Andrew J. Patterson
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Andrew J. Patterson has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
Amy Chow
From the Department of Anesthesia (AJP, RA) and Departments of Medicine and Molecular and Cellular Physiology (BK), Stanford University, Stanford, CA; Gerontology Research Center (WZ, RPX), National Institute on Aging, Baltimore, MD; Stanford University Medical School (AC), Stanford, CA; and Department of Pathology (JK), Veterans Administration Medical Center, Palo Alto, CA
1 shared publicationBrian Kobilka
From the Department of Anesthesia (AJP, RA) and Departments of Medicine and Molecular and Cellular Physiology (BK), Stanford University, Stanford, CA; Gerontology Research Center (WZ, RPX), National Institute on Aging, Baltimore, MD; Stanford University Medical School (AC), Stanford, CA; and Department of Pathology (JK), Veterans Administration Medical Center, Palo Alto, CA
1 shared publicationJon Kosek
From the Department of Anesthesia (AJP, RA) and Departments of Medicine and Molecular and Cellular Physiology (BK), Stanford University, Stanford, CA; Gerontology Research Center (WZ, RPX), National Institute on Aging, Baltimore, MD; Stanford University Medical School (AC), Stanford, CA; and Department of Pathology (JK), Veterans Administration Medical Center, Palo Alto, CA
1 shared publicationRani Agrawal
From the Department of Anesthesia (AJP, RA) and Departments of Medicine and Molecular and Cellular Physiology (BK), Stanford University, Stanford, CA; Gerontology Research Center (WZ, RPX), National Institute on Aging, Baltimore, MD; Stanford University Medical School (AC), Stanford, CA; and Department of Pathology (JK), Veterans Administration Medical Center, Palo Alto, CA
1 shared publicationRui Ping Xiao
From the Department of Anesthesia (AJP, RA) and Departments of Medicine and Molecular and Cellular Physiology (BK), Stanford University, Stanford, CA; Gerontology Research Center (WZ, RPX), National Institute on Aging, Baltimore, MD; Stanford University Medical School (AC), Stanford, CA; and Department of Pathology (JK), Veterans Administration Medical Center, Palo Alto, CA
1 shared publicationWeizhong Zhu
From the Department of Anesthesia (AJP, RA) and Departments of Medicine and Molecular and Cellular Physiology (BK), Stanford University, Stanford, CA; Gerontology Research Center (WZ, RPX), National Institute on Aging, Baltimore, MD; Stanford University Medical School (AC), Stanford, CA; and Department of Pathology (JK), Veterans Administration Medical Center, Palo Alto, CA
1 shared publication
Latest Publications
- 1 April 2004
- Published by Wolters Kluwer Health in Critical Care Medicine
- Vol. 32 (4) , 1041-1048
Protecting the myocardium: A role for the β2 adrenergic receptor in the heart
Objective The sympathetic nervous system enhances cardiac muscle function by activating β adrenergic receptors (βARs). Recent studies suggest that chronic βAR stimulation is detrimental, however, and that it may play a role in the clinical deterioration of patients with congestive heart failure. To examine the impact of chronic β1AR and β2AR subtype stimulation individually, we studied the cardiovascular effects of catecholamine infusions in βAR subtype knockout mice (β1KO, β2KO). Design Prospective, randomized, experimental study. Setting Animal research laboratory. Subjects β1KO and β2KO mice and wild-type controls. Interventions The animals were subjected to 2 wks of continuous infusion of the βAR agonist isoproterenol. Analyses of cardiac function and structure were performed during and 3 days after completion of the infusions. Functional studies included graded exercise treadmill testing, in vivo assessments of left ventricular function using Mikro-Tip catheter transducers, right ventricular pressure measurements, and analyses of organ weight to body weight ratios. Structural studies included heart weight measurements, assessments of myocyte ultrastructure using electron microscopy, and in situ terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick-end labeling staining to quantitate myocyte apoptosis. Measurements and Main Results We found that isoproterenol-treated β2KO mice experienced greater mortality rates (p = .001, chi-square test using Fisher’s exact method) and increased myocyte apoptosis at 3- and 7-day time points (p = .04 and p = .0007, respectively, two-way analysis of variance). Conclusion The results of this study suggest that in vivo β2AR activation is antiapoptotic and contributes to myocardial protection.
- 1 April 2004
- Published by Wolters Kluwer Health in Critical Care Medicine
- Vol. 32 (4) , 1041-1048
Protecting the myocardium: A role for the β2 adrenergic receptor in the heart
Objective The sympathetic nervous system enhances cardiac muscle function by activating β adrenergic receptors (βARs). Recent studies suggest that chronic βAR stimulation is detrimental, however, and that it may play a role in the clinical deterioration of patients with congestive heart failure. To examine the impact of chronic β1AR and β2AR subtype stimulation individually, we studied the cardiovascular effects of catecholamine infusions in βAR subtype knockout mice (β1KO, β2KO). Design Prospective, randomized, experimental study. Setting Animal research laboratory. Subjects β1KO and β2KO mice and wild-type controls. Interventions The animals were subjected to 2 wks of continuous infusion of the βAR agonist isoproterenol. Analyses of cardiac function and structure were performed during and 3 days after completion of the infusions. Functional studies included graded exercise treadmill testing, in vivo assessments of left ventricular function using Mikro-Tip catheter transducers, right ventricular pressure measurements, and analyses of organ weight to body weight ratios. Structural studies included heart weight measurements, assessments of myocyte ultrastructure using electron microscopy, and in situ terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick-end labeling staining to quantitate myocyte apoptosis. Measurements and Main Results We found that isoproterenol-treated β2KO mice experienced greater mortality rates (p = .001, chi-square test using Fisher’s exact method) and increased myocyte apoptosis at 3- and 7-day time points (p = .04 and p = .0007, respectively, two-way analysis of variance). Conclusion The results of this study suggest that in vivo β2AR activation is antiapoptotic and contributes to myocardial protection.