scholarly journals Importance of the coronary circulation for cardiac and metabolic performance in rainbow trout ( Oncorhynchus mykiss )

2018 ◽  
Vol 14 (7) ◽  
pp. 20180063 ◽  
Author(s):  
Andreas Ekström ◽  
Michael Axelsson ◽  
Albin Gräns ◽  
Jeroen Brijs ◽  
Erik Sandblom
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Metabolic Rate ◽  
Oxygen Supply ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Coronary Ligation ◽  
Metabolic Performance

Cardiac oxygenation is achieved via both coronary arterial and luminal venous oxygen supply routes in many fish species. However, the relative importance of these supplies for cardiac and aerobic metabolic performance is not fully understood. Here, we investigated how coronary artery ligation in rainbow trout ( Oncorhynchus mykiss ), implanted with heart rate loggers, affected cardiorespiratory performance in vivo . While coronary ligation significantly elevated resting heart rate, the standard metabolic rate was unchanged compared to sham-treated controls. However, coronary ligation reduced the maximum metabolic rate while heart rate remained unchanged following enforced exercise. Thus, coronary ligation reduced metabolic and heart rate scopes by 29% and 74%, respectively. Our findings highlight the importance of coronary oxygen supply for overall cardiorespiratory performance in salmonid fish, and suggest that pathological conditions that impair coronary flow (e.g. coronary arteriosclerosis) constrain the ability of fish to cope with metabolically demanding challenges such as spawning migrations and environmental warming.

scholarly journals It takes time to heal a broken heart: Ventricular plasticity improves heart performance after myocardial infarction in rainbow trout, Oncorhynchus mykiss

2021 ◽  
Author(s):  
Lucas A. Zena ◽  
Andreas Ekström ◽  
Albin Gräns ◽  
Catharina Olsson ◽  
Michael Axelsson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Coronary Artery ◽  
Oncorhynchus Mykiss ◽  
Coronary Occlusion ◽  
Morphological Characteristics ◽  
Coronary Artery Ligation ◽  
Resting Heart Rate ◽  
Rainbow Trout Oncorhynchus Mykiss

Coronary arteriosclerosis is a common feature of both wild and farmed salmonid fishes and may be linked to stress-induced cardiac pathologies. Yet, the plasticity and capacity for long-term myocardial restructuring and recovery following a restriction in coronary blood supply is unknown. Here, we analyzed the consequences of acute (3 days) and chronic (from 33 to 62 days) coronary occlusion (i.e., coronary artery ligation) on cardiac morphological characteristics and in vivo function in juvenile rainbow trout, Oncorhynchus mykiss. Acute coronary occlusion resulted in elevated resting heart rate and decreased inter-beat variability, which are both markers of autonomic dysfunction following acute myocardial ischemia, along with severely reduced heart rate scope (maximum – resting heart rate) relative to sham-operated trout. We also observed a loss of myocardial interstitial collagen and compact myocardium. Following long-term coronary- ligation, resting heart rate and heart rate scope normalized relative to sham-operated trout. Moreover, a distinct fibrous collagen layer separating the compact myocardium into two layers had formed. This may contribute to maintain ventricular integrity across the cardiac cycle, or alternatively, demark a region of the compact myocardium that continues to receive oxygen from the luminal venous blood. Taken together, we demonstrate that rainbow trout may cope with the aversive effects caused by coronary artery obstruction through plastic ventricular remodeling, which, at least in part, restores cardiac performance and myocardium oxygenation.

scholarly journals Targeting Cardiac Myocyte Na + -K + Pump Function With β3 Adrenergic Agonist in Rabbit Model of Severe Congestive Heart Failure

2020 ◽  
Vol 13 (9) ◽  
Author(s):  
Natasha A.S. Fry ◽  
Chia-Chi Liu ◽  
Alvaro Garcia ◽  
Elisha J. Hamilton ◽  
Keyvan Karimi Galougahi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Body Weight ◽  
Cardiac Myocyte ◽  
Rabbit Model ◽  
Severe Heart Failure ◽  
Pump Current ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Coronary Ligation

Background: Abnormally high cytosolic Na + concentrations in advanced heart failure impair myocardial contractility. Stimulation of the membrane Na + -K + pump should lower Na + concentrations, and the β3 adrenoceptor (β3 AR) mediates pump stimulation in myocytes. We examined if β3 AR-selective agonists given in vivo increase myocyte Na + -K + pump activity and reverse organ congestion in severe heart failure (HF). Methods: Indices for HF were lung-, heart-, and liver: body weight ratios and ascites after circumflex coronary artery ligation in rabbits. Na + -K + pump current, I p , was measured in voltage-clamped myocytes from noninfarct myocardium. Rabbits were treated with the β3 AR agonists CL316,243 or ASP9531, starting 2 weeks after coronary ligation. Results: Coronary ligation caused ascites in most rabbits, significantly increased lung-, heart-, and liver: body weight ratios, and decreased I p relative to that for 10 sham-operated rabbits. Treatment with CL316,243 for 3 days significantly reduced lung-, heart-, and liver: body weight ratios and prevalence of ascites in 8 rabbits with HF relative to indices for 13 untreated rabbits with HF. It also increased I p significantly to levels of myocytes from sham-operated rabbits. Treatment with ASP9531 for 14 days significantly reduced indices of organ congestion in 6 rabbits with HF relative to indices of 6 untreated rabbits, and it eliminated ascites. β3 AR agonists did not significantly change heart rates or blood pressures. Conclusions: Parallel β3 AR agonists-induced reversal of Na + -K + pump inhibition and indices of congestion suggest pump inhibition is a useful target for treatment with β3 AR agonists in congestive HF.

scholarly journals Sufentanil–medetomidine anaesthesia compared with fentanyl/fluanisone–midazolam is associated with fewer ventricular arrhythmias and death during experimental myocardial infarction in rats and limits infarct size following reperfusion

2017 ◽  
Vol 52 (3) ◽  
pp. 271-279 ◽  
Author(s):  
Ellis N ter Horst ◽  
Paul A J Krijnen ◽  
Paul Flecknell ◽  
Klaas W Meyer ◽  
Klaas Kramer ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Rate ◽  
Coronary Artery ◽  
Infarct Size ◽  
Ventricular Arrhythmias ◽  
Anaesthetic Agent ◽  
Therapeutic Interventions ◽  
Coronary Artery Ligation ◽  
Artery Ligation

To improve infarct healing following myocardial infarction in humans, therapeutic interventions can be applied during the inflammatory response. Animal models are widely used to study this process. However, induction of MI in rodents is associated with high mortality due to ventricular fibrillation (VF) during coronary artery ligation. The anaesthetic agent used during the procedure appears to influence the frequency of this complication. In this retrospective study, the effect on ventricular arrhythmia incidence during ligation and infarct size following in vivo reperfusion of two anaesthetic regimens, sufentanil–medetomidine (SM) and fentanyl/fluanisone–midazolam (FFM) was evaluated in rats. Anaesthetics were administered subcutaneously using fentanyl/fluanisone (0.5 mL/kg) with midazolam (5 mg/kg) (FFM group, n = 48) or sufentanil (0.05 mg/kg) with medetomidine (0.15 mg/kg) (SM group, n = 47). The coronary artery was ligated for 40 min to induce MI. Heart rate and ventricular arrhythmias were recorded during ligation, and infarct size was measured via histochemistry after three days of reperfusion. In the SM group, heart rate and VF incidence were lower throughout the experiment compared with the FFM group (6% versus 30%) ( P < 0.01). Fatal VF did not occur in the SM group whereas this occurred in 25% of the animals in the FFM group. Additionally, after three days of reperfusion, the infarcted area following SM anaesthesia was less than half as large as that following FFM anaesthesia (8.5 ± 6.4% versus 20.7 ± 5.6%) ( P < 0.01). Therefore, to minimize the possibility of complications related to VF and acute death arising during ligation, SM anaesthesia is recommended for experimental MI in rats.

Abstract 132: Cardiomyocyte Specific Conditional Overexpression Of Stromal Cell Derived Factor 1 Facilitates Cardiac Regeneration After Permanent Coronary Artery Ligation In Mice.

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Detlef Obal ◽  
Kenneth Brittian ◽  
Michael Book ◽  
Aruni Bhatnagar ◽  
Yiru Guo ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Stromal Cell ◽  
Cardiac Regeneration ◽  
Left Ventricular ◽  
Border Zone ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Casein Kinase 1 ◽  
Coronary Ligation ◽  
Stromal Cell Derived Factor

Background: Interruption of cardiac stromal cell derived factor 1 (SDF1)-CXCR4 axis by chronic AMD3100 administration increased myocardial injury after permanent coronary artery ligation demonstrating the important role of this chemokine in cardiac regeneration. Hypothesis: Cardiomyocyte specific conditional overexpression of SDF1 prevents heart failure after permanent coronary ligation and facilitates cardiac regeneration. Methods and Results: Tetracycline-controlled, αMyHC promoter directed overexpression of cardiac SDF1, resulted in a significant increase of SDF1 expression (SDF1: 8.1 ng/mg protein) compared to littermate WT mice (0.02 ng/mg protein) four weeks after doxycycline withdraw. SDF1 overexpression increased AKT and casein kinase 1 levels in the heart. Although there was no difference in cardiac function and scar size 1 week after infarction, SDF1 overexpression improved left ventricular (LV) ejection fraction (SDF1 [n=13]: 47±5% [mean±SEM] vs. WT [n=15]: 29±4%, p<0.05) decreased end-diastolic volume (78±10 vs. 158±30, p<0.05) and reduced infarct size measured by trichrome staining (13±3% vs. 23±3% of LV wall, p<0.05) 4 weeks after permanent ligation. Bromodeoxyuridine (BrdU) staining revealed increased regeneration indicated by a 5-fold increase in BrdU + cardiomyocyte (CM) nuclei in the borderzone of the infarct (22±3% vs. 5±1% CM nuclei, p<0.01). Increased proliferation in SDF1 mice was confirmed by a higher number of KI67 + cells compared to WT mice. Cardiomyocyte cross sectional area in the border zone was significantly reduced in SDF1 mice (365±13 μm 2 vs. 434±10 μm 2 , p<0.001) while capillary density was unchanged (2348±151/ mm 2 vs. 2498±153/ mm 2 ) compared to WT mice. Conclusion: This study demonstrates for the first time that cardiac specific overexpression of SDF1 increases myocardial regeneration and improves LV function 4 weeks after permanent coronary ligation.

Abstract 365: Targeted Delivery of IGF-1 Following Acute Myocardial Infarction

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Raffay S Khan ◽  
Jay C Sy ◽  
Milton Brown ◽  
Mario D Martinez ◽  
Niren Murthy ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Targeted Delivery ◽  
Coronary Artery Ligation ◽  
Nuclear Staining ◽  
Post Injection ◽  
Artery Ligation ◽  
Intact Cells ◽  
Double Stranded Dna

During acute myocardial infarction (MI) there is excessive necrosis of myocardial cells, leading to the release of large amounts of DNA, representing a potential target for drug delivery. Hoechst, a commonly used molecule for staining nuclei, binds to the minor groove of double-stranded DNA and can be functionalized to contain reactive groups such as free amines, sulfhydryls, and biotin moieties. Insulin-like growth factor-1 (IGF-1), a small molecule with a short half-life is protective immediately following MI, though there is potential for long-term toxicity and off-target effects. Therefore, we hypothesized that conjugating IGF-1 to Hoechst would increase targeting of IGF-1 to the injured myocardium. Hoechst-IGF1 (H-IGF1) was synthesized by binding Hoechst-biotin to biotinylated IGF-1 via a fluorescent streptavidin linker. Intact cells did not show nuclear staining with H-IGF1, while permeabilized cells had a significant increase in blue fluorescent Hoechst staining, indicating H-IGF1 was cell impermeable but could still bind DNA. Activity of H-IGF1 was demonstrated by Akt phosphorylation in cultured cardiac progenitor cells and was similar to native IGF-1. To determine in-vivo targeting of H-IGF1 to MI, mice underwent 30 minutes of coronary artery ligation followed by reperfusion (I/R). Six hours following MI, mice were injected intravenously with 70ng of H-IGF1, S-IGF1 (streptavidin bound IGF-1 only) or PBS followed by in vivo imaging at 30 and 120 minutes post-injection. At 30 minutes post-injection, we found 3.2% (2.2 of 70ng) of the injected dose of H-IGF1 in infarcted hearts compared with 1.8% (1.3 of 70ng) of S-IGF1 (n=5-7; p<0.05). To confirm that targeting of H-IGF1 was dependent on binding DNA, H-IGF1 pre-bound to double-stranded DNA was injected intravenously after I/R. This led to a significant (p<0.05) decrease in targeted IGF-1 levels. IGF-1 levels determined by ELISA 2 hours post-injection demonstrated a similar trend with increased targeting of H-IGF1 compared with S-IGF1 treated mice (4.2±0.6 ng vs. 2.4±0.2 ng; p<0.05). In conclusion, our data demonstrate that intravenous delivery of Hoechst-conjugated IGF-1 increases myocardial targeting. This provides a novel strategy for delivery of growth factors for the treatment of MI.

Myotomal slow muscle function of rainbow trout Oncorhynchus mykiss during steady swimming.

1998 ◽  
Vol 201 (10) ◽  
pp. 1659-1671 ◽  
Author(s):  
L Hammond ◽  
J D Altringham ◽  
C S Wardle
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Body Length ◽  
Muscle Activation ◽  
Activity Patterns ◽  
The Body ◽  
Entire Body ◽  
Negative Power ◽  
Rainbow Trout Oncorhynchus Mykiss

Strain and activity patterns were determined during slow steady swimming (tailbeat frequency 1.5-2.5 Hz) at three locations on the body in the slow myotomal muscle of rainbow trout Oncorhynchus mykiss using sonomicrometry and electromyography. Strain was independent of tailbeat frequency over the range studied and increased significantly from +/-3.3 % l0 at 0.35BL to +/-6 % at 0.65BL, where l0 is muscle resting length and BL is total body length. Muscle activation occurred significantly later in the strain cycle at 0.35BL (phase shift 59 degrees) than at 0.65BL (30 degrees), and the duration of activity was significantly longer (211 degrees at 0.35BL and 181 degrees at 0.65BL). These results differ from those of previous studies. The results have been used to simulate in vivo activity in isolated muscle preparations using the work loop technique. Preparations from all three locations generated net positive power under in vivo conditions, but the negative power component increased from head to tail. Both kinematically, and in the way its muscle functions to generate hydrodynamic thrust, the rainbow trout appears to be intermediate between anguilliform swimmers such as the eel, which generate thrust along their entire body length, and carangiform fish (e.g. saithe Pollachius virens), which generate thrust primarily at the tail blade.

How the efficiency of rainbow trout (Oncorhynchus mykiss) ventricular muscle changes with cycle frequency

2002 ◽  
Vol 205 (5) ◽  
pp. 697-706 ◽  
Author(s):  
Claire L. Harwood ◽  
Iain S. Young ◽  
John D. Altringham
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Cardiac Muscle ◽  
Power Output ◽  
Energy Cost ◽  
Total Efficiency ◽  
Ventricular Muscle ◽  
Cycle Frequency ◽  
Rainbow Trout Oncorhynchus Mykiss

SUMMARYDifferent species of animals require different cardiac performance and, in turn, their cardiac muscle exhibits different properties. A comparative approach can reveal a great deal about the mechanisms underlying myocardial contraction. Differences in myocardial Ca2+ handling between fish and mammals suggest a greater energy cost of activation in fish. Further, while there is considerable evidence that heart rate (or cycle frequency) should have a profound effect on the efficiency of teleost cardiac muscle, this effect has been largely overlooked. We set out to determine how cycle frequency affects the power output and efficiency of rainbow trout (Oncorhynchus mykiss) ventricular muscle and to relate this to the heart’s function in life. We measured power output and the rate of oxygen consumption (V̇O2) and then calculated efficiency over a physiologically realistic range of cycle frequencies.In contrast to mammalian cardiac muscle, in which V̇O2 increases with increasing heart rate, we found no significant change in V̇O2 in the teleost. However, power output increased by 25 % as cycle frequency was increased from 0.6 to 1.0 Hz, so net and total efficiency increased. A maximum total efficiency of 20 % was achieved at 0.8 Hz, whereas maximum power output occurred at 1.0 Hz. We propose that, since the heart operates continuously, high mechanical efficiency is a major adaptive advantage, particularly at lower heart rates corresponding to the more commonly used slower, sustainable swimming speeds. Efficiency was lower at the higher heart rates required during very fast swimming, which are used during escape or prey capture.If a fixed amount of Ca2+ is released and then resequestered each time the muscle is activated, the activation cost should increase with frequency. We had anticipated that this would have a large effect on the total energy cost of contraction. However, since V̇O2 remains constant, less oxygen is consumed per cycle at high frequencies. We suggest that a constant V̇O2 would be observed if the amount of activator Ca2+ were to decrease with frequency. This decrease in activation energy is consistent with the decrease in the systolic intracellular Ca2+ ([Ca2+]i) transient with increasing stimulation frequency seen in earlier studies.

Abstract 3366: Imaging of Peroxidase Activity in Injured Myocardium

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Matthias Nahrendorf ◽  
David E Sosnovik ◽  
John Chen ◽  
Jose-Luis Figueiredo ◽  
Peter Panizzi ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Matrix Proteins ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Non Invasive ◽  
Injured Myocardium ◽  
Reactive Chlorinating Species ◽  
Injury Causes ◽  
In Vivo Assessment

Ischemic myocardial injury causes timed recruitment of neutrophils and monocyte/macrophages, which produce significant amounts of myeloperoxidase (MPO). MPO leads to the formation of reactive chlorinating species capable of oxidizing proteins. We developed a small molecule based MPO substrate for MRI, Gd-bis-5-HT-DPTA, which is first radicalized, and then oligomerized and covalently bound to matrix proteins, all leading to enhanced R1-relaxivity and delayed wash out kinetics. Mice were subjected to coronary artery ligation and injected with 0.3mmol/kg Gd-bis-5-HT-DPTA (or Gd-DTPA as control). We performed T1-weighted cardio-respiratory gated MRI 10–120min later, followed by immunoreactive staining for MPO. 3 mice each were studied at day 1, 2, 4, 8, and >1 month after MI. Subsequently, MPO tissue activity was determined with the guaiacol method. MPO activity peaked 2 days after MI (contrast-to-noise-ratio (CNR) day 1, 26+/−4; day 2, 39+/−10; day 4, 29+/−3), and tissue levels of MPO over time correlated well with probe activity in vivo (r2=0.65, p<0.01). CNR following Gd-DTPA peaked ten minutes after injection (10.5+/−0.2), and returned to pre-injection values at 60min. In contradistinction, following injection Gd-bis-5-HT-DPTA, CNR was higher and peaked later (p<0.05 vs. Gd-DTPA, arrows depict MI in figure ). Immunoreactive staining for MPO correlated well with enhancement (r2=0.92, p<0.05). Gd-bis-5-HT-DPTA facilitates in-vivo assessment of MPO activity in injured myocardium. This approach allows non-invasive probing of the inflammatory response to ischemia and has the potential to guide the development and application of novel cardioprotective therapies.

Sign in / Sign up

Export Citation Format

Share Document