Redistribution in left ventricular regional flow following acute right ventricular pressure overload

1978 ◽  
Vol 56 (2) ◽  
pp. 185-190 ◽  
Author(s):  
Francois Sestier ◽  
Richard R. Mildenberger ◽  
Gerald A. Klassen
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Coronary Flow ◽  
Fold Increase ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Left Ventricular Myocardium ◽  
Regional Flow ◽  
Acute Pulmonary Hypertension

The left ventricular dysfunction following acute pulmonary hypertension remains unexplained. We wondered if acute pulmonary hypertension could alter the transmural flow distribution within the left ventricular myocardium, independent of coronary flow and perfusion pressure. We used a canine preparation in which the left coronary system was perfused at constant flow and induced a two- to three-fold increase in pulmonary artery pressure by banding the pulmonary artery. Regional myocardial blood flow of the left coronary system was measured using radioactive microspheres, injected into the left coronary system before and after 10–30 min of banding of the pulmonary artery. The left ventricular subendocardial: epicardial ratio fell by 12 and 31% (p < 0.05) of control value, 10 and 30 min, respectively, after banding of the pulmonary artery, the total flow to the left coronary system being kept constant. Left atrial mean pressure increased from 2.9 ± 2.4 to 3.6 ± 1.9 and 6.0 ± 2.1 (p < 0.05) following banding. The mechanism of the redistribution of coronary flow may relate to inappropriate vasodilation of the right septal myocardium with consequent relative left ventricular subendocardial hypoperfusion which might aggravate left ventricular ischemia in the presence of hypotension and hypoxia.

Measurement of myocardial PCO2 with a microelectrode: its relation to coronary sinus PCO2

1979 ◽  
Vol 236 (1) ◽  
pp. H29-H34
Author(s):  
R. B. Case ◽  
A. Felix ◽  
M. Wachter
Keyword(s):  
Coronary Sinus ◽  
Coronary Flow ◽  
Coronary Occlusion ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Co2 Efflux ◽  
Arterial Pco2 ◽  
Pco2 Electrode ◽  
The Difference

A micro-PCO2 electrode, with dimensions of 1 x 10 mm, and a 63% response time of 14 s was inserted into the left ventricular myocardium of the pentobarbital-anesthetized dog. Continuous recordings were made of myocardial PCO2 (PmCO2), arterial PCO2 (PaCO2), and coronary sinus PCO2 (CSPCO2) during variation of respiratory rate. PmCO2 and CSPCO2 were compared at varying coronary flow. PmCO2 was similar to and closely followed changes in CSPCO2. The difference between PmCO2 and CSPCO2 was -0.52 +/- 3.63 (SD) mmHg, and PmCO2 exceeded PaCO2 by 20.69 +/- 5.12 mmHg. After coronary occlusion, PmCO2, rose promptly, but CSPCO2 was only slightly elevated until the occlusion was released, when a CO2 efflux into the coronary sinus occurred. It is concluded that the electrode measures extracellular PCO2 and that extracellular and myocardial PCO2 are essentially equal. PmCO2 rises rapidly following coronary occlusion.

Left ventricular heat production measured by coronary flow and temperature gradient

1961 ◽  
Vol 16 (5) ◽  
pp. 883-890 ◽  
Author(s):  
William A. Neill ◽  
Herbert J. Levine ◽  
Richard J. Wagman ◽  
Joseph V. Messer ◽  
Norman Krasnow ◽  
...  
Keyword(s):  
Temperature Gradient ◽  
Flow Rate ◽  
Heat Production ◽  
Coronary Flow ◽  
Coronary Circulation ◽  
Heat Removal ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Coronary Perfusion

The study of energetics of the left ventricular myocardium, normally based on its oxygen consumption and mechanical work performance, can be extended by determining its heat production as well. By considering all forms of energy input and output of the left ventricle, calculations were made of left ventricular net heat production under a variety of hemodynamic conditions. One of the mechanisms for removal of the heat produced is provided by the coronary blood, which is warmed in transit through the myocardium. Direct measurements of the rate of heat removal by the coronary circulation were made from coronary flow rate and veno-arterial temperature gradient. The fraction of left ventricular net heat production which is removed by the coronary perfusion is proportional to coronary flow rate. The fraction at a given flow rate is sufficiently reproducible to permit estimation of total heat produced from the portion measured in the coronary circulation. Certain of the theoretical applications of heat data may require more accuracy than appears feasible by this method. Which of the applications discussed will prove practical remains to be determined. Submitted on February 13, 1961

Cardiac microdialysis to estimate interstitial adenosine and coronary blood flow

1990 ◽  
Vol 258 (6) ◽  
pp. H1642-H1649 ◽  
Author(s):  
D. G. Van Wylen ◽  
J. Willis ◽  
J. Sodhi ◽  
R. J. Weiss ◽  
R. D. Lasley ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow ◽  
Fold Increase ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Simultaneous Estimation ◽  
Microdialysis Probe ◽  
Regional Myocardial Ischemia

The purpose of this study was twofold: 1) to investigate the feasibility and usefulness of cardiac microdialysis for the simultaneous estimation of regional cardiac interstitial fluid (ISF) adenosine (ADO) concentration and coronary blood flow (CBF); and 2) to determine the changes in the ISF levels of ADO and CBF during cardiac stimulation or regional myocardial ischemia. Cardiac microdialysis probes were implanted in the left ventricular myocardium of chloralose-urethan-anesthetized dogs and perfused with Krebs-Henseleit buffer. The concentration of ADO in the effluent dialysate was used as an index of intramyocardial ISF ADO concentration while local CBF was measured by H2 clearance via a platinum wire within the dialysis fiber. Dialysate ADO was elevated immediately after insertion of the microdialysis probe, declined rapidly in the first 20 min, stabilized by 60 min, and remained constant for 2 h. Based on the relationship in vitro and in vivo between microdialysis probe perfusion rate and dialysate ADO concentration, ISF ADO concentration within the left ventricular myocardium was estimated to be 0.9-1.3 microM. Dobutamine (10 micrograms.kg-1.min-1) infusion resulted in a 36% increase in CBF and a 2.5-fold increase in dialysate ADO (n = 9; P less than 0.05). Regional myocardial ischemia, induced by occlusion of the left anterior descending artery (LAD), caused a 13-fold increase in dialysate ADO in the LAD perfused myocardium (n = 9; P less than 0.05). These results are consistent with the ADO hypothesis and suggest that cardiac microdialysis provides a reliable technique for the sampling of regional intramyocardial ISF.

Severe pulmonary hypertension secondary to a parachute-like mitral valve, with the left superior caval vein draining into the coronary sinus, in a girl with Turner's syndrome

2003 ◽  
Vol 13 (4) ◽  
pp. 364-366 ◽  
Author(s):  
Marc van Heerde ◽  
Jaroslav Hruda ◽  
Mark G. Hazekamp
Keyword(s):  
Pulmonary Hypertension ◽  
Mitral Valve ◽  
Coronary Sinus ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Turner's Syndrome ◽  
Turner’S Syndrome ◽  
Caval Vein ◽  
Superior Caval Vein

A 17-year-old girl with Turner's syndrome underwent two cardiac operations due to severe mitral stenosis with pulmonary hypertension, caused by a parachute-like mitral valve. The anomaly was associated with persistence of the left superior caval vein, which drained to the coronary sinus, and non-compaction of the left ventricular myocardium. The association of these lesions is rare in patients with Turner's syndrome.

Opening the pericardium during pulmonary artery constriction improves cardiac function

2004 ◽  
Vol 96 (3) ◽  
pp. 917-922 ◽  
Author(s):  
Israel Belenkie ◽  
Rozsa Sas ◽  
Jamie Mitchell ◽  
Eldon R. Smith ◽  
John V. Tyberg
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Anesthetized Dogs ◽  
Acute Pulmonary Hypertension ◽  
The Right ◽  
Pulmonary Artery Constriction

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.

scholarly journals Intracardiac hemodynamics, infarct-limiting effects and myocardial expression of microRNA 223 after necroptosis inhibition in a rat model of heterotopic allogeneic heart transplantation

2019 ◽  
Vol 24 (6) ◽  
pp. 710-715
Author(s):  
Yu. V. Dmitriev ◽  
L. V. Vasina ◽  
M. M. Galagudza
Keyword(s):  
Infarct Size ◽  
Coronary Flow ◽  
Troponin I ◽  
Myocardial Infarct ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Control Group ◽  
Left Ventricular Myocardium ◽  
Myocardial Infarct Size ◽  
Intraventricular Pressure

Objective.To investigate the effect of necroptosis inhibition on the morphofunctional state of the myocardium and the expression of microRNA 223 after heterotopic allogeneic heart transplantation in rat.Design and methods. Twenty Wistar rats were examined in the study. Animals were divided into the following groups: 1) control (n = 7), 2) dimethyl sulfoxide (DMSO) (n = 6), 3) necrostatin-1s (n = 7). Necrostatin-1s was used as an inhibitor of necroptosis, which was administered intraperitoneally in DMSO solution 1 hour before the start of the experiment at a dose of 1,65 mg/kg. HTK solution cooled to 4 °C was used as a preservation solution. Two hours after heart arrest, the heart was heterotopically transplanted in the abdominal cavity of recipient rat using the scheme “aorta-aorta, pulmonary trunc-posterior vena cava”. Three hours later, intracardiac hemodynamics was assessed by recording the pressure in the left ventricle, heart rate and coronary flow rate in Langendorff-perfused heart. The expression level of microRNA 223–5p and –3p in left ventricular myocardium was assessed using real-time polymerase chain reaction. The plasma levels of troponin I were assessed by enzyme immunoassay. Myocardial infarct size was measured planimetrically at the end of the experiment by staining myocardium with triphenyltetrazolium chloride.Results. Inhibition of necroptosis significantly improved the morphofunctional state of the myocardium, which manifested in a decrease of myocardial infarct size in the necrostatin-1s group compared with the control group and DMSO group. Thus, in the necrostatin-1s group, myocardial infarct size was 25 ± 8,7 %, which was smaller than in the control and DMSO groups (56 ± 9,5 and 57 ± 8,7 %, respectively; p < 0,05). Also in the necrostatin-1s group, lower diastolic intraventricular pressure was recorded, as well as higher values of pulse intraventricular pressure and coronary flow rate than in control group and DMSO group (p < 0,05). Left ventricular myocardium in the necrostatin-1s group demonstrated higher expression of the antinecroptotic miRNA 223–5p and –3p as compared with the control and DMSO groups, as well as lower plasma levels of troponin I (p < 0,05).Conclusions.Pharmacological inhibition of necroptosis in heterotopically transplanted donor heart is accompanied by marked cardioprotective effects and increases the expression of antinecroptotic microRNA 223–5p and –3p. 

scholarly journals Effects of Telmisartan on Myocardial Protein Profiles in Hypertensive Rats

2021 ◽  
Vol 34 (3) ◽  
pp. 299-299
Author(s):  
Yu Feng ◽  
Man-li Zhou ◽  
Jian-zhang Wang ◽  
Jia-qi Zhang ◽  
Shu-le Qian ◽  
...  
Keyword(s):  
Heat Shock ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Sterile Water ◽  
Protein Profiles ◽  
Related Protein ◽  
Hypertensive Rats ◽  
Treatment Groups ◽  
Proteasome 26S

Abstract Background To investigate the effects of telmisartan on the protein profiles of the left ventricular myocardium in spontaneously hypertensive rats (SHR). Methods Sixteen SHR were randomly divided into control and telmisartan treatment groups. Rats were treated with sterile water (10 ml/kg) or telmisartan (4.33 mg/kg) by gavage for 12 weeks. Wistar-Kyoto (WKY) rats treated with sterile water (10 ml/kg) as controls. At the end of 12 weeks of control or telmisartan treatment, rats were sacrificed, and hearts were collected for protein preparations, isotope labeling, and mass spectrometric analysis. Results In total, there were 23 differentially expressed proteins in the left ventricular myocardium between control and telmisartan treatment groups in SHR. Compared with the telmisartan group, the upregulated proteins in the SHR were dual-specificity mitogen-activated protein kinase kinase 3-like, transgelin, and haptoglobin subtype 2. The downregulated proteins in the SHR were as follows: von Willebrand factor (fragment), kininogen 1, small ribonucleoprotein-related protein, fibrinogen beta chain, protein mass 3 (fragment), proteasome 26s, heat shock protein 27-related protein 1, tenascin X, fibronectin subtype 2, transferrin receptor protein, platelets 1, cathepsin L1, complement factor B, isoform CRA_b, fibrinogen isomer, immunoglobulin heavy chain (γ polypeptide), and α 1 antiprotease. Conclusions Telmisartan differentially regulates myocardial protein expression in hypertensive rats including heat shock protein 27, fibrinogen, fibronectin, proteasome 26s and transgelin, as well as proteins in biochemical, metabolic, and signal transduction pathways. These changes in protein expression may contribute to the antihypertrophic effects of telmisartan in hypertension.

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