Effects of a coronary alpha 1-constriction on transmural left ventricular flow and contractile function

1992 ◽  
Vol 262 (4) ◽  
pp. H965-H972 ◽  
Author(s):  
P. A. Gwirtz ◽  
J. M. Dodd-O ◽  
H. F. Downey ◽  
H. J. Mass ◽  
B. A. Barron ◽  
...  
Keyword(s):  
Contractile Function ◽  
Stellate Ganglion ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximal Rate ◽  
Circumflex Artery ◽  
Ventricular Systolic Pressure ◽  
Adrenergic Antagonist

Modulation of myocardial contractile function and perfusion by alpha 1-adrenergic receptors were examined in anesthetized dogs during left stellate ganglion stimulation. In 11 dogs, stellate stimulation significantly increased heart rate, mean arterial pressure, left ventricular systolic pressure, maximal rate of left ventricular pressure generation, segmental shortening and rate of shortening in anterior and posterior ventricular regions, and myocardial oxygen extraction. Myocardial lactate extraction decreased. The selective alpha 1-adrenergic antagonist prazosin (0.5 mg) injected into the circumflex artery during stellate stimulation caused significant additional increases in maximal rate of left ventricular pressure generation by 19 +/- 5% and in rate of shortening in posterior subendocardium by 20 +/- 6%. No changes were observed in posterior subepicardial or anterior subendocardial segmental contractile function. Myocardial oxygen and lactate extractions returned to their control values following prazosin injection. Regional left ventricular perfusion was measured using tracer microspheres in five additional dogs. Stellate stimulation increased subepicardial and subendocardial perfusion by 30%. Prazosin increased both subepicardial and subendocardial perfusion by an additional 36%. Stellate stimulation increased norepinephrine concentration in the coronary sinus, but no further increase was noted after blockage of alpha 1-receptors by prazosin. Thus, during sympathetic stimulation, an alpha 1-vasoconstriction existed uniformly across the left ventricular wall. However, blockade of this vasoconstriction was associated with an increase in contractile function only in the deeper muscle layers.

Effects of vasoactive intestinal peptide on myocardial performance

1994 ◽  
Vol 266 (2) ◽  
pp. H399-H405 ◽  
Author(s):  
N. P. Xenopoulos ◽  
R. J. Applegate
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Contractile Function ◽  
Time Derivative ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Adrenergic Blockade ◽  
Volume Relation ◽  
First Time

It is now recognized that stimulation of the vagus releases both acetylcholine (ACh) and vasoactive intestinal peptide (VIP). Whereas ACh depresses cardiac function, recent data indicate that VIP may have a cardiostimulatory effect. Exogenously administered VIP appears to enhance left ventricular (LV) contractile function; however, whether endogenously released VIP alters LV performance is not known. Accordingly, we evaluated the effects of exogenous VIP and endogenously released VIP during vagal stimulation after muscarinic and beta-adrenergic blockade (VS-B) on LV performance using pressure-volume analysis. Eight anesthetized open-chest dogs instrumented to measure LV pressure and volume (conductance catheter) were pretreated with atropine (0.1 mg/kg) and propranolol (1 mg/kg). The cervical vagi were transected. Hemodynamic data were obtained at steady state and during transient vena caval occlusion. Exogenous intravenous VIP (0.05 microgram/kg-1 x min-1) increased HR minimally [2.1 +/- 0.9% increase; P = not significant (NS)] but significantly increased maximum first time derivative of left ventricular pressure (dP/dtmax; 29.4 +/- 19.9% increase; P < 0.05) and the slope of the end-systolic pressure-volume relation (Ees; 3.1 +/- 1.3 to 8.9 +/- 4.2 mmHg/ml; P < 0.05). Minimum first time derivative of left ventricular pressure (dP/dtmin) decreased 22 +/- 16.2% (P < 0.05), and the time constant of isovolumic relaxation (tau) decreased 38 +/- 18% (P < 0.05). During VS-B (20 Hz, 15 v, 5 min), HR increased significantly (98 +/- 11 to 130 +/- 26 beats/min; P < 0.05). Ees also increased significantly (3.3 +/- 1.6 vs. 5.2 +/- 2.8 mmHg/ml; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Time dependence of regional systolic left ventricular relationships in intact hearts

1990 ◽  
Vol 258 (5) ◽  
pp. H1348-H1356
Author(s):  
W. P. Miller ◽  
S. H. Nellis ◽  
A. J. Liedtke
Keyword(s):  
Time Course ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Long Term Memory ◽  
Volume Loading ◽  
Ventricular Systolic Pressure ◽  
Length Relationship ◽  
Heart Preparation

In intact hearts the beat-to-beat left ventricular systolic pressure-length relationship is not uniquely defined, but rather is history dependent and appears hysteretic. The purpose of these studies was to assess the time course of this phenomenon. In an open chest swine heart preparation, left ventricular pressure, regional lengths, and wall thickness were measured. Loading conditions were altered by the infusion of volume into the left ventricle to increase peak systolic pressure approximately 30 mmHg. The resultant interbeat systolic pressure-dimension relationships were hysteretic. The first part of the study (n = 13) was to test whether the myocardium exhibited a long-term memory of prior mechanical events. Measurements obtained 30 and 120 s after volume loading revealed no residual differences in pressure or dimension compared with preinjection values. Thus the phenomenon was transient and complete (reversible) by 30 s. To better characterize this event, the temporal effects of myocardial loading were studied (n = 8). A randomized comparison of two different rates of volume infusions (27 +/- 2 vs. 56 +/- 2 ml/s, P less than 0.001) was performed. Varying the volume loading resulted in similar increases in peak left ventricular pressure (35 +/- 3 vs. 31 +/- 3 mmHg) but at different increments of development, i.e., greater than 5-7 cardiac cycles at the slower rate of volume infusion vs. greater than 2-3 cardiac cycles (P less than 0.001) at the faster rate. The isochronal systolic pressure-dimension relationships were quantitated by measuring the area of the hysteretic relationship and its slope.(ABSTRACT TRUNCATED AT 250 WORDS)

Reflex cardiovascular depression induced by capsaicin injection into canine liver

1982 ◽  
Vol 242 (6) ◽  
pp. H955-H960
Author(s):  
J. H. Ashton ◽  
G. A. Iwamoto ◽  
J. C. Longhurst ◽  
J. H. Mitchell
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Afferent Fiber ◽  
Pressure Rise ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Ventricular Systolic Pressure ◽  
Cardiovascular Depression

Capsaicin was injected into the portal circulation of 29 dogs after a blood delay pathway was constructed between the liver and right heart, through which capsaicin-contaminated blood could be replaced while systemic hemodynamics were maintained constant. Capsaicin (500 micrograms) rapidly decreased left ventricular systolic pressure (-10%), mean arterial pressure (-12%), heart rate (-4%), renal vascular resistance (-7%), maximal rate of left ventricular pressure rise (dP/dtmax) (-12%), and dP/dt at 25 mmHg developed left ventricular pressure (-15%) in animals with paced hearts. Left ventricular end-diastolic pressure did not change. Vagus nerve interruption at the level of the diaphragm did not alter hemodynamic changes occurring during capsaicin injections, but anterior hepatic nerve interruption eliminated the changes, suggesting that the cardiovascular responses were reflex in origin and that the principal afferent pathway traverses the hepatic nerve. This study demonstrates that activation of afferent fiber receptors within the liver tissue can contribute to neural regulation of the cardiovascular system, but the natural stimulus for these receptors is not known.

Varying elastance concept may explain coronary systolic flow impediment

1989 ◽  
Vol 257 (5) ◽  
pp. H1471-H1479 ◽  
Author(s):  
R. Krams ◽  
P. Sipkema ◽  
N. Westerhof
Keyword(s):  
Coronary Flow ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Time Varying ◽  
Ventricular Systolic Pressure ◽  
Low Load ◽  
Left Ventricular Systolic Pressure ◽  
Vascular Compartment

We measured phasic arterial coronary inflow in the blood-perfused isolated cat heart (n = 5) with a balloon in the left ventricle under well-defined conditions, i.e., constant perfusion pressure, constant vasomotor tone (maximal vasodilation), and heart rate. The normalized amplitude (A) between systolic flow (Fs) and diastolic flow (Fd) [A = (Fd - Fs)/Fd] was related to systolic left ventricular pressure (Ps, range 1.6-17 kPa, 1 kPa = 7.5 mmHg) for different isovolumic beats obtained by changes in balloon volume and for low load isobarically ejecting beats (pressure 0.2 kPa). The data were fitted to A = a + bPs with a = 0.70 +/- 0.15 (SD) and b = 0.005 +/- 0.005 kPa-1. This relation indicates a very weak effect of left ventricular systolic pressure on normalized flow amplitude. Thus the hypothesis that left ventricular pressure is the sole determinant impeding coronary flow could not be confirmed. However, our data could be explained on basis of the time-varying elastance concept (H. Suga, K. Sagawa, and A. A. Shoukas. Circ. Res. 32: 314-322, 1973). The intravascular and luminal (cavity) compartments both are assumed to be subject to a time-varying elastance. The time-varying luminal elastance is similar for isovolumic and isobaric beats. We assume that the elastance of the vascular compartment also behaves the same for these beats, and therefore coronary flow is affected similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jingtao Na ◽  
Haifeng Jin ◽  
Xin Wang ◽  
Kan Huang ◽  
Shuang Sun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Expression Patterns ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Luciferase Reporter ◽  
Left Ventricular Ejection ◽  
Tunel Staining ◽  
Ventricular Ejection Fraction

Abstract Background Heart failure (HF) is a clinical syndrome characterized by left ventricular dysfunction or elevated intracardiac pressures. Research supports that microRNAs (miRs) participate in HF by regulating  targeted genes. Hence, the current study set out to study the role of HDAC3-medaited miR-18a in HF by targeting ADRB3. Methods Firstly, HF mouse models were established by ligation of the left coronary artery at the lower edge of the left atrial appendage, and HF cell models were generated in the cardiomyocytes, followed by ectopic expression and silencing experiments. Numerous parameters including left ventricular posterior wall dimension (LVPWD), interventricular septal dimension (IVSD), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LEVDP), heart rate (HR), left ventricular pressure rise rate (+ dp/dt) and left ventricular pressure drop rate (-dp/dt) were measured in the mice. In addition, apoptosis in the mice was detected by means of TUNEL staining, while RT-qPCR and Western blot analysis were performed to detect miR-18a, HDAC3, ADRB3, cMyb, MMP-9, Collagen 1 and TGF-β1 expression patterns. Dual luciferase reporter assay validated the targeting relationship between ADRB3 and miR-18a. Cardiomyocyte apoptosis was determined by means of flow cytometry. Results HDAC3 and ADRB3 were up-regulated and miR-18a was down-regulated in HF mice and cardiomyocytes. In addition, HDAC3 could reduce the miR-18a expression, and ADRB3 was negatively-targeted by miR-18a. After down-regulation of HDAC3 or ADRB3 or over-expression of miR-18a, IVSD, LVEDD, LVESD and LEVDP were found to be decreased but LVPWD, LVEF, LVFS, LVSP, + dp/dt, and −dp/dt were all increased in the HF mice, whereas fibrosis, hypertrophy and apoptosis of HF cardiomyocytes were declined. Conclusion Collectively, our findings indicate that HDAC3 silencing confers protection against HF by inhibiting miR-18a-targeted ADRB3.

Role of reflexes following myocardial necrobiosis

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
Author(s):  
G. Ascanio ◽  
F. Barrera ◽  
E. V. Lautsch ◽  
M. J. Oppenheimer
Keyword(s):  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Hemodynamic Changes ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood ◽  
Bilateral Vagotomy ◽  
Left Ventricular Systolic Pressure

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.

Effects of alpha-adrenergic blockade on cardiovascular responses to static exercise in cats

1986 ◽  
Vol 250 (1) ◽  
pp. R1-R4
Author(s):  
T. G. Waldrop ◽  
M. Bielecki ◽  
W. J. Gonyea ◽  
J. H. Mitchell
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Static Exercise ◽  
Ventricular Systolic Pressure ◽  
Pressure Transducers ◽  
Adrenergic Mechanism ◽  
Alpha Blockade

Static exercise performed by conscious cats elicits increases in heart rate (HR), left ventricular systolic pressure (LVSP), and the maximal rate of left ventricular pressure development [LV(dP/dt)max]. The increased HR is mediated primarily by withdrawal of parasympathetic tone, whereas a beta-adrenergic mechanism is responsible for the LV(dP/dt)max increase. In the present study the cardiovascular responses to static exercise in awake cats was recorded before and after alpha-adrenergic blockade. Pressure transducers were implanted into the left ventricle of cats who had been trained operantly to perform static exercise. Significant increases in LVSP, LV(dP/dt)max and HR occurred in all cats during static exercise before blockade. In contrast, alpha-adrenergic blockade (phentolamine, 2.5 mg/kg iv) abolished the exercise-induced increase in LVSP but did not prevent increases in HR and LV(dP/dt)max. The cats performed fewer exercise bouts per day during alpha-blockade than when unblocked. We conclude that an alpha-adrenergic mechanism mediates the increase in LVSP in response to static exercise in conscious cats.

Stability of cardiodynamic and some blood parameters in the baboon following intravenous anaesthesia with ketamine and diazepam

1998 ◽  
Vol 69 (1) ◽  
Author(s):  
W.J. Du Plooy ◽  
P.J. Schutte ◽  
J. Still ◽  
L. Hay ◽  
C.P. Kahler
Keyword(s):  
Blood Pressure ◽  
Continuous Infusion ◽  
Total Duration ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Blood Parameters ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Pressure Curve ◽  
Arterial Blood

The stability of cardiodynamic and some blood parameters during a slow, continuous infusion of a combination of ketamine and diazepam is reported. Contractility (dP/dt), myocardial relaxation (Tln), left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), arterial blood pressure and certain blood parameters were assessed in 3 male and 3 female juvenile baboons (Papio ursinus). Anaesthesia was induced with 15 mg/kg ketamine IM and maintained with a continuous IV infusion (40-60 mℓ/h) of ketamine and diazepam. The mixture consisted of 2 mℓ ketamine (100 mg/mℓ), 2 mℓ diazepam (5 mg/mℓ) and 50 mℓ saline. A period of 75 + 10 min was allowed for preparation of the animals, after which lead II of the ECG, femoral artery blood pressure and left ventricular pressure were recorded at 15-min intervals for a period of 2 h: the total duration of anaesthesia was 195 min. Arterial blood samples were analysed at 30-min intervals for blood gases, electrolytes, glucose and insulin. Left ventricular parameters were derived from the left ventricular pressure curve. Tln, LVSP and LVEDP showed small fluctuations. Contractility decreased (p < 0.037) at the 195-min interval. No arrhythmias or ECG changes were seen, while blood pressure decreased gradually. Serum calcium concentration decreased and blood glucose levels increased gradually over time. Anaesthesia and analgesia were sufficient and no other drugs were necessary. The animals appeared sedated and dazed 60-80 min after the procedure. A continuous infusion of a combination of ketamine and diazepam for a duration of 150 min can provide stable anaesthesia for cardiodynamic measurements.

Systolic pressure gradients across the aortic valve and in the ascending aorta

1965 ◽  
Vol 209 (3) ◽  
pp. 557-563 ◽  
Author(s):  
Thomas E. Driscol ◽  
Richard W. Eckstein
Keyword(s):  
Aortic Valve ◽  
Pressure Gradient ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximum Pressure ◽  
Early Systole ◽  
Systolic Pressure Gradient

Left ventricular and aortic pressure pulses and the pressure gradient across the aortic valve were recorded in anesthetized and unanesthetized dogs. Aortic pressure recorded immediately above the valve increased 5–15 msec before it was exceeded by left ventricular pressure. The maximum systolic pressure gradient occurred in early systole and remained positive throughout the ejection period. When aortic pressure was recorded 1–3 cm distal to the valve, these pressure pulse relationships were altered so that 1) the rise in aortic pressure was delayed, 2) the early systolic maximum pressure gradient was increased, and 3) aortic pressure exceeded ventricular pressure during the latter half of systole. The changes in early systole are due to a delay in the pulse wave reaching the more distal recording site. The mean systolic pressure gradient between two sites within the ascend-ing aorta was found to be negative, i.e., opposite to the direction of forward flow. The negative pressure gradient probably accounts for the reversal of the transvalvular pressure gradient in late systole when aortic pressure was recorded distal to the valve.

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