Contamination of lymph from the major prenodal cardiac lymphatic in dogs

1999 ◽  
Vol 276 (5) ◽  
pp. H1795-H1800
Author(s):  
Hans J. Geissler ◽  
Karen L. Davis ◽  
Glen A. Laine ◽  
Michael L. Brennan ◽  
Uwe Mehlhorn ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Flow Rate ◽  
Lymphatic System ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Lymph Flow ◽  
Left Ventricular Myocardium ◽  
Anatomic Variations ◽  
Lymphatic Function

Cannulation of the canine major prenodal cardiac lymphatic (MPCL) is the most common approach for the investigation of myocardial lymphatic function. However, the assumption that the MPCL drains pure cardiac lymph has been questioned. We studied variations of MPCL anatomy and investigated whether noncardiac lymph is drained by this lymphatic. After dye was injected into the lungs and left ventricular myocardium in 21 dogs, dissection of the cardiac lymphatic system yielded 3 anatomic variations. In variations 1 and 2 (81% of dogs), a mixture of cardiac and pulmonary lymph was drained via the MPCL. In variation 3 (19% of dogs) no connection was found between MPCL and pulmonary lymphatics. In variations 1 and 2, alteration of tidal volume resulted in significant changes of lymph flow rate. The pulmonary contribution to MPCL lymph flow was estimated as 34% in variation 2. We conclude that MPCL lymph may contain not only cardiac lymph but also significant pulmonary contamination. This finding should be considered in the interpretation of lymph data from cannulation of the canine MPCL.

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

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.

scholarly journals Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yankun Lyu ◽  
Vipin K. Verma ◽  
Younjee Lee ◽  
Iosif Taleb ◽  
Rachit Badolia ◽  
...  
Keyword(s):  
Heart Function ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Excitation Contraction Coupling ◽  
Transverse Tubular System ◽  
Contraction Coupling ◽  
Senescent Phenotype ◽  
Cellular Microstructure ◽  
T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

scholarly journals Myxomatous Mitral Valve Disease with Mitral Valve Prolapse and Mitral Annular Disjunction: Clinical and Functional Significance of the Coincidence

2021 ◽  
Vol 8 (2) ◽  
pp. 9
Author(s):  
Nina C. Wunderlich ◽  
Siew Yen Ho ◽  
Nir Flint ◽  
Robert J. Siegel
Keyword(s):  
Mitral Valve ◽  
Mitral Valve Disease ◽  
Morphological Changes ◽  
Morphological Characteristics ◽  
Mitral Annulus ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Valve Disease ◽  
Left Ventricular Myocardium ◽  
Basal Portion

The morphological changes that occur in myxomatous mitral valve disease (MMVD) involve various components, ultimately leading to the impairment of mitral valve (MV) function. In this context, intrinsic mitral annular abnormalities are increasingly recognized, such as a mitral annular disjunction (MAD), a specific anatomical abnormality whereby there is a distinct separation between the mitral annulus and the left atrial wall and the basal portion of the posterolateral left ventricular myocardium. In recent years, several studies have suggested that MAD contributes to myxomatous degeneration of the mitral leaflets, and there is growing evidence that MAD is associated with ventricular arrhythmias and sudden cardiac death. In this review, the morphological characteristics of MAD and imaging tools for diagnosis will be described, and the clinical and functional aspects of the coincidence of MAD and myxomatous MVP will be discussed.

β-blockade abolishes the augmented cardiac tPA release induced by transactivation of heterodimerised bradykinin receptor-2 and β2-adrenergic receptor in vivo

2014 ◽  
Vol 112 (11) ◽  
pp. 951-959 ◽  
Author(s):  
Morten Eriksen ◽  
Arnfinn Ilebekk ◽  
Alessandro Cataliotti ◽  
Cathrine Rein Carlson ◽  
Torstein Lyberg ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Sympathetic Nerves ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Adrenergic Stimulation ◽  
Β2 Adrenergic Receptor ◽  
Β Blocker

SummaryBradykinin (BK) receptor-2 (B2R) and β2-adrenergic receptor (β2AR) have been shown to form heterodimers in vitro. However, in vivo proofs of the functional effects of B2R-β2AR heterodimerisation are missing. Both BK and adrenergic stimulation are known inducers of tPA release. Our goal was to demonstrate the existence of B2R-β2AR heterodimerisation in myocardium and to define its functional effect on cardiac release of tPA in vivo. We further investigated the effects of a non-selective β-blocker on this receptor interplay. To investigate functional effects of B2R-β2AR heterodimerisation (i. e. BK transactivation of β2AR) in vivo, we induced serial electrical stimulation of cardiac sympathetic nerves (SS) in normal pigs that underwent concomitant BK infusion. Both SS and BK alone induced increases in cardiac tPA release. Importantly, despite B2R desensitisation, simultaneous BK infusion and SS (BK+SS) was characterised by 2.3 ± 0.3-fold enhanced tPA release compared to SS alone. When β-blockade (propranolol) was introduced prior to BK+SS, tPA release was inhibited. A persistent B2R-β2AR heterodimer was confirmed in BK-stimulated and nonstimulated left ventricular myocardium by immunoprecipitation studies and under non-reducing gel conditions. All together, these results strongly suggest BK transactivation of β2AR leading to enhanced β2AR-mediated release of tPA. Importantly, non-selective β-blockade inhibits both SS-induced release of tPA and the functional effects of B2R-β2AR heterodimerisation in vivo, which may have important clinical implications.

Impact of cardiopulmonary bypass and cardioplegic arrest on myocardial lymphatic function

1995 ◽  
Vol 268 (1) ◽  
pp. H178-H183 ◽  
Author(s):  
U. Mehlhorn ◽  
K. L. Davis ◽  
E. J. Burke ◽  
D. Adams ◽  
G. A. Laine ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Myocardial Edema ◽  
Dry Weight ◽  
Myocardial Contraction ◽  
Left Ventricular ◽  
Lymph Flow ◽  
Cardioplegic Arrest ◽  
Lymphatic Function

Cardioplegic arrest (CPA) is associated with interstitial myocardial edema, which has been shown to impair myocardial function. The accumulation of interstitial myocardial edema may be enhanced by impaired myocardial lymph flow. The purpose of this study was to investigate the effects of CPA on myocardial lymphatic function. In nine anesthetized dogs, we cannulated a prenodal cardiac lymphatic and measured myocardial lymph flow rate (QL), myocardial lymph driving pressure (PL), and myocardial lymph hyaluronan (Hya) concentration. We determined left ventricular function using pressure-volume curves derived by sonomicrometry and micromanometry. The dogs were placed on cardiopulmonary bypass (CPB) (28 degrees C) and subjected to 60 min of hypothermic, crystalloid CPA. With the onset of asystole both QL and PL decreased significantly from 70.7 +/- 31.8 (SD) to 3.3 +/- 4.0 microliters/min and from 19.9 +/- 8.0 to 10.4 +/- 1.8 mmHg, respectively (P < 0.01). Following return of sinus rhythm after separation from CPB, QL and PL increased significantly to 135.4 +/- 28.0 microliters/min and 27.3 +/- 7.5 mmHg, respectively (P < 0.01). Post-CPA myocardial edema was demonstrated by gravimetric wet-to-dry weight determination of 3.67 +/- 0.20 (normal 2.90 +/- 0.20, P < 0.001) and was associated with significantly decreased left ventricular function. Myocardial Hya turnover rate was 1.3 +/- 1.0% per day under baseline conditions and increased significantly to 2.7 +/- 0.9% per day post-CPA (P < 0.01). We conclude that organized myocardial contraction is the major determinant of myocardial lymph flow. Myocardial lymph flow impairment during CPA may contribute to post-CPA myocardial edema and left ventricular dysfunction.

scholarly journals Heart transplantation in an adult patient with isolated noncompaction of the left ventricular myocardium

Medicina ◽  
2010 ◽  
Vol 46 (3) ◽  
pp. 193 ◽  
Author(s):  
Sigita Glaveckaitė ◽  
Kęstutis Ručinskas ◽  
Jelena Čelutkienė ◽  
Vytė Maneikienė ◽  
Diana Zakarkaitė ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Adult Patient ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Important Process ◽  
Ventricular Noncompaction ◽  
Myocardial Development ◽  
Myocardial Fibers ◽  
Heart Lesions

Isolated noncompaction of the ventricular myocardium is defined as a rare cardiomyopathy caused by intrauterine arrest of compaction of the myocardial fibers and meshwork, an important process in myocardial development, in absence of any coexisting congenital heart lesions. A lot of controversies exist about diagnostic criteria, nomenclature, origin, pathogenesis, and prognosis of this disease. Here, we describe an adult patient with isolated left ventricular noncompaction who presented with worsening congestive heart failure and was successfully treated with heart transplantation.

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