Patients with heart disease are frequently treated with supplemental oxygen. Although oxygen can exhibit vasoactive properties in many vascular beds, its effects on the coronary circulation have not been fully characterized. To examine whether supplemental oxygen administration affects coronary blood flow (CBF) in a clinical setting, we measured in 18 patients with stable coronary heart disease the effects of breathing 100% oxygen by face mask for 15 min on CBF (via coronary Doppler flow wire), conduit coronary diameter, CBF response to intracoronary infusion of the endothelium-dependent dilator ACh and to the endothelium-independent dilator adenosine, as well as arterial and coronary venous concentrations of the nitric oxide (NO) metabolites nitrotyrosine, NO(2)(-), and NO(3)(-). Relative to breathing room air, breathing of 100% oxygen increased coronary resistance by approximately 40%, decreased CBF by approximately 30%, increased the appearance of nitrotyrosine in coronary venous plasma, and significantly blunted the CBF response to ACh. Oxygen breathing elicited these changes without affecting the diameter of large-conduit coronary arteries, coronary venous concentrations of NO(2)(-) and NO(3)(-), or the coronary vasodilator response to adenosine. Administering supplemental oxygen to patients undergoing cardiac catheterization substantially increases coronary vascular resistance by a mechanism that may involve oxidative quenching of NO within the coronary microcirculation.

Objectives: To provide a multiorganizational statement to update recommendations for critical care pharmacy practice and make recommendations for future practice. A position paper outlining critical care pharmacist activities was last published in 2000. Since that time, significant changes in healthcare and critical care have occurred. Design: The Society of Critical Care Medicine, American College of Clinical Pharmacy Critical Care Practice and Research Network, and the American Society of Health-Systems Pharmacists convened a joint task force of 15 pharmacists representing a broad cross-section of critical care pharmacy practice and pharmacy administration, inclusive of geography, critical care practice setting, and roles. The Task Force chairs reviewed and organized primary literature, outlined topic domains, and prepared the methodology for group review and consensus. A modified Delphi method was used until consensus (> 66% agreement) was reached for each practice recommendation. Previous position statement recommendations were reviewed and voted to either retain, revise, or retire. Recommendations were categorized by level of ICU service to be applicable by setting and grouped into five domains: patient care, quality improvement, research and scholarship, training and education, and professional development. Main Results: There are 82 recommendation statements: 44 original recommendations and 38 new recommendation statements. Thirty-four recommendations represent the domain of patient care, primarily relating to critical care pharmacist duties and pharmacy services. In the quality improvement domain, 21 recommendations address the role of the critical care pharmacist in patient and medication safety, clinical quality programs, and analytics. Nine recommendations were made in the domain of research and scholarship. Ten recommendations were made in the domain of training and education and eight recommendations regarding professional development. Conclusions: Critical care pharmacists are essential members of the multiprofessional critical care team. The statements recommended by this taskforce delineate the activities of a critical care pharmacist and the scope of pharmacy services within the ICU. Effort should be made from all stakeholders to implement the recommendations provided, with continuous effort toward improving the delivery of care for critically ill patients.

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Objectives: Provide a multiorganizational statement to update the statement from a paper in 2000 about critical care pharmacy practice and makes recommendations for future practice. Design: The Society of Critical Care Medicine, American College of Clinical Pharmacy Critical Care Practice and Research Network, and the American Society of Health-Systems Pharmacists convened a joint task force of 15 pharmacists representing a broad cross-section of critical care pharmacy practice and pharmacy administration, inclusive of geography, critical care practice setting, and roles. The Task Force chairs reviewed and organized primary literature, outlined topic domains, and prepared the methodology for group review and consensus. A modified Delphi method was used until consensus (> 66% agreement) was reached for each practice recommendation. Previous position statement recommendations were reviewed and voted to either retain, revise, or retire. Recommendations were categorized by level of ICU service to be applicable by setting, and grouped into five domains: patient care, quality improvement, research and scholarship, training and education, and professional development. Main Results: There are 82 recommendation statements: forty-four original recommendations and 38 new recommendation statements. Thirty-four recommendations were made for patient care, primarily relating to critical care pharmacist duties and pharmacy services. In the quality improvement domain, 21 recommendations address the role of the critical care pharmacist in patient and medication safety, clinical quality programs, and analytics. Nine recommendations were made in the domain of research and scholarship. Ten recommendations are in the domain of training and education and eight recommendations regarding professional development. Conclusions: The statements recommended by this taskforce delineate the activities of a critical care pharmacist and the scope of pharmacy services within the ICU. Effort should be made from all stakeholders to implement the recommendations provided, with continuous effort toward improving the delivery of care for critically ill patients.

We proposed that mitral cell ␤1-adrenoceptor activation mediates rat pup odor preference learning. Here we evaluate ␤1-, ␤2-, ␣1-, and ␣2-adrenoceptor agonists in such learning. The ␤1-adrenoceptor agonist, dobutamine, and the ␣1-adrenoceptor agonist, phenylephrine, induced learning, and both exhibited an inverted U-curve dose-response relationship to odor preference learning. Phenylephrine-induced learning occurred in the presence of propranolol to prevent indirect activation of ␤-adrenoceptors. ␣1-Adrenoceptor mediation may represent a novel mechanism inducing learning or may increase cAMP in mitral cells via indirect activation of GABA B receptors. Neither the ␤2-adrenoceptor agonist, salbutamol, nor the ␣2-adrenoceptor agonist, clonidine, induced learning.Since initial ground breaking studies in Aplysia (for a review, see Pittenger and Kandel 2003) and later Drosophila (Yin and Tully 1996), there has been interest in the hypothesis that the cyclic adenosine monophosphate/protein kinase A/cyclic adenosine monophosphate response element binding protein (cAMP/PKA/ CREB) cascade might be a universal mechanism underlying learning and memory. In mammalian models there is also supporting evidence for such an assertion, but in adult rat models the associative pathways involved in recruiting cAMP activation in learning are difficult to identify (Alberini 1999). The rat pup odor preference learning model offers an advantage in that respect as the role of ␤-adrenoceptor activation as an unconditioned stimulus is well established (Sullivan et al. 1989(Sullivan et al. , 1991aSullivan and Wilson 1991;Langdon et al. 1997), and more recently, a causal role for cAMP in this form of associative learning has been demonstrated .In 2003, we proposed that early odor preference learning in the week-old rat pup induced by pairing a novel odor with tactile stimulation (stroking), or with injection of the nonselective ␤-agonist isoproterenol, was mediated by the activation of ␤1-adrenoceptors on mitral cells that interacted with glutamatergic odor input to the same cells (Yuan et al. 2003b). This interaction was proposed to produce alterations in mitral cell connectivity that altered the pup's memory of, and preference for, the novel odor. We showed that ␤1-adrenoceptors are predominantly localized on mitral cells and that they are colocalized there with 5-HT 2A receptors (Yuan et al. 2003b), which facilitate learning by potentiating the cAMP response initiated by ␤1-adrenoceptors. We have also found that cAMP has a causal role in odor preference learning consistent with our hypothesis (Yuan et al. 2003a,b).All previous work with odor preference learning and ␤-adrenoceptor activation has used the nonselective ␤-adrenoceptor agonist isoproterenol. It has not been demonstrated that selective ␤1-adrenoceptor activation produces learning. Isoproterenol, infused directly into the olfactory bulb (Sullivan et al. 2000) or given systemically (Sullivan et al. 1991a;Langdon et al. 1997), induces odor preference learning when paired with a nov...