Cardiac electrophysiology: normal and ischemic ionic currents and the ECG.

Basic cardiac electrophysiology is foundational to understanding normal cardiac function in terms of rate and rhythm and initiation of cardiac muscle contraction. The primary clinical tool for assessing cardiac electrical events is the electrocardiogram (ECG), which provides global and regional information on rate, rhythm, and electrical conduction as well as changes in electrical activity associated with cardiac disease, particularly ischemic heart disease. This teaching review is written at a level appropriate for first- and second-year medical students.

Using thermal stress to model aspects of disease states.

Exposure to acute heat or cold stress elicits numerous physiological responses aimed at maintaining body temperatures. Interestingly, many of the physiological responses, mediated by the cardiovascular and autonomic nervous systems, resemble aspects of, or responses to, certain disease states. The purpose of this Perspective is to highlight some of these areas in order to explore how they may help us better understand the pathophysiology underlying aspects of certain disease states.

Oxygen modulation of superoxide radical injury in the krebs-perfused, isolated rabbit heart.

Myocardial malondialdehyde concentration (MDA) as an index of membrane lipoperoxidation was measured in previously ischemic isolated rabbit hearts reperfused with Krebs solution equilibrated with different oxygen concentrations. Hearts were subjected to a ischemic period of 30 min at 4 degrees C and then reperfused at 37 degrees C with a Krebs-Henseleit solution equilibrated with 95% oxygen (group 1), 65% oxygen (group 2), or 21% oxygen (group 3). MDA concentration in nanomoles per gram protein (mean +/- SEM) at the end of reperfusion in group 1 (n = 5) was 357 +/- 18; in group 2 (n = 5) 282 +/- 18; and in group 3 (n = 5) 246 +/- 16 (p =.

Role of nitric oxide and reactive oxygen species in platelet-activating factor-induced microvascular leakage.

Platelet-activating factor (PAF), released during inflammatory responses, increases microvascular permeability to fluid and macromolecules. Previous studies in the hamster cheek pouch microcirculation have shown that PAF-induced increases in permeability can be diminished by pretreatment with a nitric oxide synthase inhibitor indicating that nitric oxide is required for PAF to cause leakage, although nitric oxide itself does not cause leakage. We evaluated the hypothesis that PAF stimulates the production of reactive oxygen species (ROS) that then react with nitric oxide to form a new species that signals the increase in vascular permeability.