atrial-natriuretic-factor and Ventricular-Fibrillation

atrial-natriuretic-factor has been researched along with Ventricular-Fibrillation* in 6 studies

Trials

1 trial(s) available for atrial-natriuretic-factor and Ventricular-Fibrillation

ArticleYear
Administration of atrial natriuretic peptide attenuates reperfusion phenomena and preserves left ventricular regional wall motion after direct coronary angioplasty for acute myocardial infarction.
    Circulation journal : official journal of the Japanese Circulation Society, 2003, Volume: 67, Issue:5

    To evaluate the effects of synthetic human atrial natriuretic peptide (hANP) on myocardial reperfusion injury and left ventricular remodeling, 19 patients within 12 h of a first attack of anterior myocardial infarction (AMI) underwent intracoronary injection of 25 microg of hANP immediately after coronary angioplasty, combined with intravenous infusion of 0.025 microg x kg(-1) x min(-1) of hANP initiated on admission for 1 week (hANP group); 18 similar patients had saline administered (control group). The incidences of premature ventricular contraction, ventricular tachycardia and/or fibrillation in the hANP group were significantly less than in the control group after coronary angioplasty. Left ventricular ejection fraction was significantly greater and left ventricular end-diastolic volume index was significantly smaller 6 months after coronary angioplasty. Left ventricular regional wall motion of the infarcted segments significantly increased. Thus, hANP remarkably suppressed reperfusion phenomena and preserved left ventricular function through improvement of regional wall motion of the infarcted segments after coronary angioplasty.

    Topics: Angioplasty, Balloon, Coronary; Atrial Natriuretic Factor; Blood Pressure; Coronary Circulation; Female; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Myocardial Reperfusion Injury; Ventricular Fibrillation; Ventricular Function, Left

2003

Other Studies

5 other study(ies) available for atrial-natriuretic-factor and Ventricular-Fibrillation

ArticleYear
Effects of pre-, peri-, and postmyocardial infarction treatment with losartan in rats: effect of dose on survival, ventricular arrhythmias, function, and remodeling.
    American journal of physiology. Heart and circulatory physiology, 2005, Volume: 288, Issue:4

    Angiotensin receptor blockers (ARBs) reduce adverse left ventricular (LV) remodeling and improve LV function and survival when started postmyocardial infarction (MI). ARBs also reduce ventricular arrhythmias during ischemia-reperfusion injury when started pre-MI. No information exists regarding their efficacy and safety when started pre-MI and continued peri- and post-MI. We evaluated whether the ARB losartan improves the outcome when started pre-MI and continued peri- and post-MI. Male Wistar rats (n = 502) were treated for 7 days pre-MI with losartan at a high dose (30 mg.kg(-1).day(-1)), progressively increasing dose (3 mg.kg(-1).day(-1) increased to 10 mg.kg(-1).day(-1) 10 days and 30 mg.kg(-1).day(-1) 20 days post-MI), or no treatment. Ambulatory systolic blood pressure and Holter monitoring were performed for 24 h post-MI. Echocardiography was done 30 days post-MI, and LV remodeling, cardiac hemodynamics, and fetal gene expression were assessed 38 days post-MI. High-dose losartan reduced 24-h post-MI survival compared with the progressive dose and control (21.9% vs. 36.6% and 38.1%, P = 0.033 and P = 0.009, respectively). This was associated with greater hypotension in the high dose and no change in ventricular arrhythmias in all groups. In 24-h post-MI survivors, the progressive dose group had reduced mortality from 24 h to 38 days (8.5% vs. 28.6% for control vs. 38.9% for high dose, P = 0.032 and P = 0.01, respectively). Survivors of both losartan groups demonstrated improved LV remodeling, cardiac hemodynamics, preserved GLUT-4, and reduced cardiac fetal gene expression. Pretreatment with ARBs does not reduce 24-h post-MI ventricular arrhythmias or survival, and high doses increase mortality by causing excessive hypotension. In 24-h post-MI survivors, progressively increasing doses of losartan have multiple beneficial effects, including improved survival.

    Topics: Actins; Angiotensin II Type 1 Receptor Blockers; Animals; Atrial Natriuretic Factor; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Cardiac Volume; Dose-Response Relationship, Drug; Echocardiography; Glucose Transporter Type 4; Incidence; Losartan; Male; Monosaccharide Transport Proteins; Muscle Proteins; Myocardial Infarction; Myosin Heavy Chains; Polymerase Chain Reaction; Rats; Rats, Wistar; RNA, Messenger; Tachycardia, Ventricular; Ventricular Fibrillation; Ventricular Pressure; Ventricular Remodeling

2005
Inhibition of angiotensin-converting enzyme reduces susceptibility of hypertrophied rat myocardium to ventricular fibrillation.
    Circulation journal : official journal of the Japanese Circulation Society, 2002, Volume: 66, Issue:11

    Left ventricular (LV) hypertrophy increases susceptibility to reperfusion arrhythmias and the angiotensin-converting enzyme inhibitor, ramipril, may reduce that susceptibility via regression of LV hypertrophy. Rats (n=12 per group) were subjected to abdominal aortic constriction (AC) or sham-operation (SH) and from 3 to 6 weeks after surgery, 3 AC groups received ramipril (0.01, 0.1, or 1 mg/kg per day p.o.) while the SH and 1 AC group received vehicle. Six weeks after surgery (ie after 3 weeks of treatment), the hearts were excised and subjected to independent Langendorf perfusion of left and right coronary beds. The left coronary bed was then subjected to ischemia (7 min) and reperfusion (5 min). Hypertrophied hearts from the vehicle AC group showed a significant increase in the incidence of reperfusion-induced ventricular fibrillation (VF) compared with control hearts from the SH group (92%* vs 33%: *p<0.05); this difference was abolished by ramipril (42%, 50%, and 42%, at 0.01, 0.1, or 1 mg/kg per day, respectively). The LV weight/body weight ratio was significantly increased in all AC groups (regardless of ramipril treatment) relative to the SH group. At the cellular level, myocyte length was significantly increased in the vehicle AC group, but was normalized by ramipril treatment (1 mg/kg per day). At the molecular level, atrial natriuretic factor (ANF) mRNA expression was also significantly increased in the vehicle AC group, but was again normalized by ramipril treatment (1 mg/kg per day). In conclusion, short-term treatment with ramipril reduced susceptibility to severe ventricular arrhythmias in hypertrophied rat hearts. This protection was achieved in the absence of a significant reduction in LV weight, but was accompanied by regression of myocyte hypertrophy, as reflected by reductions in cell size and ANF expression.

    Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Atrial Natriuretic Factor; Cardiomegaly; Disease Models, Animal; Heart Ventricles; Male; Myocardial Reperfusion Injury; Myocytes, Cardiac; Ramipril; Rats; Rats, Wistar; RNA, Messenger; Ventricular Fibrillation

2002
Effect of atrial natriuretic peptide on electrical defibrillation efficacy.
    Journal of cardiovascular electrophysiology, 1998, Volume: 9, Issue:9

    In vitro studies have suggested that human atrial natriuretic peptide (ANP) modulates the electrophysiologic properties of myocardial cells. This study assessed whether ANP could influence defibrillation efficacy.. In 35 anesthetized dogs, the transcardiac defibrillation threshold (DFT) as well as hemodynamic and electrophysiologic variables were determined before and during treatment with ANP (n = 11), hydralazine (n = 11), or saline (n = 13). ANP (1.5 microg/kg + 0.2 microg/kg per min) increased the plasma concentration of cyclic GMP (a second messenger for ANP) and significantly decreased aortic blood pressure (mean 100+/-11 mmHg to 83+/-15 mmHg). ANP also prolonged ventricular repolarization (effective refractory period 157+/-7 msec to 165+/-11 msec) and markedly reduced DFT (5.4+/-1.2 J to 3.8+/-0.7 J [P < 0.01]) without changing pulmonary artery pressure or sinus cycle length. Neither saline nor hydralazine (1.5 mg/kg) had a significant effect on DFT (saline 4.7+/-2.1 J to 4.6+/-2.4 J; hydralazine 4.3+/-2.0 J to 4.2+/-1.9 J), although hydralazine caused pronounced hypotension (mean aortic pressure 103+/-9 mmHg to 74+/-13 mmHg).. These results suggest that ANP increases defibrillation efficacy, and that this effect is not necessarily shared by other vasodilating agents.

    Topics: Animals; Atrial Natriuretic Factor; Cyclic GMP; Dogs; Electric Countershock; Electrocardiography; Hemodynamics; Hydralazine; Infusions, Intravenous; Treatment Outcome; Vasodilator Agents; Ventricular Fibrillation

1998
The N-terminus, C-terminus, and vessel dilator of the ANF prohormone are present in the urine and increase with ventricular fibrillation.
    Biochemical and biophysical research communications, 1990, Dec-31, Volume: 173, Issue:3

    The N-terminus consisting of amino acids (a.a.) 1-98 (i.e., proANF 1-98), C-terminus (i.e., ANF; a.a. 99-126) and midportion of N-terminus consisting of a.a. 31-67 (proANF 31-67; Vessel Dilator) of the 126 a.a. ANF prohormone were present in the urine in 5-to-8-fold increased concentrations versus their plasma concentrations in 6 dogs under basal conditions. With acute coronary occlusion the right atrial plasma concentrations of these peptides increased two-to-three-fold, while in the urine only proANF 31-67 increased (3.5-fold). Ventricular fibrillation caused a 4-to-10-fold increased secretion into the right atrial chamber with a simultaneous 3-to-4.7-fold increase in the urine of proANF 1-98, proANF 31-67, and ANF. This investigation demonstrates that proANF 1-98, proANF 31-67 and ANF are normally present in urine and increase in the urine with cardiac stimuli that cause their release from the heart.

    Topics: Animals; Atrial Natriuretic Factor; Dogs; Heart Ventricles; Kidney; Natriuresis; Peptide Fragments; Protein Precursors; Radioimmunoassay; Ventricular Fibrillation

1990
Atrial natriuretic factor protects the isolated working ischaemic rat heart against the action of angiotensin II.
    Journal of hypertension. Supplement : official journal of the International Society of Hypertension, 1988, Volume: 6, Issue:4

    The interaction between atrial natriuretic factor [synthetic human ANF-(103-126)] and angiotensin II (Ang II) and its influence on reperfusion arrhythmias, cardiodynamics, enzyme loss and metabolic changes were investigated in isolated ischaemic working rat hearts. Acute regional myocardial ischaemia was induced by coronary artery occlusion which was associated with ventricular fibrillation. Perfusion with 1 X 10(-9) mol/l Ang II markedly aggravated these arrhythmias. Perfusion with 1 X 10(-7) mol/l ANF, in contrast, gave protection against ventricular fibrillation and prevented Ang II-induced aggravation of ventricular fibrillation. Atrial natriuretic factor improved cardiodynamics, in particular, during reperfusion, whereas Ang II impaired cardiodynamics and increased the release of creatine kinase and lactate dehydrogenase. These adverse effects of Ang II were absent when ANF was simultaneously perfused. Compared with control hearts, myocardial tissue levels of glycogen, ATP and creatine phosphate were increased in hearts perfused with either ANF or ANF plus Ang II, whereas lactate levels decreased. Perfusion with Ang II alone led to deterioration in these metabolic parameters. These results in isolated working rat hearts suggest that ANF protects against the consequences of ischaemia and reperfusion and that functional antagonism between ANF and Ang II may contribute to this.

    Topics: Angiotensin II; Animals; Arrhythmias, Cardiac; Atrial Natriuretic Factor; Coronary Circulation; Coronary Disease; Myocardial Reperfusion Injury; Rats; Rats, Inbred Strains; Ventricular Fibrillation

1988
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