Delay in opening the infarct related coronary artery increases plasma atrial natriuretic peptide levels.

Plasma atrial natriuretic peptide (ANP) levels were measured in rabbits during the late healing phase of myocardial infarcts. Significant differences in plasma ANP levels (P < 0.02) were found between rabbits that had undergone very late (6 h) or early reperfusion (20 and 45 min of ischemia) of the infarct related coronary artery. Differences in ANP levels were independent of infarct size, ventricular remodeling and infarct expansion. We conclude late reperfusion of infarct related artery, independent of myocardial salvage, is associated with increased circulating ANP plasma levels.

Haptoglobin and malaria.

Haptoglobin gene knockout mice and wild-type controls were infected with Plasmodium berghei ANKA or Plasmodium chabaudi. The peak parasitaemia and parasite burden were higher in Hp-/- mice than in Hp+/+ mice. The increase in spleen weight following malaria infection was smaller in Hp-/- mice than in Hp+/+ animals. The occurrence of cerebral malaria in P. berghei ANKA infection was not different in Hp gene knockout mice and their controls.

Tissue distribution of indoleamine 2,3-dioxygenase in normal and malaria-infected tissue.

An immunohistochemical method was developed, using a polyclonal antibody, to detect the enzyme indoleamine 2,3-dioxygenase (IDO) in normal and malaria-infected tissue. Plasmodium berghei ANKA, a cerebral malaria (CM) model, and P. berghei K173, a non-cerebral malaria (NCM) model, were used. It was found that vascular endothelial cells were the primary site of IDO expression in both models of malaria infection and that this response was systemic, with the vascular endothelium of brain, heart, lung, spleen and uterus all staining positive. These results suggest that IDO is part of a systemic host response to parasite infection. Although high levels of IDO production alone may not cause pathology, it is possible that when its production is combined with other features of CM, such as breakdown of the blood-brain barrier (BBB), metabolites of the kynurenine pathway may be able to influence the otherwise tightly regulated, immunologically privileged site of the CNS and cause some of the symptoms and pathology observed.

A method to determine the fractal dimension of the cross-sectional jaggedness of the infarct scar edge.

This study describes the use of a shareware software package available from the National Institutes of Health for computing the fractal dimension. Specifically, when fractal analysis is used in its correct context it provides for a quantitative description of the space filling properties of two-dimensional objects. A rabbit model of post myocardial infarction is described where the cross-sectional infarct edge is reconstructed and its jaggedness determined by calculating its fractal dimension via the pixel dilation method. The fractal dimensions of the anterior and posterior lateral infarct edges were calculated to have a mean of 1.16 and 1.29, respectively. In conclusion, the fractal technique can be used to describe the complex jaggedness of the infarct edge. This case study also illustrates the fact that the complexity of an infarcted area is not uniform across the scar. For example, we found that the space filling properties of the anterior and posterior borders of a myocardial infarct can differ by more than 2-fold.

A semi-quantitative PCR method for the detection of low levels of apoptotic DNA fragmentation in a heart failure model.

Cells that are apoptotic and comprise less than 2% of the total cellular population are difficult to detect by conventional methods (i.e., DNA ladder). We discuss a new methodological technique, PCR-amplified DNA ladder, to detect very low levels of DNA fragmentation (indicative of apoptosis) in a myocardial infarct heart failure model. Results and methodology are contrasted with the traditional DNA ladder technique.