TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Assiri, Abdullah S.
AU  - Yassin, Hanaa Z.
AU  - Ammar, Hania I.
AU  - Obradović, Milan M.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/716
AB  - Cardiovascular disease (CVD) is among the most major causes of morbidity and mortality worldwide. Great progress has been made in the management of CVD which has been influenced by the use of experimental animal models. These models provided information at cellular and molecular levels and allowed the development of treatment strategies. CVD models have been developed in many species, including large animals (e.g. pigs and dogs) and small animals (e.g. rats and mice). Although, no model can solely reproduce clinical HF, simulations of heart failure (HF) are available to experimentally tackle certain queries not easily resolved in humans. Induced HF may also be produced experimentally through myocardial infarction (MI), pressure loading, or volume loading. Volume loading is useful to look at hormone and electrolyte disturbances, while pressure loading models is helpful to study ventricular hypertrophy, cellular imbalance and vascular changes in HF. Coronary heart disease is assessed in MI animal models. In this review we describe various experimental models used to study the pathophysiology of HF.
T2  - Current Vascular Pharmacology
T1  - Heart Failure Models: Traditional and Novel Therapy
VL  - 13
IS  - 5
SP  - 658
EP  - 669
DO  - 10.2174/1570161113666150212151506
ER  - 

@article{
author = "Haidara, Mohamed A. and Assiri, Abdullah S. and Yassin, Hanaa Z. and Ammar, Hania I. and Obradović, Milan M. and Isenović, Esma R.",
year = "2015",
abstract = "Cardiovascular disease (CVD) is among the most major causes of morbidity and mortality worldwide. Great progress has been made in the management of CVD which has been influenced by the use of experimental animal models. These models provided information at cellular and molecular levels and allowed the development of treatment strategies. CVD models have been developed in many species, including large animals (e.g. pigs and dogs) and small animals (e.g. rats and mice). Although, no model can solely reproduce clinical HF, simulations of heart failure (HF) are available to experimentally tackle certain queries not easily resolved in humans. Induced HF may also be produced experimentally through myocardial infarction (MI), pressure loading, or volume loading. Volume loading is useful to look at hormone and electrolyte disturbances, while pressure loading models is helpful to study ventricular hypertrophy, cellular imbalance and vascular changes in HF. Coronary heart disease is assessed in MI animal models. In this review we describe various experimental models used to study the pathophysiology of HF.",
journal = "Current Vascular Pharmacology",
title = "Heart Failure Models: Traditional and Novel Therapy",
volume = "13",
number = "5",
pages = "658-669",
doi = "10.2174/1570161113666150212151506"
}

Haidara, M. A., Assiri, A. S., Yassin, H. Z., Ammar, H. I., Obradović, M. M.,& Isenović, E. R.. (2015). Heart Failure Models: Traditional and Novel Therapy. in Current Vascular Pharmacology, 13(5), 658-669.
https://doi.org/10.2174/1570161113666150212151506

Haidara MA, Assiri AS, Yassin HZ, Ammar HI, Obradović MM, Isenović ER. Heart Failure Models: Traditional and Novel Therapy. in Current Vascular Pharmacology. 2015;13(5):658-669.
doi:10.2174/1570161113666150212151506 .

Haidara, Mohamed A., Assiri, Abdullah S., Yassin, Hanaa Z., Ammar, Hania I., Obradović, Milan M., Isenović, Esma R., "Heart Failure Models: Traditional and Novel Therapy" in Current Vascular Pharmacology, 13, no. 5 (2015):658-669,
https://doi.org/10.2174/1570161113666150212151506 . .

TY  - JOUR
AU  - Bin-Jaliah, Ismaeel
AU  - Ammar, Hania I.
AU  - Mikhailidis, Dimitri P.
AU  - Dallak, Mohammed A.
AU  - Al-Hashem, Fahaid H.
AU  - Haidara, Mohamed A.
AU  - Yassin, Hanaa Z.
AU  - Bahnasi, Abeer A.
AU  - Rashed, Laila A.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3883
AB  - The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (Delta P/Delta t(max)) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P LT .001), RPP (P LT .001), and Delta P/Delta t(max) (P LT .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.
T2  - Angiology
T1  - Cardiac Adaptive Responses After Hypoxia in an Experimental Model
VL  - 61
IS  - 2
SP  - 145
EP  - 156
DO  - 10.1177/0003319709352486
ER  - 

@article{
author = "Bin-Jaliah, Ismaeel and Ammar, Hania I. and Mikhailidis, Dimitri P. and Dallak, Mohammed A. and Al-Hashem, Fahaid H. and Haidara, Mohamed A. and Yassin, Hanaa Z. and Bahnasi, Abeer A. and Rashed, Laila A. and Isenović, Esma R.",
year = "2010",
abstract = "The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (Delta P/Delta t(max)) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P LT .001), RPP (P LT .001), and Delta P/Delta t(max) (P LT .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.",
journal = "Angiology",
title = "Cardiac Adaptive Responses After Hypoxia in an Experimental Model",
volume = "61",
number = "2",
pages = "145-156",
doi = "10.1177/0003319709352486"
}

Bin-Jaliah, I., Ammar, H. I., Mikhailidis, D. P., Dallak, M. A., Al-Hashem, F. H., Haidara, M. A., Yassin, H. Z., Bahnasi, A. A., Rashed, L. A.,& Isenović, E. R.. (2010). Cardiac Adaptive Responses After Hypoxia in an Experimental Model. in Angiology, 61(2), 145-156.
https://doi.org/10.1177/0003319709352486

Bin-Jaliah I, Ammar HI, Mikhailidis DP, Dallak MA, Al-Hashem FH, Haidara MA, Yassin HZ, Bahnasi AA, Rashed LA, Isenović ER. Cardiac Adaptive Responses After Hypoxia in an Experimental Model. in Angiology. 2010;61(2):145-156.
doi:10.1177/0003319709352486 .

Bin-Jaliah, Ismaeel, Ammar, Hania I., Mikhailidis, Dimitri P., Dallak, Mohammed A., Al-Hashem, Fahaid H., Haidara, Mohamed A., Yassin, Hanaa Z., Bahnasi, Abeer A., Rashed, Laila A., Isenović, Esma R., "Cardiac Adaptive Responses After Hypoxia in an Experimental Model" in Angiology, 61, no. 2 (2010):145-156,
https://doi.org/10.1177/0003319709352486 . .