Rats are protected from the stress of chronic pressure overload compared with mice.

Szczegóły
Abstrakt

Tytuł:: Rats are protected from the stress of chronic pressure overload compared with mice.
Autorzy:: Nishimura K; Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Oydanich M; Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Zhang J; Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Babici D; Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Fraidenraich D; Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Vatner DE; Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Vatner SF; Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Źródło:: American journal of physiology. Regulatory, integrative and comparative physiology [Am J Physiol Regul Integr Comp Physiol] 2020 May 01; Vol. 318 (5), pp. R894-R900. Date of Electronic Publication: 2020 Mar 25.
Typ publikacji:: Comparative Study; Journal Article; Research Support, N.I.H., Extramural
Język:: English
Imprint Name(s):: Original Publication: Bethesda, Md. : American Physiological Society
MeSH Terms:: Ventricular Function, Left*
Ventricular Pressure*
Ventricular Remodeling*
Hypertrophy, Left Ventricular/*physiopathology
Ventricular Dysfunction, Left/*physiopathology
Animals ; Aorta/physiopathology ; Aorta/surgery ; Capillaries/metabolism ; Capillaries/physiopathology ; Coronary Circulation ; Disease Models, Animal ; Hypertrophy, Left Ventricular/etiology ; Hypertrophy, Left Ventricular/metabolism ; Ki-67 Antigen/metabolism ; Ligation ; Mice, Inbred C57BL ; Muscle Development ; Myocytes, Cardiac/metabolism ; Neovascularization, Physiologic ; Proto-Oncogene Proteins c-kit/metabolism ; Rats, Sprague-Dawley ; Signal Transduction ; Species Specificity ; Time Factors ; Troponin I/metabolism ; Ventricular Dysfunction, Left/etiology ; Ventricular Dysfunction, Left/metabolism
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Grant Information:: R21 AG053514 United States AG NIA NIH HHS; R01 HL119464 United States HL NHLBI NIH HHS; R01 HL102472 United States HL NHLBI NIH HHS; R01 HL130848 United States HL NHLBI NIH HHS; R01 HL106511 United States HL NHLBI NIH HHS; R01 HL137368 United States HL NHLBI NIH HHS; R01 HL124282 United States HL NHLBI NIH HHS; R01 HL137405 United States HL NHLBI NIH HHS; UL1 TR003017 United States TR NCATS NIH HHS; S10 OD025238 United States OD NIH HHS
Contributed Indexing:: Keywords: angiogenesis; cardiac function; heart failure; pressure overload
Substance Nomenclature:: 0 (Ki-67 Antigen)
0 (Troponin I)
EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
Entry Date(s):: Date Created: 20200327 Date Completed: 20200720 Latest Revision: 20210502
Update Code:: 20240105
PubMed Central ID:: PMC7272766
DOI:: 10.1152/ajpregu.00370.2019
PMID:: 32209023
: Czasopismo naukowe

The goal of this investigation was to compare the effects of chronic (4 wk) transverse aortic constriction (TAC) in Sprague-Dawley rats and C57BL/6J mice. TAC, after 1 day, induced similar left ventricular (LV) pressure gradients in both rats ( n = 7) and mice ( n = 7) (113 ± 5.4 vs. 103 ± 11.5 mmHg), and after 4 wk, the percent increase in LV hypertrophy, as reflected by LV/tibial length (51% vs 49%), was similar in rats ( n = 12) and mice ( n = 12). After 4 wk of TAC, LV systolic and diastolic function were preserved in TAC rats. In contrast, in TAC mice, LV ejection fraction decreased by 31% compared with sham, along with increases in LV end-diastolic pressure (153%) and LV systolic wall stress (86%). Angiogenesis, as reflected by Ki67 staining of capillaries, increased more in rats ( n = 6) than in mice ( n = 6; 10 ± 2 vs. 6 ± 1 Ki67-positive cells/field). Myocardial blood flow fell by 55% and coronary reserve by 28% in mice with TAC ( n = 4), but they were preserved in rats ( n = 4). Myogenesis, as reflected by c-kit-positive myocytes staining positively for troponin I, is another mechanism that can confer protection after TAC. However, the c-kit-positive cells in rats with TAC were all negative for troponin I, indicating the absence of myogenesis. Thus, rats showed relative tolerance to severe pressure overload compared with mice, with mechanisms involving angiogenesis but not myogenesis.

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