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Books on the topic 'Vasodilators'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 August 2024

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1

John, Gaddum. Vasodilator substances of the tissues. Cambridge: Cambridge University Press, 1986.

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2

Feletou, Michel. EDHF: The complete story. Boca Raton, FL: CRC/Taylor & Francis, 2006.

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3

1895-1967, Kilborn Leslie G., ed. Adrenalin vasodilator mechanisms in the cat at different ages. [Toronto]: University Library, pub. by the Librarian, 1994.

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4

Pang, Catherine C. Y. The effects of drugs on the venous system. Austin: R.G. Landes, 1994.

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5

U, Abshagen, ed. Clinical pharmacology of antianginal drugs. Berlin: Springer-Verlag, 1985.

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6

S, Manning Allan, and Szendey George L, eds. Prenylamine: A novel approach to myocardial protection. New York, N.Y: Raven Health Care Communications, 1988.

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7

Deutsche Gesellschaft für Neurochirurgie. Tagung. Stabilizing craniocervical operations: Calcium antagonists in SAH : current legal issues. Berlin: Springer-Verlag, 1990.

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8

Brett, Stephen James. Inhaled vasodilator therapy, nitric oxide and pulmonary inflammation. Birmingham: University of Birmingham, 1998.

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9

M, Vanhoutte Paul, Shepherd John T. 1919-, International Union of Physiological Sciences. Congress, and International Symposium on Mechanisms of Vasodilatation (4th : 1986 : Rochester, Minn.), eds. Vasodilatation: Vascular smooth muscle, peptides, autonomic nerves, and endothelium. New York: Raven Press, 1988.

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10

Frank, Cuttitta, and Martínez Alfredo, eds. Adrenomedulin. Amsterdam: IOS Press, 1998.

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11

1962-, Martínez Alfredo, and Cuttitta Frank, eds. Adrenomedullin. Amsterdam: IOS Press, 1998.

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12

B, Garthoff, ed. Experimental hypertension and therapeutic progress: Vasodilation and beyond. Berlin: Springer-Verlag, 1995.

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13

Karsten, Schrör, and Pace-Asciak C, eds. Mediators in the cardiovascular system: Regional ischemia. Basel, Switz: Birkhäuser Verlag, 1995.

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14

N, Cohn Jay, and Rittinghausen R, eds. Mononitrates: [International Symposium on Mononitrates, Montreux, Switzerland, June 14-16, 1984]. Berlin: Springer-Verlag, 1985.

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15

Groeneveld, A. B. J., and Alexandre Lima. Vasodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0035.

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Vasodilators are commonly used in the intensive care unit (ICU) to control arterial blood pressure, unload the left or the right heart, control pulmonary artery pressure, and improve microcirculatory blood flow. Vasodilator refers to drugs acting directly on the smooth muscles of peripheral vessel walls and drugs are usually classified based on their mechanism (acting directly or indirectly) or site of action (arterial or venous vasodilator). Drugs that have a predominant effect on resistance vessels are arterial dilators and drugs that primarily affect venous capacitance vessels are venous dilators. Drugs that interfere with sympathetic nervous system, block renin-angiotensin system, phosphodiesterase inhibitors, and nitrates are some examples of drugs with indirect effect. Vasodilator drugs play a major therapeutic role in hypertensive emergencies, primary and secondary pulmonary hypertension, acute left heart, and circulatory shock. This review discusses the main types of vasodilators drugs commonly used in the ICU.
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16

Chousterman, Benjamin, and Didier Payen. Pulmonary vasodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0039.

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Pulmonary vasodilators (PV) are commonly used in the intensive care unit (ICU) to treat pulmonary hypertension and/or hypoxaemia. The choice of drug is based on its pharmacokinetic and pharmacodynamic properties. The inhaled route of administration is preferred to treat hypoxaemia as it improves the ventilation/perfusion ratio. Systemic administration of PVs can lead to a decrease of mean arterial pressure and a worsening of hypoxaemia. Despite their beneficial effects, PVs have not shown improvement in mortality in acute respiratory distress syndrome patients. Rebound of hypoxaemia and/or pulmonary arterial hypertension should be prevented during PV treatment discontinuation with a slow de-escalation protocol. This chapter reviews the use of the main PV available for use in the ICU.
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17

Just, H., W. D. Bussmann, and F. Burkart. Vasodilators in Chronic Heart Failure. Springer, 2011.

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18

Just, H., W. D. Bussmann, and F. Burkart. Vasodilators in Chronic Heart Failure. Springer London, Limited, 2012.

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19

Shen, Howard. MemoCharts Pharmacology: Vasodilators (Review chart). Minireview, 2004.

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20

Heidrich, H. Proof of Therapeutical Effectiveness of Nootropic and Vasoactive Drugs: Advances in Clinical and Experimental Nicergoline Research. Springer, 1986.

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21

Proof of therapeutical effectiveness of nootropic and vasoactive drugs: Advances in clinical and experimental nicergoline research. Berlin: Springer-Verlag, 1986.

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22

Feletou, Michel, and Paul Vanhoutte. EDHF: The Complete Story. CRC, 2005.

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23

Feletou, Michel. Edhf: The Complete Story. Taylor & Francis Group, 2012.

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24

Vanhoutte, Paul M., Michel Feletou, Paul Vanhoutte, and Michel Félétou. EDHF: The Complete Story. Taylor & Francis Group, 2005.

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25

Arterial Vasodilation: Mechanisms and Therapy. Lea & Febiger, 1993.

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26

Finch, Michael Brendan. Haemodynamic effects of some peripheral vasodilators in normal man and in patients with Raynaud's syndrome. 1986.

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27

Kågström, Jens. Regulation of gastrointestinal blood flow in fish by vasoactive neuropeptides: With emphasis on putative vasodilators. 1997.

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28

Clinical Pharmacology of Antianginal Drugs. Island Press, 1985.

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29

Adam, W. E., W. Bleifeld, U. Abshagen, and D. G. Gibson. Clinical Pharmacology of Antianginal Drugs. Springer London, Limited, 2012.

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30

Charlier, R., Bacq Z. M, and P. Alexander. Coronary Vasodilators : International Series of Monographs on Pure and Applied Biology Division: Modern Trends in Physiological Sciences. Elsevier Science & Technology Books, 2013.

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31

Schwarte, Lothar A., Stephan A. Loer, J. K. Götz Wietasch, and Thomas W. L. Scheeren. Cardiovascular drugs in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0019.

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Anaesthetists should be familiar with currently available cardiovascular drugs used to maintain cardiovascular stability and achieve haemodynamic goals in surgical patients. The first part of this chapter summarizes antihypertensive agents, and the second part discusses positive inotropic drugs and vasopressors, which can be used perioperatively. Selection of vasoactive agents should be guided by the therapeutic goal (e.g. decreasing or increasing blood pressure or blood flow) and the underlying pathophysiology. Choice of catecholamines in a given situation should be based on the desired effects, that is, goals that can be monitored. Generally speaking, it is easier to affect blood pressure than cardiac output, and how to optimize regional and microcirculatory blood flow remains uncertain. Regardless of the chosen intervention, its haemodynamic effects should be closely monitored and always evaluated against the clinical effects. Recent developments include the definition of haemodynamic goals (goal-directed therapy) and clinical end-points, which seem to decrease morbidity and mortality, regardless of the goals defined and interventions used. With regard to mortality, use of inotropic agents has been associated with adverse outcomes, whereas the use of vasodilators has not. Inotropes in combination with vasodilators have the highest mortality.
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32

Vanhoutte, Paul M. Edhf 2002. Taylor & Francis Group, 2001.

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33

Vanhoutte, Paul M. Edhf 2002. CRC, 2001.

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34

Vanhoutte, Paul M. Edhf 2002. Taylor & Francis Group, 2001.

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35

Vanhoutte, Paul M. Edhf 2002. Taylor & Francis Group, 2001.

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36

Vanhoutte, Paul M. Edhf 2002. Taylor & Francis Group, 2001.

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37

Vanhoutte, Paul M. Edhf 2002. Taylor & Francis Group, 2001.

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38

Vanhoutte, Paul M. Edhf 2002. Taylor & Francis Group, 2001.

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39

Patel, Mikin V., and Steven Zangan. Optimizing Carbon Dioxide Peripheral Arteriography. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0103.

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Angiography relies on the use of contrast medium for visualization of the vessel. Iodinated contrast can be contraindicated in patients with renal impairment or iodinated contrast allergy, so carbon dioxide (CO2) gas can be a useful alternative. A number of technical and postural parameters can optimize CO2 angiography, and vasodilators can be used to improve imaging of peripheral vessels. Although CO2 has distinct advantages, the limitations of CO2 angiography must be well understood. Operators should be aware that CO2 angiography can lead to overestimation of vessel size and can lead to complications such as transient ischemia of tissues, alterations of blood chemistry, neurotoxicity, and “vapor lock.”
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40

The Effects of Drugs in the Venous System. Landes Bioscience, 1994.

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41

Vanhoutte, Paul M. Vasodilator Mechanisms (Bibliotheca Cardiologica). S. Karger AG (Switzerland), 1985.

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42

Kreit, John W. Acute Respiratory Distress Syndrome (ARDS). Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0012.

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Acute Respiratory Distress Syndrome reviews the definitions, causes, pathophysiology, and management of this relatively common, life-threatening disorder. This chapter describes how to ensure adequate tissue oxygen delivery while minimizing ventilator-induced lung injury and provides an in-depth review of how to determine the optimum level of positive end-expiratory pressure (PEEP). The first topic addressed is the precipitating factors and pathophysiology of acute respiratory distress syndrome. Next the chapter turns to mechanical ventilation, and covers the subjects of adequate oxygenation, ventilator-induced lung injury, ancillary therapies, ventilatory therapies, and high I:E ventilation. The topics addressed in the area of non-ventilatory therapies include: prone positioning of the patient, neuromuscular blockade, inhaled vasodilators, and extracorporeal membrane oxygenation (ECMO).
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43

Marino, Philip, and Laura Price. Diagnosis and management of pulmonary hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0169.

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The diagnosis of pulmonary hypertension (PH) and associated right ventricular (RV) dysfunction or failure in the setting of critical illness relies on the use of non-invasive tools including echocardiography, and in some cases invasive haemodynamic monitoring. The management for PH and RV failure in the ICU may be challenging, and is dependent on local expertise and drug availability.Systemic vasoactive agents and pulmonary vasodilators play an important role. Patients with pulmonary arterial hypertension, pulmonary embolism or chronic thromboembolic PH should be anticoagulated; those with haemodynamically unstable PE may require thrombolysis.The characteristics of individual agents must be considered and monitored carefully.Few clinical studies or ICU-specific guidelines exist. Surgical options exist for patients with PH and RV failure. This chapter reviews the diagnostic and management strategies of PH and RV failure in the ICU setting.
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44

Dalzell, Jonathan R., Colette E. Jackson, Roy Gardner, and John JV McMurray. Acute heart failure: early pharmacological therapy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0052.

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Acute heart failure syndromes consist of a spectrum of clinical presentations due to an impairment of some aspect of the cardiac function. They represent a final common pathway for a vast array of pathologies and may be either a de novo presentation or, more commonly, a decompensation of pre-existing chronic heart failure. Despite being one of the most common medical presentations, there are no definitively proven prognosis-modifying treatments. The mainstay of current therapy is oxygen and intravenous diuretics. However, within this spectrum of presentations, there is a crucial dichotomy which governs the ultimate treatment approach, i.e. the presence, or absence, of cardiogenic shock. Patients without cardiogenic shock may receive vasodilators, whilst shocked patients should be considered for treatment with inotropic therapy or mechanical circulatory support, when appropriate and where available.
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45

Dalzell, Jonathan R., Colette E. Jackson, Roy Gardner, and John JV McMurray. Acute heart failure: early pharmacological therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0052_update_001.

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Acute heart failure syndromes consist of a spectrum of clinical presentations due to an impairment of some aspect of the cardiac function. They represent a final common pathway for a vast array of pathologies and may be either a de novo presentation or, more commonly, a decompensation of pre-existing chronic heart failure. Despite being one of the most common medical presentations, there are no definitively proven prognosis-modifying treatments. The mainstay of current therapy is oxygen and intravenous diuretics. However, within this spectrum of presentations, there is a crucial dichotomy which governs the ultimate treatment approach, i.e. the presence, or absence, of cardiogenic shock. Patients without cardiogenic shock may receive vasodilators, whilst shocked patients should be considered for treatment with inotropic therapy or mechanical circulatory support, when appropriate and where available.
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46

Gaddum, J. H. Vasodilator Substances of the Tissue. Cambridge University Press, 1987.

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47

Vasodilator substances of the tissues. Cambridge [Cambridgeshire]: Cambridge University Press, 1986.

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48

Muhlen, Bengt Von Zur. Antihypertensive Treatment and Endothelial Vasodilatory Function. Uppsala Universitet, 2001.

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49

Lindgren, Sam. Vasodilator effects of selective phosphodiesterase inhibitors. 1990.

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50

Bunjes, Werner E. Medical and pharmaceutical dictionary. Thieme-Stratton, 1985.

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