31Dec/16

Pulmonary Edema in PH & PVOD – Potential Causes of PVOD Misdiagnosis

*DISCLAIMER: These are my own thoughts and opinions based on my research and are not meant to be taken as medical advice.* Below is a potential explanation for how edema could occur in Pulmonary Hypertension (PH) patients receiving vasodilator therapy, thus leading to them being potentially misdiagnosed for Pulmonary Veno-Occlusive Disease (PVOD)… It makes sense to think that because a PH patient does not respond to vasodilator therapy well, or experiences edema due to vasodilator therapy, it may be an indication that they have PVOD. The theory goes that vasodilators can “open” up the vasculature (even in PH patients) and if the veins are “occluded” or non-responsive/rigid, then there is a large pressure difference that occurs when the blood flows from the “open” to “closed/rigid” section causing backpressure and edema: “PAH-specific vasodilator therapies may cause an augmentation of pulmonary arteriolar blood flow against the fixed resistance of occluded pulmonary venules and veins.… Read More...
13Aug/16

Pulmonary Hypertension – Atherosclerosis of the Lungs?

The passage below is from “Metabolic Regulation: A Human Perspective”, by Keith N. Frayn. I sometimes read things with a “PH filter” (and sometimes with a more global filter depending on context), and this particular passage was read with my “PH filter”… It got me thinking about the relationship of elevated non-esterified fatty acid concentrations in the plasma, adipose tissue, atherosclerosis, and if there is any connection between those and pulmonary hypertension. For some perspective, fatty acid metabolism is dysregulated in PH patients, with decreased fatty acid oxidation in myocardium and potentially increased lipid accumulation in myocardium and other tissues, increasing risk of lipotoxicity.… Read More...
31Jul/16

The Pentose Phosphate Path and PH, Part I – RBCs, G6PD, & GSH

The pentose phosphate pathway (PPP) is a metabolic pathway that parallels glycolysis. In cells, within the cytosol, glucose is converted into glucose 6-phosphate (catalyzed by the enzyme hexokinase), which can then either 1) enter glycolysis (and subsequent glucose oxidation via citric acid cycle) to produce ATP, or 2) enter the PPP. The PPP (diagram below) is primarily an anabolic pathway; the primary purpose being the following: to produce molecules (specifically 5 carbon sugars, and Ribose-5-phosphate) used for fatty acid synthesis, nucleic acid synthesis, and protein synthesis. However, another important purpose of the PPP is to produce NADPH, a high energy electron carrier.… Read More...
31Jul/16

Thought Of The Day – AMPK, Pulmonary Vasculature & RV

Today’s thought stems from a quote I found reading Metabolic Regulation: A Human Perspective by Keith N. Frayn. This is one of my new favorite books… Quote: “AMPK senses energy status of the cell: when there is a drain on ATP, AMP rises and the AMPK is activated, leading in turn to inhibition of ATP utilizing pathways (particularly biosynthetic pathways) and activation of ATP-generating pathways (glucose uptake, glycolysis, fatty acid oxidation).” Thought: AMPK (5′ AMP-activated protein kinase) activation in some form, either via dietary means, or as a drug target, would seem to be a good idea for the pulmonary vasculature as it would potentially prevent proliferation of PASMC’s and PAEC’s, and perhaps even adventitial fibroblasts (because of the “preventing biosynthetic pathway” feature stated above).… Read More...