The Experts below are selected from a list of 3516 Experts worldwide ranked by ideXlab platform

Arumugam Sudalai - One of the best experts on this subject based on the ideXlab platform.

Km Shaffi - One of the best experts on this subject based on the ideXlab platform.

  • Use of the Hypertensive Agent Angiotensin Ii for Modifying Oxygen Delivery to Tumours
    Advances in experimental medicine and biology, 1994
    Co-Authors: Gillian M. Tozer, Km Shaffi, D. G. Hirst
    Abstract:

    Ischaemia-induced tumour hypoxia can limit the effectiveness of radiotherapy. Regions of deficient blood flow within tumours also limit the access of blood-borne anti-cancer Agents. Vasoconstrictor drugs, such as angiotensin II, have potential for improving the oxygen status of tumours via an increase in their blood flow. This would occur if the tumour perfusion pressure could be increased without increasing tumour vascular resistance. An increase in absolute tumour blood flow following i.v. infusion of angiotensin II has been reported in the literature (Hori et al.,1991,Tanda et al.,1991,Tokuda et al.,1990).The aims of this study were 1) to determine the relationship between blood flow response to angiotensin II and perfusion pressure and 2) to investigate whether angiotensin II induces any improvement in blood flow to very poorly perfused tumour regions which are critical for the outcome of both radiotherapy and chemotherapy.

  • Modification of tumour blood flow using the Hypertensive Agent, angiotensin II
    British journal of cancer, 1993
    Co-Authors: Gillian M. Tozer, Km Shaffi
    Abstract:

    The effects of different doses of angiotensin II (0.02 to 0.5 microgram kg-1 min-1 on mean arterial blood pressure, tissue blood flow and tissue vascular resistance were investigated in BD9 rats. Blood flow was measured using the uptake of 125I- or 14C-labelled iodoantipyrine (125I-IAP and 14C-IAP). Spatial heterogeneity of blood flow within tumours, before and after angiotensin II infusion, was also measured using 14C-IAP and an autoradiographic procedure. Mean arterial blood pressure rose steeply with angiotensin II dose. Blood flow to skeletal muscle, skin overlying the tumour, contralateral skin, small intestine and kidney tended to decline in a dose-dependent manner. Blood flow to the tumour was also reduced (to 80% of control values) but there was no dose response. Blood flow to the heart was slightly increased and blood flow to the brain was unaffected by angiotensin II. Vascular resistance, in all tissues, was increased by angiotensin II infusion. The increase in tumour tissue was similar to that found in skeletal muscle and small intestine and is likely to be caused by a direct vasoconstricting effect of the drug rather than autoregulation of tumour blood flow in the face of an increase in perfusion pressure. The reduction in overall blood flow at the highest perfusion pressure was due to a preferential effect of angiotensin II at the tumour periphery. These results show that some tumours, at least, can respond directly to the effects of vasoactive Agents.

Gillian M. Tozer - One of the best experts on this subject based on the ideXlab platform.

  • Use of the Hypertensive Agent Angiotensin Ii for Modifying Oxygen Delivery to Tumours
    Advances in experimental medicine and biology, 1994
    Co-Authors: Gillian M. Tozer, Km Shaffi, D. G. Hirst
    Abstract:

    Ischaemia-induced tumour hypoxia can limit the effectiveness of radiotherapy. Regions of deficient blood flow within tumours also limit the access of blood-borne anti-cancer Agents. Vasoconstrictor drugs, such as angiotensin II, have potential for improving the oxygen status of tumours via an increase in their blood flow. This would occur if the tumour perfusion pressure could be increased without increasing tumour vascular resistance. An increase in absolute tumour blood flow following i.v. infusion of angiotensin II has been reported in the literature (Hori et al.,1991,Tanda et al.,1991,Tokuda et al.,1990).The aims of this study were 1) to determine the relationship between blood flow response to angiotensin II and perfusion pressure and 2) to investigate whether angiotensin II induces any improvement in blood flow to very poorly perfused tumour regions which are critical for the outcome of both radiotherapy and chemotherapy.

  • Modification of tumour blood flow using the Hypertensive Agent, angiotensin II
    British journal of cancer, 1993
    Co-Authors: Gillian M. Tozer, Km Shaffi
    Abstract:

    The effects of different doses of angiotensin II (0.02 to 0.5 microgram kg-1 min-1 on mean arterial blood pressure, tissue blood flow and tissue vascular resistance were investigated in BD9 rats. Blood flow was measured using the uptake of 125I- or 14C-labelled iodoantipyrine (125I-IAP and 14C-IAP). Spatial heterogeneity of blood flow within tumours, before and after angiotensin II infusion, was also measured using 14C-IAP and an autoradiographic procedure. Mean arterial blood pressure rose steeply with angiotensin II dose. Blood flow to skeletal muscle, skin overlying the tumour, contralateral skin, small intestine and kidney tended to decline in a dose-dependent manner. Blood flow to the tumour was also reduced (to 80% of control values) but there was no dose response. Blood flow to the heart was slightly increased and blood flow to the brain was unaffected by angiotensin II. Vascular resistance, in all tissues, was increased by angiotensin II infusion. The increase in tumour tissue was similar to that found in skeletal muscle and small intestine and is likely to be caused by a direct vasoconstricting effect of the drug rather than autoregulation of tumour blood flow in the face of an increase in perfusion pressure. The reduction in overall blood flow at the highest perfusion pressure was due to a preferential effect of angiotensin II at the tumour periphery. These results show that some tumours, at least, can respond directly to the effects of vasoactive Agents.

Kurt Kimpinski - One of the best experts on this subject based on the ideXlab platform.

  • role of melatonin in blood pressure regulation an adjunct anti Hypertensive Agent
    Clinical and Experimental Pharmacology and Physiology, 2018
    Co-Authors: Jacquie Baker, Kurt Kimpinski
    Abstract:

    Cardiovascular diseases account for approximately one-third of all deaths each year. Of this, hypertension accounts for approximately 9.4 million deaths. Melatonin, the primary circadian hormone, has been substantiated as an effective and safe adjunct anti-Hypertensive Agent. In support of this, melatonin receptors have been identified within the central and peripheral nervous system, as well as the cardiovascular system, including various vascular tissues. Therefore, it is not surprising that recent research has emerged highlighting a key role of melatonin in autonomic regulation of blood pressure. In animals, pinealectomies elicit peripheral vasoconstriction and hypertension. In studies involving humans, both healthy controls and patient populations of essential and nocturnal hypertension, melatonin administration demonstrates significant hypotensive effects that yield clinically significant results. However, the precise mechanism by which melatonin elicits its hypotensive effects in humans require further investigation. This review focuses on melatonin, its role within the cardiovascular system and the emerging implications for its use as an anti-Hypertensive Agent. Additionally, this review will discuss the current thinking on potential mechanisms behind the hypotensive effects of melatonin including: endothelium-dependent vasodilation, anti-oxidant defence mechanisms and sympatho-vagal autonomic regulation.

Ram Chandra Gupta - One of the best experts on this subject based on the ideXlab platform.

  • lc determination of the anti ischemic and anti Hypertensive Agent cdri 93 478 in rat serum
    Journal of Pharmaceutical and Biomedical Analysis, 2001
    Co-Authors: Jawahar Lal, Ram Chandra Gupta
    Abstract:

    Abstract CDRI-93/478 is a potent anti-ischemic and anti-Hypertensive Agent. This compound is in advanced stage of pre-clinical trials. A high-performance liquid chromatographic (HPLC) method was developed for the analysis of CDRI-93/478 in rat serum, a species used for safety evaluation. The HPLC analysis, applicable to 1 ml volumes of serum, involved double extraction of serum samples with diethyl ether at alkaline pH followed by separation on a spheri-5 cyano column and the use of fluorescence detector at excitation wavelength 250 nm and emission wavelength 372 nm. The method was sensitive with a limit of quantitation of 10 ng ml −1 in rat serum and the recovery was more than 84%. The linearity was satisfactory as indicated by correlation of >0.99, in addition to the visual examination of the calibration curves. The precision and accuracy were acceptable as indicated by relative standard deviation (R.S.D.) ranging from 1.73 to 9.51%, bias values ranging from −7.31 to 8.68%. Moreover, CDRI-93/478 was stable in rat serum after being subjected to three freeze–thaw cycles. In-process stability evaluation showed the stability of the compound in processed samples lasted up to 168 h. The assay was found to be sensitive, specific, accurate, precise, and reliable for use in pharmacokinetic or toxicokinetic studies.

  • LC determination of the anti-ischemic and anti-Hypertensive Agent CDRI-93/478 in rat serum.
    Journal of pharmaceutical and biomedical analysis, 2001
    Co-Authors: Jawahar Lal, Ram Chandra Gupta
    Abstract:

    Abstract CDRI-93/478 is a potent anti-ischemic and anti-Hypertensive Agent. This compound is in advanced stage of pre-clinical trials. A high-performance liquid chromatographic (HPLC) method was developed for the analysis of CDRI-93/478 in rat serum, a species used for safety evaluation. The HPLC analysis, applicable to 1 ml volumes of serum, involved double extraction of serum samples with diethyl ether at alkaline pH followed by separation on a spheri-5 cyano column and the use of fluorescence detector at excitation wavelength 250 nm and emission wavelength 372 nm. The method was sensitive with a limit of quantitation of 10 ng ml −1 in rat serum and the recovery was more than 84%. The linearity was satisfactory as indicated by correlation of >0.99, in addition to the visual examination of the calibration curves. The precision and accuracy were acceptable as indicated by relative standard deviation (R.S.D.) ranging from 1.73 to 9.51%, bias values ranging from −7.31 to 8.68%. Moreover, CDRI-93/478 was stable in rat serum after being subjected to three freeze–thaw cycles. In-process stability evaluation showed the stability of the compound in processed samples lasted up to 168 h. The assay was found to be sensitive, specific, accurate, precise, and reliable for use in pharmacokinetic or toxicokinetic studies.