Samhita S. Rhodes, Ph.D.
Affiliations: | Marquette University, Milwaukee, WI, United States |
Area:
Signal Processing, Cardiac Electrophysiology, fMRIGoogle:
"Samhita Rhodes"Mean distance: 17.88 (cluster 23)
Parents
Sign in to add mentor| Kristina Marie Ropella | grad student | 2003 | Marquette University | |
| (Analysis of the relationship between myoplasmic ionized calcium and contractile function in guinea pig intact hearts.) | ||||
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Publications
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| Rhodes SS, Camara AK, Aldakkak M, et al. (2015) Stretch-induced increase in cardiac contractility is independent of myocyte Ca2+ while block of stretch channels by streptomycin improves contractility after ischemic stunning. Physiological Reports. 3 |
| Rhodes SS, Camara AK, Heisner JS, et al. (2012) Reduced mitochondrial Ca2+ loading and improved functional recovery after ischemia-reperfusion injury in old vs. young guinea pig hearts. American Journal of Physiology. Heart and Circulatory Physiology. 302: H855-63 |
| Riess ML, Rhodes SS, Stowe DF, et al. (2009) Comparison of cumulative planimetry versus manual dissection to assess experimental infarct size in isolated hearts. Journal of Pharmacological and Toxicological Methods. 60: 275-80 |
| Heinen A, Aldakkak M, Stowe DF, et al. (2007) Reverse electron flow-induced ROS production is attenuated by activation of mitochondrial Ca2+-sensitive K+ channels. American Journal of Physiology. Heart and Circulatory Physiology. 293: H1400-7 |
| Camara AK, Aldakkak M, Heisner JS, et al. (2007) ROS scavenging before 27 degrees C ischemia protects hearts and reduces mitochondrial ROS, Ca2+ overload, and changes in redox state. American Journal of Physiology. Cell Physiology. 292: C2021-31 |
| Heinen A, Camara AK, Aldakkak M, et al. (2007) Mitochondrial Ca2+-induced K+ influx increases respiration and enhances ROS production while maintaining membrane potential. American Journal of Physiology. Cell Physiology. 292: C148-56 |
| An J, Rhodes SS, Jiang MT, et al. (2006) Anesthetic preconditioning enhances Ca2+ handling and mechanical and metabolic function elicited by Na+-Ca2+ exchange inhibition in isolated hearts. Anesthesiology. 105: 541-9 |
| Rhodes SS, Camara AK, Ropella KM, et al. (2006) Ischemia reperfusion dysfunction changes model-estimated kinetics of myofilament interaction due to inotropic drugs in isolated hearts. Biomedical Engineering Online. 5: 16 |
| Rhodes SS, Ropella KM, Camara AK, et al. (2006) Ischemia-reperfusion injury changes the dynamics of Ca2+-contraction coupling due to inotropic drugs in isolated hearts. Journal of Applied Physiology (Bethesda, Md. : 1985). 100: 940-50 |
| Riess ML, Camara AK, Rhodes SS, et al. (2005) Increasing heart size and age attenuate anesthetic preconditioning in guinea pig isolated hearts. Anesthesia and Analgesia. 101: 1572-6 |