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Opioids are the most potent analgesics available and have long been the standard treatment for both acute and chronic pain. However, they are not being used to their full potential in certain areas of pain management, such as chronic cancer and noncancer pain. There are a variety of reasons for this, ranging from political ideology to uncorroborated concerns about the safety and tolerability of opioids, including patient addiction and dependency. This review addresses the increasing quantity of comparative data that facilitate the differentiation of opioids with respect to their safety and tolerability. [ABSTRACT FROM AUTHOR]

Opioids are the most potent analgesics available and have long been the standard treatment for both acute and chronic pain. However, they are not being used to their full potential in certain areas of pain management, such as chronic cancer and noncancer pain. There are a variety of reasons for this, ranging from political ideology to uncorroborated concerns about the safety and tolerability of opioids, including patient addiction and dependency. This review addresses the increasing quantity of comparative data that facilitate the differentiation of opioids with respect to their safety and tolerability. [ABSTRACT FROM AUTHOR]

Angiogenesis is an important issue in cancer research and opioids are often used to treat pain in cancer patients. Therefore it is important to know if the use of opioids is associated with an aberrant stimulation of tumour growth triggered by the stimulation of angiogenesis in cancer patients. Some studies in the literature already suggested the presence of the ì3 opioid receptor, known as the receptor for many opioids, on endothelial cells, which are key players in the process of angiogenesis. In this study we used endothelial cells, known to express the ì3 opioid receptor (MOR3), to evaluate the effects of morphine on angiogenesis. We first investigated the effect of morphine on the proliferation of endothelial cells. We showed that morphine is able to stimulate vascular endothelial cell proliferation in vitro. This effect of morphine is mediated by the MAPK pathway as pre-treatment with PD98059 inhibited this excessive proliferation. Because previous studies indicated NO as a downstream messenger we investigated the role of NO in the aberrant proliferation of endothelial cells. Our data could not confirm these findings using intracellular NO measurements and quantitative fluorescence microscopy. The potential use and pitfalls of opioids in cancer patients is discussed in light of these negative findings. [ABSTRACT FROM AUTHOR]