Myocardial metabolic alterations after contrast angiography.

Contrast media used during angiography are known to produce transient alterations in cardiovascular physiology. However, little information is available concerning what alterations, if any, occur in myocardial metabolism after contrast angiography. Sixteen patients with symptoms of ischemic heart disease undergoing elective left ventriculography were studied. Coronary sinus and arterial blood samples were obtained for free fatty acids, glucose and lactate before and after performing left ventriculography with Renografin-76. Coronary blood flow was determined by the thermodilution technique. Five minutes after ventriculography, the arterial level of free fatty acids had decreased by 18.0 +/- 4.9 percent (mean +/- standard deviation) from the baseline (before angiography) samples (probability [p] less than 0.001). Associated with this decrease in arterial free fatty acids was an increase in the myocardial uptake of this substrate. At 5 minutes after left ventriculography, the free fatty acid uptake had increased 48.5 +/- 33.0 percent compared with the baseline value (p less than 0.001). After the injection of contrast medium, there was no significant change in the arterial levels of glucose or lactate. However, significant decreases in the myocardial uptake of glucose and lactate were demonstrated (-72.5 +/- 44.5 percent [p less than 0.001] and -43.2 +/- 22.9 percent [p less than 0.001], respectively) at 5 minutes. The changes in arterial free fatty acids and in the myocardial uptake of the various substrates persisted throughout the sampling period of 20 minutes after ventriculography. These results demonstrate that contrast medium significantly alters myocardial metabolism. These metabolic alterations persist longer than the hemodynamic changes induced by contrast angiography.

Ascorbic acid inhibits replication and infectivity of avian RNA tumor virus.

Ascorbic acid, at nontoxic concentrations, causes a substantial reduction in the ability of avian tumor viruses to replicate in both primary avian tendon cells and chicken embryo fibroblasts. The virus-infected cultures appear to be less transformed in the presence of ascorbic acid by the criteria of morphology, reduced glucose uptake, and increased collagen synthesis. The vitamin does not act by altering the susceptibility of the cells to initial infection and transformation, but instead appears to interfere with the spread of infection through a reduction in virus replication and virus infectivity. The effect is reversible and requires the continuous presence of the vitamin in the culture medium.

The uncoupled regulation of fibronectin and collagen synthesis in Rous sarcoma virus transformed avian tendon cells.

We have investigated the regulation of fibronectin and procollagen synthesis in normal and Rous sarcoma virus transformed primary avian tendon cells. These two proteins interact at the cell periphery and both are reportedly lost upon transformation. We thus examined whether their synthesis was coordinately regulated in Rous sarcoma virus-infected cells. It was found that while the synthesis of both pro alpha 1 and pro alpha 2 peptides was reduced upon transformation, the synthesis of fibronectin was not altered. Nevertheless, long term radiolabeling demonstrated that fibronectin levels were reduced in transformed cells. It is concluded that the reduction in levels of these components at the surface is brought about by different mechanisms; collagen levels being regulated by procollagen synthesis and fibronectin levels by degradation and/or release into the culture medium. The possibility is discussed that fibronectin is lost from the cell periphery of primary avian tendon cells as a consequence of decreased levels of anchoring collagen molecules.

Primary avian tendon cells in culture. An improved system for understanding malignant transformation.

Primary avian tendon (PAT) cells which maintain their differentiated state in culture are rapidly transformed by Rous sarcoma virus. By criteria of morphology, increased rate of 2-deoxyglucose uptake, and loss of density dependent growth control, PAT cells transform as well as their less differentiated counterpart, chick embryo fibroblasts. In addition, the percentage of collagen produced by PAT cells drops on transformation by an order of magnitude, from 23 to 2.5%, but is unaffected by viral replication of a transformation-defective mutant. The responsiveness of normal and transformed PAT cells to various environmental factors changes dramatically upon transformation. Normal PAT cells respond to the presence of ascorbate and high cell density by raising the level of collagen synthesis from 5 to 23%. Transformed PAT cells are totally unresponsive. These and previously reported results lead us to postulate that the break-down in the normal regulatory mechanisms used by the cell to maintain the differentiated state is related to or is responsible for the onset of malignant transformation.