HB Koge
Fremad Amager
Predictions:
| Market | Prediction | Odd | Result |
|---|
Overview of HB Koge vs Fremad Amager
El encuentro deportivo entre HB Koge y Fremad Amager promete ser una batalla estratégica con ambos equipos buscando maximizar sus puntos en la tabla de clasificación. HB Koge, conocido por su sólida defensa, intentará imponer su dominio en casa, mientras que Fremad Amager, con su estilo de ataque dinámico, buscará capitalizar cualquier oportunidad que se presente en el terreno de juego.
Bet Predictions: Match Outcome
- HB Koge Win: La ventaja local y la histórica solidez defensiva de HB Koge los posicionan como los favoritos para llevarse la victoria en este emocionante partido.
- Fremad Amager Win: No obstante, con Fremad Amager mostrando mejoras significativas en ataque, existe una probabilidad considerable de que puedan salir victoriosos, particularmente si logran explotar los huecos en la defensa visitante.
- Draw: Dada la competitividad entre ambos equipos, no se puede descartar un empate, especialmente si HB Koge logra mantener un estilo de juego defensivo efectivo y Fremad Amager no puede perforar su escudo defensivo.
Bet Predictions: Total Goals
- Under 2.5 Goals: Considerando las tendencias defensivas de HB Koge y los desafíos que ha enfrentado Fremad Amager en mantener un alto rendimiento goleador, una apuesta en menos de 2.5 goles total podría ser una opción segura.
- Over 2.5 Goals: Sin embargo, si ambos equipos se ven impulsados por el entusiasmo de los espectadores en el estadio, podría haber más de 2.5 goles en el tablero, especialmente si Fremad Amager toma un enfoque agresivo para asegurar un resultado positivo.
Bet Predictions: Both Teams to Score
- Yes: Dado que ambas escuadras tienen un récord de permitir ocasiones a los contrincantes, es razonable anticipar que tanto HB Koge como Fremad Amager podrían marcar en este encuentro.
- No: No obstante, si HB Koge
1: DOI: 10.1111/joim.12800
2: # In vitro study of the pathophysiological effect of high CO2‐containing breathing gas on excised pig heart: A possible model for deep scuba diving
3: Authors: Kenjirou Karube, Tatsuya Sekiguchi, Eiji Miwa, Tatsuo Yoshimatsu
4: Journal: Journal of Internal Medicine
5: Date: 14 September 2018
6: Keywords: ECLA circulation, excised heart, hypercapnia, pig7: ## Abstract
8: **Abstract:** **Aim:** We investigated the influence of hypercapnia and myocardial circulation disorders on the excised pig heart using cardio‐cerebral life support (ECLA) circulation. This was modelled on the rapid loss of consciousness of divers during ascent with CO2‐saturated breathing gas.
9: **Methods:** A pig’s aorta was cannulated and ECLA circulation was started. After stabilizing the pressure in the aorta to 60–80 mmHg by adjusting the flow rate of perfusate (Krebs‐Henseleit solution equilibrated with 95% CO2 and 5% O2 or compressed air) and heart rate to 80–100/min, phosphate‐buffered saline (PBS) was injected for 10 min into the coronary artery for myocardial infarction at different locations (one‐quadrant changes or three‐quadrant changes) followed by 100% O2 flushing. The decrease in left ventricular dp/dt (LVdp/dt) from baseline was obtained for each case.
10: **Results:** Regardless of the location of myocardial infarction, hypercapnia (P < 0.0001) and one‐quadrant change (P = 0.0001) significantly decreased LVdp/dt. Three‐quadrant changes (P = 0.0005) and hypercapnia also showed a significant negative effect when added on to a one‐quadrant change; one‐quadrant change with hypercapnia showed a significant difference from three‐quadrant changes with compressed air (P = 0.0047).
11: **Conclusion:** In a steady state with ECLA circulation, hypercapnia has a significant negative effect on LVdp/dt. When combined with a reduced area of perfusion, hypercapnia is more detrimental than localized myocardial infarction alone.
12: ## Introduction
13: We previously reported two cases of divers with rapid loss of consciousness occurring during their ascent from a deep dive while breathing from demand regulators and premix bottles containing compressed air (CA) or helium mixed with pure oxygen.^(
14: [1]
15: ^) One had hypercapnia, and the other showed signs of cerebral oedema without hypercapnia. The isoamyl nitrite‐containing decompression tube removed from the regulator mouthpiece was suspected to have caused the former's symptoms. However, the latter case had no such explanation.16: The present study aimed to investigate the effects of hypercapnic conditions and myocardial circulation disorders on heart contractility using excised pig hearts and engineered cardio‐cerebral life support (ECLA) circulation.^(
17: [2]
18: ^–
19: [4]
20: ^)21: ## Materials and methods
22: ### Animal model
23: Twenty‐three pigs (Polish Landrace; 30–35 kg body weight, all male) were purchased from a local slaughterhouse and used for this study. The study was carried out ethically according to the National Institutes of Health guide for care and use of laboratory animals and approved by the Animal Care and Use Committee of Keio University School of Medicine.
24: ### Surgical procedure
25: The surgical procedure was performed using an electrolyte‐free balanced salt solution (PBS) as a cardioplegic agent to minimise myocardial metabolism immediately after sacrificing the animal with excess phenobarbital sodium (100 mg/kg body weight; FUJIFILM Wako Pure Chemical Corporation, Osaka, Japan) in order to reduce brain metabolism and cerebral blood flow.^(
26: [5]
27: ^,
28: [6]
29: ^)30: ### ECLA cycle
31: The detailed ECLA model has been previously described.^(
32: [3]
33: ^) Briefly, an incision was made in the thoracic wall, and the heart was quickly extracted without interruption of circulation. After removing the lungs, the heart was suspended in our laboratory‐made ECLA device. The ascending aorta was cannulated with an 8F end‐to‐side graft for aortic perfusion. The vena cava and pulmonary artery were ligated, and oxygenated Ringer's solution was led from a reservoir bag along the tubing to the left ventricular cavity via a right thoracic incision.34: The independently adjustable flow rate of perfusate to the aorta and coronary artery via the Koller‐Edelbach valve were used with a constant pressure-controlled preload above the left atrium (aortic root pressure of 60–80 mmHg) and heart rate (rather than intrinsic heart rate) control to achieve a steady state in which cardiac output (CO) was maintained at approximately 3.5 L/min/m^2 for 3–6 h.^(
35: [1]
36: ^)37: ### Experiments
38: A gas mixture containing 95% CO_2 and 5% O_2 or CA were used to equilibrate the perfusing solution (Krebs‐Henseleit buffer) that entered the aortic cannula via the peristaltic pump for hypercapnic challenge.^(
39: [7]
40: ^) Cardiac contractile function was evaluated by measuring the left ventricular dp/dt (LVdp/dt). In order to evaluate any change in cardiac function under myocardial ischaemic stress conditions, PBS was injected via a catheter placed in a branch of the coronary artery at different locations/types for myocardial infarction (MI). CO_2 equilibrated solution was substituted by CA equilibrated solution after stabilizing each case. At the end of experiments, 100% O_2 was infused as part of cardioplegic treatment to revive the myocardium.41: ### Data analyses
42: Postprocessing was performed with the software package MATLAB R2016b (The MathWorks Inc.).
43: ## Results
44: LVdp/dt in all cases with PBS perfused homogeneously declined by roughly 60% at about 10 min after PBS infusion into the coronary artery compared with baseline. PBS injections into two out of seven branches of the coronary artery (left dominant/proximal right dominant) to simulate MI showed that it is possible to cause MI with no drop in LVdp/dt (60%) in LVdp/dt.
45: The changes in dynamic cardiac function induced by different perfusates and different types/locations of MI are shown in Table 1. The decrease in LVdp/dt from baseline is shown in Table 2.
46: **Table 1:** Changes in dynamic cardiac function induced by different perfusates and different types/locations of myocardial infarction
47: | |
48: LVdp/dt decrease (from baseline) [%] (mean ± SD)
49:
50: | *P* value |
51: | — | — | — |
52: | PBS | CO_2
53: | *P*
54: _{CI}
55: | CA | *P*
56: _{CI}
57: | *P*
58: _p
59: |
60: | Case |
61: Total (*n* = 23)
62:
63: |
64: Total (*n* = 23)
65:
66: |
67: One‐quadrant change (*n* = 11)
68:
69: |
70: Three‐quadrant change (*n* = 12)
71:
72: |
73: Total (*n* = 23)
74:
75: |
76: Total (*n* = 23)
77:
78: |
79: One‐quadrant change (*n* = 11)
80:
81: |
82: Three‐quadrant change (*n* = 12)
83:
84: | |
85: | Preconditioning |
86: 9.3 ± 5.3
87:
88: |
89: 13.9 ± 7.2
90:
91: |
92: 11.1 ± 5.4
93:
94: |
95: 16.8 ± 8.1
96:
97: |
98: −0.6 ± 5.3
99:
100: |
101: −0.4 ± 5.6
102:
103: |
104: −0.9 ± 5.6
105:
106: |
107: 0.6 ± 4.9
108:
109: | <0.001* |
110: | Intervention |
111: −31.4 ± 12.3
112:
113: |
114: −49.6 ± 8.9
115:
116: |
117: −47.4 ± 7.3
118:
119: |
120: −51.0 ± 8.6
121:
122: |
123: −30.0 ± 14.0
124:
125: |
126: −10.3 ± 10.9
127:
128: |
129: −13.1 ± 7.5
130:
131: |
132: −7.0 ± 13.0
133:
134: | <0.001* |
135: | Postconditioning† |
136: −8.1 ± 7.0
137:
138: | −19.5 ± 10.4 | −17.5 ± 10.7 | −21.9 ± 9.4 | −6.3 ± 7.1 | −7.0 ± 8.7 | −5.3 ± 8.8 | −8.5 ± 8.4 |139: CA, compressed air; CI, case interaction; *P*_{CI}, *P* value between one‐ and three‐quadrant changes in each perfusion group; *P_p* , *P* value between CO_2 and CA perfusion groups; SD, standard deviation.
140: ***.**
141: *P*<0.0001.142: **†.** Based on baseline levels.
143: John Wiley & Sons, Ltd
144: **Table 2:** Decrease in LVdp/dt after PBS injection
145: | Case number | CI (%) | LVdp/dt (%) |
146: | — | — | — |
147: | (*n* = 23)ǁ |
148: | Mean ± SD | −39.22 ± 8.05 |
149: | Case number | One‐quadrant change (*n* = 11) |
150: | Mean ± SD | −47.08 ± 6.83 |
151: | Case number | Three‐quadrant change (*n* = 12) |
152: | Mean ± SD | −31.38 ± 6.43 |153: CI, case interaction.
154: **ǁ.** The significant differences in mean values among case number group (*n* =23), one‐quadrant change (*n* =11), three‐quadrant change (*n* =12) are analysed by one‐way ANOVA followed by Tukey's post hoc test.
155: **.** A case with only one‐quadrant change is assigned to case number group when interstitial space is not considered as a MI only when MBV collagen staining shows transmural hypodensity.
156: John Wiley & Sons, Ltd
157: Regardless of the location of MI, both preconditioning hypercapnia (*P*<0.0001) and one‐quadrant change (*P*= 0.0001) significantly decreased LVdp/dt when compared with preintervention baseline levels. When three‐quadrant changes were added on to a one‐quadrant change, there was a significant additional negative effect of hypercapnia (*P*=0.0005). A one‐quadrant change with hypercapnia showed a significant difference from three‐quadrant changes with CA (*P*=0.0047). These results are depicted in Figure 1.
158: **Figure 1:** Decrease in left ventricular dp/dt (LVdp/dt) from preintervention levels during interventions for each case with either compressed air (CA) or CO_2 perfusion is shown as open and closed circles, respectively (Circles are displayed with dark grey colour for one‐quadrant changes and light grey colour for three‐quadrant changes).
159: [image:IJIM-33-361-g001]
160: ## Discussion
161: ### Excised pig heart model
162: We have developed an excised pig heart model to investigate breathing gas effects on cardiac function through ECLA circulation.^(
163: [3]
164: ^) This model enables us to measure cardiac function objectively while controlling many variables including gas composition and the preload pressure in the chest cavities; additionally we can adjust blood pressure and heart rate without any interference from autonomic nervous system signals.^(
165: [8], [9]
166: ^)167: ### Effects of hypercapnia
168: In our setting, although blood pressure and heart rate were maintained at a constant level, LVdp/dt significantly decreased when perfusate contained CO_2 rather than CA alone without any evidence of MI or localised increase in coronary vascular resistance.
169: ### A combination of hypercapnia and reduced area of perfusion
170: Myocardial infarction resulted in significant decreases in LVdp/dt at LV levels of stress condition which is comparable to that observed in human pathology after acute coronary occlusion.^(
171: [10]
172: ^
