08 +/- 0.03 ml-1, P < 0.05). Data were analyzed before and after pericardiectomy at three matched levels of left atrial pressure (LAP; 7, 13, and 20 mmHg). The J-to-KFTI ratio increased significantly with volume infusion and was significantly less after pericardiectomy than before (1.2 +/- 0.7 vs. 1.2 +/- 0.6, 1.8 +/- 0.6 vs. 2.2 +/- 0.9, and 2.0 +/- 0.8 vs. 2.6 +/- 0.9 at low, mid, and high levels of LAP, respectively; P < 0.05 at mid and high levels of LAP). Peak early transmitral velocity increased with both volume infusion and pericardiectomy. We conclude that pericardiectomy increases LA compliance and early LV filling rate and is accompanied by a relatively greater augmentation in conduit than reservoir function of the left atrium.

Response of primate heart to emotional stress before and after cardiac denervation

1976 ◽  
Vol 230 (4) ◽  
pp. 988-995 ◽  
Author(s):  
DC Randall ◽  
MP Kaye ◽  
WC Randall ◽  
JV Brady ◽  
KH Martin
Keyword(s):  
Emotional Stress ◽  
Cardiovascular Response ◽  
Time Derivative ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Nervous Control ◽  
Small Magnitude ◽  
Ventricular Systolic Pressure ◽  
Cardiac Denervation ◽  
Before And After

Eleven chair-restrained rhesus monkeys were classically conditioned to a 1-min, 900-Hz tone (CSf) followed by food and a 1-min, 3.4-5Hz tone (CSs) followed by shock. Each conditional stimulus produced large, sudden, and highly significant (P less than .01) increases in left ventricular systolic pressure (LVP), its first time derivative (d(LVP)/dt), and heart rate (HR). The animal's hearts were sugically denervated following control studies of the conditional responses. Two to four weeks later, these responses were reexamined by again presenting CSf and CSs to five surviving monkeys following a format identical to that used in the control experiments. Complete cardiac denervation virtually eliminated the sudden increases in each of the measured variables. Denervation also "unmasked" small-magnitude, delayed chronotropic and inotropic responses during CSs (but not CSf). These effects were ascribed to the action of circulating catecholamines known to be secreted during "emotional" stress. Four monkeys studied for 6 mo or more postoperatively showed evidence for varying degrees of cardiac reinnervation. Loss of nervous control of the nonhuman primate heart greatly compromises the cardiovascular response to these environmental and behavioral stress situations.

PGE2 and arachidonate inhibit the baroreflex in conscious dogs via cardiac receptors

1989 ◽  
Vol 256 (4) ◽  
pp. H999-H1005 ◽  
Author(s):  
M. J. Panzenbeck ◽  
W. Tan ◽  
M. A. Hajdu ◽  
K. G. Cornish ◽  
I. H. Zucker
Keyword(s):  
Heart Rate ◽  
Arachidonic Acid ◽  
Vena Cava ◽  
Surgical Techniques ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Baroreflex Control ◽  
Maximum Slope ◽  
Intracoronary Infusion

Prostaglandin (PG) I2 and PGE2 are known to stimulate left ventricular receptors with nonmyelinated vagal afferents. The present experiments were performed to determine the effects of intracoronary infusion of PGE2 (10-50 ng.kg-1.min-1) and arachidonic acid (50-100 micrograms.kg-1.min-1) on the baroreflex control of heart rate in conscious dogs. Dogs were anesthetized with pentobarbital sodium and were instrumented using sterile surgical techniques. After recovery, baroreflex pressure-heart rate curves were constructed by varying arterial pressure with partial occlusions of the descending aorta or inferior vena cava. Intracoronary infusion of PGE2 significantly inhibited the maximum heart rate achieved during unloading of baroreceptors, attenuated the heart rate range, and decreased the maximum slope of the baroreflex curve; PGE2 had no significant effect on the minimum heart rate during hypertension. Intravenous infusion of PGE2 did not cause significant baroreflex inhibition, and pericoronary nerve block in three dogs prevented the effects of intracoronary PGE2. Intracoronary infusion of arachidonic acid had effects on the baroreflex control of heart rate similar to those of PGE2. The effects of arachidonic acid infusion were prevented by cyclooxygenase blockade. Thus intracoronary PGE2 and arachidonic acid inhibit the baroreflex control of heart rate most likely via stimulation of left ventricular receptors with vagal C-fiber afferents. The effects of arachidonic acid were secondary to synthesis of prostaglandins.

Sign in / Sign up

Export Citation Format

Share Document