Nitric oxide modulates cardiac performance in the heart of Anguilla anguilla

2001 ◽  
Vol 204 (10) ◽  
pp. 1719-1727 ◽  
Author(s):  
S. Imbrogno ◽  
L. De Iuri ◽  
R. Mazza ◽  
B. Tota
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Anguilla Anguilla ◽  
Cardiac Performance ◽  
Stroke Work ◽  
Nos Inhibitors ◽  
Cgmp Pathway ◽  
Triton X ◽  
Endocardial Endothelium

Nothing is known about the effects of nitric oxide (NO) on cardiac performance in fish. Using an in vitro working heart preparation that generates physiological values of output pressure, cardiac output and ventricular work and power, we assessed the effects of NO on the cardiac performance of the eel Anguilla anguilla. We examined basal cardiac performance (at constant preload, afterload and heart rate), the effects of cholinergic stimulation and the Frank-Starling response (preload-induced increases in cardiac output at constant afterload and heart rate). The NO synthase (NOS) inhibitors N(G)-monomethyl-l-arginine (l-NMMA) and l-N(5)(1-iminoethyl)ornithine (l-NIO), the guanylate cyclase inhibitor 1H-(1,2,4)oxadiazolo-(4,3-a)quinoxalin-1-one (ODQ) and Triton X-100, a detergent that damages the endocardial endothelium, all increased stroke volume (V(S)) and stroke work (W(S)). In contrast, the endogenous NOS substrate l-arginine, tested before and after treatment with haemoglobin, the NO donor 3-morpholinosydnonimine, tested with and without the superoxide scavenger superoxide dismutase, and the stable cGMP analogue 8-bromoguanosine 3′,5′-cyclic monophosphate (8-Br-cGMP) decreased V(S) and W(S). Acetylcholine chloride produced a biphasic effect. At nanomolar concentrations, in 34 % of the preparations, it induced a NO-cGMP-dependent positive inotropism that required the integrity of the endocardial endothelium. Pretreatment with Triton X-100 or with NO-cGMP pathway inhibitors (l-NMMA, l-NIO, N(G)-nitro-l-arginine methyl ester, Methylene Blue and ODQ) abolished the positive effect of acetylcholine. In contrast, at micromolar concentrations, acetylcholine produced a negative effect that involved neither the endocardial endothelium nor the NO-cGMP pathway. Pre-treatment with l-arginine (10(−)(6)mol l(−)(1)) was without effect, whereas l-NIO (10(−)(5)mol l(−)(1)) significantly reduced the Frank-Starling response. Taken together, these three experimental approaches provide evidence that NO modulates cardiac performance in the eel heart.

scholarly journals Endocardial endothelium in the avascular heart of the frog: morphology and role of nitric oxide.

1997 ◽  
Vol 200 (24) ◽  
pp. 3109-3118 ◽  
Author(s):  
S U Sys ◽  
D Pellegrino ◽  
R Mazza ◽  
A Gattuso ◽  
L J Andries ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Stroke Volume ◽  
Systolic Function ◽  
Rana Esculenta ◽  
Confocal Scanning Laser Microscopy ◽  
Stroke Work ◽  
Ventricular Performance ◽  
Cgmp Pathway ◽  
Endocardial Endothelium

Endocardial endothelial morphology and the physiological modulatory role of nitric oxide (NO) were studied in an in vitro preparation of the working intact heart of the frog Rana esculenta, which lacks coronary vasculature and is thus devoid of a coronary vascular endothelium. En face confocal scanning laser microscopy of samples of perfused fixed hearts demonstrated the presence of NO synthase as a cytoplasmic constituent of the endocardial endothelial cells. Stroke volume (as a measure of performance in paced frog hearts) and stroke work (as an index of systolic function) increased by approximately 5 % after inhibition of the NO-cGMP pathway with 10(-4 )mol l-1 NG-nitro-l-arginine methyl ester and by approximately 8 % after inhibition with 10(-6 )mol l-1 Methylene Blue. In contrast, stroke volume and stroke work decreased by approximately 22 % after activation of the NO-cGMP pathway with sodium nitroprusside (10(-4 )mol l-1), while 3-morpholinosydnonimine (5x10(-8) to 10(-5 )mol l-1) caused a decrease of between 15 and 30 % and 8-bromo-cGMP (10(-6 )mol l-1) a decrease of approximately 8 %. These responses were significantly attenuated after exposure of the ventricular luminal to Triton X-100 (0.05 %, 0.1 ml), which itself increased performance (by over 10 %) without detectable morphological changes. These results show that the endocardial endothelium of Rana esculenta produces amounts of NO sufficient to modulate ventricular performance.

Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?

2001 ◽  
Vol 281 (5) ◽  
pp. R1624-R1632 ◽  
Author(s):  
Virginia L. Brooks ◽  
Kathy A. Clow ◽  
Lisa S. Welch ◽  
George D. Giraud
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Mesenteric Artery ◽  
Vascular Tone ◽  
Ascending Aorta ◽  
No Production ◽  
Vascular Conductance ◽  
Vascular Beds ◽  
Conscious Rabbits

Pregnancy produces marked systemic vasodilation, but the mechanism is unknown. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased vascular conductance, but that the contribution varies among vascular beds. Rabbits were instrumented with aortic and vena caval catheters and ultrasonic flow probes implanted around the ascending aorta, superior mesenteric artery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intravenous injection of N ω-nitro-l-arginine (l-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first before pregnancy (NP) and then at the end of gestation (P). l-NA produced similar increases in arterial pressure between groups, but the following responses were larger ( P < 0.05) when the rabbits were pregnant: 1) decreases in total peripheral conductance [−3.7 ± 0.3 (NP), −5.0 ± 0.5 (P) ml · min−1 · mmHg−1], 2) decreases in mesenteric conductance [−0.47 ± 0.05 (NP), −0.63 ± 0.07 (P) ml · min−1 · mmHg−1], 3) decreases in terminal aortic conductance [−0.43 ± 0.05 (NP), −0.95 ± 0.19 ml · min−1 · mmHg−1 (P)], and 4) decreases in heart rate [−41 ± 4 (NP), −62 ± 5 beats/min (P)]. Nevertheless, total peripheral and terminal aortic conductances remained elevated in the pregnant rabbits ( P < 0.05) after l-NA. Furthermore, decreases in cardiac output and femoral conductance were not different between the reproductive states. We conclude that the contribution of NO to vascular tone increases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate. Finally, unknown factors in addition to NO must also underlie the basal vasodilation observed during pregnancy.

L-NAME antagonizes vasopressin V2-induced vasodilatation in dogs

1994 ◽  
Vol 266 (1) ◽  
pp. H99-H106 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Endothelial Cells ◽  
Cardiac Output ◽  
Arginine Vasopressin ◽  
Electromagnetic Flowmeter ◽  
Hemodynamic Effects ◽  
Blood Pressure Responses ◽  
Chronically Instrumented Dogs

Experiments were performed in conscious chronically instrumented dogs to study the mechanism of hemodynamic effects mediated by selective vasopressin V2 agonists. In one group of dogs (n = 5) instrumented for the measurement of arterial pressure and cardiac output (electromagnetic flowmeter), the infusion of NG-nitro-L-arginine methyl ester (L-NAME; 20 or 40 micrograms.kg-1 x min-1) prevented or significantly inhibited the increase in cardiac output, heart rate and systemic conductance induced by injections of 1-desamino-8-D-arginine vasopressin (DDAVP, desmopressin) and 4-valine-8-D-arginine vasopressin (VDAVP), two selective V2 agonists. L-NAME infusion did not modify the aortic adenosine 3',5'-cyclic monophosphate increase induced by DDAVP infusion. In a second group of dogs similarly prepared (n = 4), the administration of L-arginine (10 mg.kg-1 x min-1) at the same time as that of L-NAME (20 micrograms.kg-1 x min-1) completely prevented the hemodynamic effects of L-NAME and restored the response to DDAVP administration. In a third group of dogs (n = 4), the infusion of a bradykinin B2 antagonist, at a rate that significantly inhibited the cardiac output, heart rate, and blood pressure responses to bradykinin, did not modify the hemodynamic response to DDAVP infusion. We conclude that the hemodynamic effects of selective V2 agonists in dogs are not mediated by bradykinin release but instead via a V2-like receptor on endothelial cells that triggers the release of nitric oxide.

Differential role of nitric oxide in regional sympathetic responses to stimulation of NTS A2a adenosine receptors

2005 ◽  
Vol 288 (2) ◽  
pp. H638-H649 ◽  
Author(s):  
Tadeusz J. Scislo ◽  
Nobusuke Tan ◽  
Donal S. O'Leary
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Neural Responses ◽  
No Donors ◽  
A2a Adenosine Receptors ◽  
Cgs 21680 ◽  
Nos Inhibitors ◽  
Sympathetic Responses ◽  
Deta Nonoate ◽  
Stimulation Of

Our previous studies showed that preganglionic adrenal (pre-ASNA), renal (RSNA), lumbar, and postganglionic adrenal sympathetic nerve activities (post-ASNA) are inhibited after stimulation of arterial baroreceptors, nucleus of the solitary tract (NTS), and glutamatergic and P2x receptors and are activated after stimulation of adenosine A1 receptors. However, stimulation of adenosine A2a receptors inhibited RSNA and post-ASNA, whereas it activated pre-ASNA. Because the effects evoked by NTS A2a receptors may be mediated via activation of nitric oxide (NO) mechanisms in NTS neurons, we tested the hypothesis that NO synthase (NOS) inhibitors would attenuate regional sympathetic responses to NTS A2a receptor stimulation, whereas NO donors would evoke contrasting responses from pre-ASNA versus RSNA and post-ASNA. Therefore, in chloralose/urethane-anesthetized rats, we compared hemodynamic and regional sympathetic responses to microinjections of selective A2a receptor agonist (CGS-21680, 20 pmol/50 nl) after pretreatment with NOS inhibitors Nω-nitro-l-arginine methyl ester (10 nmol/100 nl) and 1-[2-(trifluoromethyl)phenyl]imidazole (100 pmol/100 nl) versus pretreatment with vehicle (100 nl). In addition, responses to microinjections into the NTS of different NO donors [40 and 400 pmol/50 nl sodium nitroprusside (SNP); 0.5 and 5 nmol/50 nl 3,3-bis(aminoethyl)-1-hydroxy-2-oxo-1-triazene (DETA NONOate, also known as NOC-18), and 2 nmol/50 nl 3-(2-hydroxy-2-nitroso-1-propylhydrazino)-1-propanamine (PAPA NONOate, also known as NOC-15)], the NO precursor l-arginine (10–50 nmol/50 nl), and sodium glutamate (500 pmol/50 nl) were evaluated. SNP, DETA NONOate, and PAPA NONOate activated pre-ASNA and inhibited RSNA and post-ASNA, whereas l-arginine and glutamate microinjected into the same site of the NTS inhibited all these sympathetic outputs. Decreases in heart rate and depressor or biphasic responses accompanied the neural responses. Pretreatment with NOS inhibitors reversed the normal depressor and sympathoinhibitory responses to stimulation of NTS A2a receptors into pressor and sympathoactivatory responses and attenuated the heart rate decreases; however, it did not change the increases in pre-ASNA. We conclude that NTS NO mechanisms differentially affect regional sympathetic outputs and differentially contribute to the pattern of regional sympathetic responses evoked by stimulation of NTS A2a receptors.

Cardiac performance in semi-isolated heart of the crab Carcinus maenas

1994 ◽  
Vol 266 (3) ◽  
pp. R781-R789
Author(s):  
J. L. Wilkens ◽  
B. R. McMahon
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Isolated Heart ◽  
Carcinus Maenas ◽  
Ventricular Volume ◽  
Whole Body ◽  
Shore Crab ◽  
Stroke Work ◽  
Adaptive Responses

A semi-isolated, in situ heart preparation of the shore crab, Carcinus maenas, supported by its alary ligaments, pumps vigorously for hours at a mean heart rate of 49.7 beats/min and cardiac output of 30 ml.kg-1.min-1. These hearts show no adaptive responses to changes in pericardial sinus pressure, outflow resistance, or afterload. Direct perfusion-induced stretch of the heart wall causes increases in contractile force but minimal changes in heart rate. Stroke work and power are lower than comparable values for animals with myogenic hearts and closed circulatory systems. The values for heart rate and cardiac output are lower than in vivo values and may in part reflect the technique used as well as intrinsic performance of the heart without neural and neurohormonal inputs. Morphometrically the heart represents 0.2% of whole body weight, and the mean stroke volume of 0.35-0.45 ml/kg represents an ejection fraction of 27-34% of ventricular volume (1.4 ml/kg).

Cardiac performance: optimal heart rate for maximal cardiac output

1979 ◽  
Vol 39 (1) ◽  
pp. 79-85 ◽  
Author(s):  
Arnfinn Ilebekk ◽  
MÅLfrid Molaug Miller ◽  
JØRgen Thorvaldson ◽  
Fredrik Kiil
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiac Performance ◽  
Maximal Cardiac Output

Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling

2007 ◽  
Vol 293 (5) ◽  
pp. H3140-H3149 ◽  
Author(s):  
Steven N. Mink ◽  
Zhao-Qin Cheng ◽  
Ratna Bose ◽  
Hans Jacobs ◽  
Krika Kasian ◽  
...  
Keyword(s):  
G Protein ◽  
Inhibitory Effect ◽  
G Protein Signaling ◽  
Protein Signaling ◽  
Parasympathetic Nerves ◽  
Adrenergic Response ◽  
Nos Inhibitors ◽  
Inhibitory G Protein ◽  
Triton X ◽  
Endocardial Endothelium

We previously showed that lysozyme (Lzm-S), derived from leukocytes, caused myocardial depression in canine sepsis by binding to the endocardial endothelium to release nitric oxide (NO). NO then diffuses to adjacent myocytes to activate the cGMP pathway. In a canine right ventricular trabecular (RVT) preparation, Lzm-S also decreased the inotropic response to field stimulation (FSR) during which the sympathetic and parasympathetic nerves were simulated to measure the adrenergic response. In the present study, we determined whether the pathway by which Lzm-S decreased FSR was different from the pathway by which Lzm-S reduced steady-state (SS) contraction. Furthermore, we determined whether the decrease in FSR was due to a decrease in sympathetic stimulation or enhanced parasympathetic signaling. In the RVT preparation, we found that the inhibitory effect of Lzm-S on FSR was prevented by NO synthase (NOS) inhibitors. A cGMP inhibitor also blocked the depressant activity of Lzm-S. However, in contrast to the Lzm-S-induced decline in SS contraction, chemical removal of the endocardial endothelium by Triton X-100 to eliminate endothelial NO release did not prevent the decrease in FSR. An inhibitory G protein was involved in the effect of Lzm-S, since FSR could be restored by treatment with pertussis toxin. Atropine prevented the Lzm-S-induced decline in FSR, whereas β1- and β2-adrenoceptor function was not impaired by Lzm-S. These results indicate that the Lzm-S-induced decrease in FSR results from a nonendothelial release of NO. NO then acts through inhibitory G protein to enhance parasympathetic signaling.

Cardiac Output in the Large Cephalopod Octopus Dofleini

1965 ◽  
Vol 42 (3) ◽  
pp. 475-480
Author(s):  
KJELL JOHANSEN
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Work ◽  
Free Swimming ◽  
Blood Samples ◽  
Fick Principle ◽  
Arterial Blood ◽  
Percentage Saturation ◽  
Intravascular Catheters

The cardiac output in Octopus dofleini has been measured, making use of the Fick principle. The measurements were made on intact animals, resting or free-swimming, after previous chronic implantation of intravascular catheters for collection of blood samples. The respiratory exchange was measured with a specially designed respirometer. In addition to cardiac output the following parameters were measured or computed: oxygen consumption; oxygen tension, oxygen content and percentage saturation of venous and arterial blood; arterial pressure; heart rate; stroke volume and stroke work. A detailed discussion of the results obtained is limited by the lack of comparable information for other invertebrates.

scholarly journals Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure

2020 ◽  
Vol 319 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Joseph Mannozzi ◽  
Jasdeep Kaur ◽  
Marty D. Spranger ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Muscle Metaboreflex ◽  
Effective Arterial Elastance

Dynamic exercise elicits robust increases in sympathetic activity in part due to muscle metaboreflex activation (MMA), a pressor response triggered by activation of skeletal muscle afferents. MMA during dynamic exercise increases arterial pressure by increasing cardiac output via increases in heart rate, ventricular contractility, and central blood volume mobilization. In heart failure, ventricular function is compromised, and MMA elicits peripheral vasoconstriction. Ventricular-vascular coupling reflects the efficiency of energy transfer from the left ventricle to the systemic circulation and is calculated as the ratio of effective arterial elastance ( Ea) to left ventricular maximal elastance ( Emax). The effect of MMA on Ea in normal subjects is unknown. Furthermore, whether muscle metaboreflex control of Ea is altered in heart failure has not been investigated. We utilized two previously published methods of evaluating Ea [end-systolic pressure/stroke volume ( EaPV)] and [heart rate × vascular resistance ( EaZ)] during rest, mild treadmill exercise, and MMA (induced via partial reductions in hindlimb blood flow imposed during exercise) in chronically instrumented conscious canines before and after induction of heart failure via rapid ventricular pacing. In healthy animals, MMA elicits significant increases in effective arterial elastance and stroke work that likely maintains ventricular-vascular coupling. In heart failure, Ea is high, and MMA-induced increases are exaggerated, which further exacerbates the already uncoupled ventricular-vascular relationship, which likely contributes to the impaired ability to raise stroke work and cardiac output during exercise in heart failure.

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