Liposome‐encapsulated hemoglobin (HbV) transfusion rescues rats undergoing progressive lethal 85% hemorrhage as a result of an anti‐arrhythmogenic effect on the myocardium

2021 ◽  
Author(s):  
Bonpei Takase ◽  
Yuko Higashimura ◽  
Haruka Asahina ◽  
Masayuki Ishihara ◽  
Hiromi Sakai
Keyword(s):  
Arrhythmogenic Effect

scholarly journals Ageing: A Possible Clue to the Arrhythmogenic Effect of Hemodyalisis

Nephron ◽  
1988 ◽  
Vol 50 (1) ◽  
pp. 82-82 ◽  
Author(s):  
Alberto Cocchi ◽  
Giuseppe Zuccalà ◽  
Pierugo Carbonin ◽  
Roberto Mori ◽  
Raffaele Antonelli Incalzi
Keyword(s):  
Arrhythmogenic Effect

Arrhythmogenic effects of catecholamines are decreased in heart failure induced by rapid pacing in dogs

1993 ◽  
Vol 265 (5) ◽  
pp. H1654-H1662 ◽  
Author(s):  
H. G. Li ◽  
D. L. Jones ◽  
R. Yee ◽  
G. J. Klein
Keyword(s):  
Heart Failure ◽  
Ventricular Arrhythmias ◽  
Control Group ◽  
Purkinje Fibers ◽  
Failure Group ◽  
Failing Heart ◽  
Minimal Dose ◽  
Arrhythmogenic Effect ◽  
Rapid Pacing ◽  
Arrhythmogenic Effects

Increased circulating catecholamines are considered to be arrhythmogenic in heart failure. It is unclear whether increased circulating catecholamines contribute directly to ventricular arrhythmias or are only markers of the severity of heart failure. The present study determined the sensitivity of the failing heart to the arrhythmogenic effect of exogenous norepinephrine in a rapid pacing-induced model of heart failure in dogs (240 beats for 4 wk, n = 14). A similarly operated, non-paced group served as controls (n = 9). Cardiac sensitivity to the arrhythmogenic effect of catecholamines was determined by measuring the minimal dose of exogenous norepinephrine that induced ventricular tachycardia (arrhythmogenic threshold dose, ATD). ATD significantly increased after development of heart failure in heart-failure group (1.62 +/- 0.32 microgram/kg at baseline vs. 16.65 +/- 3.48 micrograms/kg at restudy, P < 0.01), whereas no significant change was noted in the control group (1.08 +/- 0.36 microgram/kg at baseline vs. 2.53 +/- 0.36 micrograms/kg at restudy, P > 0.10). Action potential duration was unchanged by superfusion with 10(-7) M isoproterenol in both ventricular muscles (230.2 +/- 6.1 vs. 229.7 +/- 5.3 ms, P = NS) and Purkinje fibers (273.2 +/- 6.5 vs. 283.8 +/- 4.2 ms, P = NS) from the failing hearts, although isoproterenol induced a shortening in the control group (204.8 +/- 0.9 vs. 181.3 +/- 1.6 ms in ventricular muscles, P < 0.01; 313.8 +/- 6.5 vs. 279.5 +/- 5.7 ms in Purkinje fibers, P < 0.01). We conclude that the failing heart has a decreased sensitivity to the arrhythmogenic effect of catecholamines.

Atrial Flutter Associated with Carboplatin Administration

2011 ◽  
Vol 45 (11) ◽  
pp. 1451-1451 ◽  
Author(s):  
Sammy Zakaria ◽  
Kit Yu Lu ◽  
Veronique Nussenblatt ◽  
Ilene Browner
Keyword(s):  
Atrial Flutter ◽  
Causal Link ◽  
Cardiac Monitoring ◽  
Cardiac Complications ◽  
Medication Regimen ◽  
Cardiac Events ◽  
Drug Induced ◽  
Arrhythmogenic Effect ◽  
Adverse Cardiac Events ◽  
Effect Of Treatment

Objective: To report a novel case of atrial flutter associated with carboplatin administration and review chemotherapy-related cardiac toxicities, focusing on platinum-containing compounds. Case Report: A 69-year-old man with extensive small cell lung cancer and asymptomatic cardiovascular and cerebrovascular disease was inconsistently adherent to his medication regimen. While undergoing carboplatin infusion, he developed atrial flutter. He had no other immediate arrhythmogenic causes of atrial flutter and the arrhythmia spontaneously reverted to sinus rhythm after 24 hours. His condition remained stable until he died 8 days later. The cause of death was unknown and the family declined postmortem examination. Discussion: Although this patient's cardiac history and nonadherence to his medications may have increased his susceptibility to develop atrial arrhythmias, the Naranjo probability scale reveals a possible relationship between atrial flutter and Infusion of carboplatin. A literature search revealed other adverse cardiac events due to platinum compounds; however, to our knowledge, this case is the first to describe an association with atrial flutter. A definitive causal link cannot be determined, but this may have been the result of a direct arrhythmogenic effect of treatment or to a novel hypersensitivity reaction. Given the potential deleterious impact of drug-induced arrhythmias, we have reported this case to the Food and Drug Administration as a new adverse effect of carboplatin. Conclusions: Providers should consider cardiac monitoring during carboplatin infusion in patients with known cardiac disease or at high risk of cardiac complications.

Activation of Peripheral Delta Opioid Receptors Increases Cardiac Tolerance to Arrhythmogenic Effect of Ischemia/Reperfusion

2014 ◽  
Vol 21 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Leonid N. Maslov ◽  
Peter R. Oeltgen ◽  
Yury B. Lishmanov ◽  
Stephen A. Brown ◽  
Eva I. Barzakh ◽  
...  
Keyword(s):  
Opioid Receptors ◽  
Ischemia Reperfusion ◽  
Delta Opioid Receptors ◽  
Arrhythmogenic Effect

Investigating the dual nature of endothelin-1: Ischemia or direct arrhythmogenic effect?

Life Sciences ◽  
2000 ◽  
Vol 66 (26) ◽  
pp. 2527-2541 ◽  
Author(s):  
Tamás Szabó ◽  
László Gellér ◽  
Béla Merkely ◽  
László Selmeci ◽  
Alexander Juhász-Nagy ◽  
...  
Keyword(s):  
Dual Nature ◽  
Endothelin 1 ◽  
Arrhythmogenic Effect

Comparison of the arrhythmogenic effect of myocardial infarction in the cat and dog

1979 ◽  
Vol 13 (3) ◽  
pp. 152-159 ◽  
Author(s):  
R. D. REYNOLDS ◽  
G. J. KELLIHER ◽  
D. M. RITCHIE ◽  
J. ROBERTS ◽  
A. B. BEASLEY
Keyword(s):  
Myocardial Infarction ◽  
Arrhythmogenic Effect

Effect of different levels of briefly sustained ventricular pressure on arrhythmia in the isolated working rat heart

1991 ◽  
Vol 81 (6) ◽  
pp. 715-721 ◽  
Author(s):  
M. A. James ◽  
J. V. Jones
Keyword(s):  
Wall Stress ◽  
Ventricular Pressure ◽  
Ventricular Wall ◽  
Hypertensive Rats ◽  
Arrhythmogenic Effect ◽  
Rat Hearts ◽  
Short Period ◽  
Working Heart ◽  
Different Levels ◽  
Working Rat Heart

1. The effect of different levels of ventricular pressure upon the prevalence of ventricular arrhythmias has been studied in 42 rat hearts by using the isolated working heart model. 2. The results have shown that there is an increased prevalence of arrhythmia at the highest levels of pressure tested in hearts from both normal and hypertensive rats. In hearts from normal rats total ectopic counts were 304 at 140 mmHg and 150 at 60 mmHg (P < 0.05). In hearts from hypertensive rats total ectopic counts were 4217 at 180 mmHg and 2179 at 100 mmHg (P < 0.05). 3. Hearts from hypertensive rats demonstrated significantly more ectopic activity than hearts from normal rats at all test pressures. Median values for ectopic counts for each study period were 68 in hearts from hypertensive rats and seven in hearts from normotensive rats (P < 0.001). 4. There was evidence that the increased arrhythmia observed was not due to ischaemia or fatigue, and it seems likely that these effects of raised pressure are due to its effect on ventricular wall stress. The differences between various pressures were relatively small, but do suggest that a sustained increase in ventricular wall stress is arrhythmogenic. 5. This small arrhythmogenic effect over the relatively short period of these studies may be of much greater significance when considered in the context of the prolonged periods for which the diseased heart may be subjected to raised wall stress.

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