-
Alimentary Pharmacology & Therapeutics Sep 2020
Topics: Hepatorenal Syndrome; Humans; Lypressin; Terlipressin; Vasoconstrictor Agents
PubMed: 32852817
DOI: 10.1111/apt.15943 -
The Medical Letter on Drugs and... Mar 2023
Topics: Humans; Terlipressin; Hepatorenal Syndrome; Vasoconstrictor Agents; Octreotide; Treatment Outcome
PubMed: 36897603
DOI: 10.58347/tml.2023.1672c -
Current Hypertension Reports May 2017This review is intended to briefly describe the primary mechanistic pathways by which several common drugs can increase blood pressure. We also propose potential... (Review)
Review
PURPOSE OF REVIEW
This review is intended to briefly describe the primary mechanistic pathways by which several common drugs can increase blood pressure. We also propose potential management strategies based on the underlying mechanisms responsible for the blood pressure elevation.
RECENT FINDINGS
As hypertension is a significant risk factor for cardiovascular events, healthcare providers must evaluate patients' concomitant medications that may contribute to elevations in blood pressure. The presence of these medications, if not properly addressed, can lead to consequences such as an inadvertent diagnosis of hypertension, as well as the potential need for unnecessary intensification of antihypertensive regimens in those already treated. Blood pressure elevation is an unfortunate by-product of multiple medications. The substances discussed in this review can elicit significant and persistent elevations in blood pressure, and health care providers must first evaluate whether the drug is necessary. If one exists, it is best to select a similar agent with lower risk of increasing blood pressure; if unavoidable, then clinicians should select an appropriate management strategy to compensate for the rise in blood pressure.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Blood Pressure; Glucocorticoids; Gonadal Steroid Hormones; Humans; Hypertension; Risk Factors; Sympathomimetics; Vasoconstrictor Agents; Water-Electrolyte Imbalance
PubMed: 28451850
DOI: 10.1007/s11906-017-0736-z -
Emergency Medicine Australasia : EMA Apr 2018Although comprehensive guidelines for treatment of sepsis exist, current research continues to refine and revise several aspects of management. Imperatives for rapid... (Review)
Review
Although comprehensive guidelines for treatment of sepsis exist, current research continues to refine and revise several aspects of management. Imperatives for rapid administration of broad-spectrum antibiotics for all patients with sepsis may not be supported by contemporary data. Many patients may be better served by a more judicious approach allowing consideration of investigation results and evidence-based guidelines. Conventional fluid therapy has been challenged with early evidence supporting balanced, restricted fluid and early vasopressor use. Albumin, vasopressin and hydrocortisone have each been shown to support blood pressure and reduce catecholamine requirements but without effect on mortality, and as such should be considered for ED patients with septic shock on a case-by-case basis. Measurement of quality care in sepsis should incorporate quality of blood cultures and guideline-appropriateness of antibiotics, as well as timeliness of therapy. Local audit is an essential and effective means to improve practice. Multicentre consolidation of data through agreed minimum sepsis data sets would provide baseline quality data, required for the design and evaluation of interventions.
Topics: Anti-Bacterial Agents; Emergency Service, Hospital; Hemodynamics; Humans; Sepsis; Time Factors; Vasoconstrictor Agents
PubMed: 29569847
DOI: 10.1111/1742-6723.12951 -
International Journal of Molecular... Feb 2021Cocaine is one of the most widely abused illicit drugs worldwide and has long been recognised as an agent of cardiac dysfunction in numerous cases of drug overdose....
Cocaine is one of the most widely abused illicit drugs worldwide and has long been recognised as an agent of cardiac dysfunction in numerous cases of drug overdose. Cocaine has previously been shown to up-regulate cytoskeletal rearrangements and morphological changes in numerous tissues; however, previous literature observes such changes primarily in clinical case reports and addiction studies. An investigation into the fundamental cytoskeletal parameters of migration, adhesion and proliferation were studied to determine the cytoskeletal and cytotoxic basis of cocaine in cardiac cells. Treatment of cardiac myocytes with cocaine increased cell migration and adhesion ( < 0.05), with no effect on cell proliferation, except with higher doses eliciting (1-10 μg/mL) its diminution and increase in cell death. Cocaine downregulated phosphorylation of cofilin, decreased expression of adhesion modulators (integrin-β3) and increased expression of ezirin within three hours of 1 μg/mL treatments. These functional responses were associated with changes in cellular morphology, including alterations in membrane stability and a stellate-like phenotype with less compaction between cells. Higher dose treatments of cocaine (5-10 μg/mL) were associated with significant cardiomyocyte cell death ( < 0.05) and loss of cellular architecture. These results highlight the importance of cocaine in mediating cardiomyocyte function and cytotoxicity associated with the possible loss of intercellular contacts required to maintain normal cell viability, with implications for cardiotoxicity relating to hypertrophy and fibrogenesis.
Topics: Animals; Cardiotoxicity; Cell Adhesion; Cell Movement; Cell Survival; Cells, Cultured; Cocaine; Cytoskeleton; Myocytes, Cardiac; Rats; Vasoconstrictor Agents
PubMed: 33668403
DOI: 10.3390/ijms22052263 -
European Journal of Anaesthesiology Jul 2022
Topics: Humans; Hypotension; Norepinephrine; Phenylephrine; Vasoconstrictor Agents
PubMed: 35759290
DOI: 10.1097/EJA.0000000000001697 -
Pharmacotherapy Mar 2019Septic shock is a life-threatening disorder associated with high mortality rates requiring rapid identification and intervention. Vasoactive agents are often required to... (Review)
Review
Septic shock is a life-threatening disorder associated with high mortality rates requiring rapid identification and intervention. Vasoactive agents are often required to maintain goal hemodynamics and preserve tissue perfusion. However, guidance regarding the proper administration of adjunct agents for the management of septic shock is limited in patients who are refractory to norepinephrine. This review summarizes vasopressor agents and describes the nuanced application of these agents in patients with septic shock, specifically focusing on clinical scenarios with limited guidance including patients who are nonresponsive to first-line agents and individuals with mixed shock states, tachyarrhythmias, obesity, valvular abnormalities, or other comorbid conditions.
Topics: Hemodynamics; Humans; Norepinephrine; Shock, Septic; Vasoconstrictor Agents
PubMed: 30644586
DOI: 10.1002/phar.2220 -
FASEB Journal : Official Publication of... May 2022The F prostanoid receptor (FP), which accounts for the therapeutic effect of PGF in uterine atony that leads to postpartum hemorrhage and maternal morbidity, could...
The F prostanoid receptor (FP), which accounts for the therapeutic effect of PGF in uterine atony that leads to postpartum hemorrhage and maternal morbidity, could possibly mediate vasoconstrictor effect in small or resistance arteries to elevate blood pressure that limits the clinical use of the agent in patients with cardiovascular disorders. This study aimed to test the above hypothesis with genetically altered mice. Ex vivo and in vivo experiments were performed on control wild-type (WT) mice and mice with deficiencies in FP (FP ) or thromboxane (Tx)-prostanoid receptor (the original receptor of TxA ; TP ), and/or those with an additional deficiency in E prostanoid receptor-3 (one of the vasoconstrictor receptors of PGE ; EP3 ). Here, we show that PGF indeed evoked vasoconstrictor responses in the above-mentioned tissues of WT mice, which were however unaltered by FP . Interestingly, such contractile responses were reversed into dilations by TP /EP3 . A similar pattern of results was observed with the pressor effect of PGF under in vivo conditions. However, TP alone (which could largely remove the contractile responses) did not result in relaxation to PGF . Also, either the ex vivo vasodilator effect or the in vivo depressor response of PGF obtained after the removal of TP and EP3-mediated actions was unaltered by FP . Therefore, both the ex vivo vasoconstrictor action in small or resistance arteries and the systemic pressor effect of PGF can reflect vasoconstrictor activities derived from the non-FP receptors TP and EP3 outweighing a concurrently activated dilator effect, which is again independent of FP.
Topics: Animals; Female; Mice; Prostaglandins; Prostaglandins F; Receptors, Prostaglandin; Receptors, Thromboxane; Vasoconstrictor Agents
PubMed: 35349198
DOI: 10.1096/fj.202101908R -
FASEB Journal : Official Publication of... Feb 2019The vasoconstrictor and/or pressor effects of prostaglandin (PG)F participate in the development of vascular pathologies and limit the clinical use of the agent. This...
The vasoconstrictor and/or pressor effects of prostaglandin (PG)F participate in the development of vascular pathologies and limit the clinical use of the agent. This study aimed to determine the receptor types responsible for the vasoconstrictor activity of PGF and whether they mediate the pressor response evoked by the prostanoid under in vivo conditions. Experiments were performed on genetically altered mice and/or on vessels from these mice or humans. Here we show that deletion of the thromboxane-prostanoid receptor (TP) abolished or drastically diminished the contraction to PGF in isolated mouse vessels (some of which were resistance arteries) and reduced the elevation in blood pressure evoked by the prostanoid under in vivo conditions. In accordance, TP antagonism abolished the contraction in small arteries of human omentum. Further deletion of E prostanoid receptor type 3 (EP3) removed the PGF-evoked contraction that remained in some TP arteries and added to the effect of TP on the elevation in blood pressure evoked by the prostanoid under in vivo conditions. In contrast, the uterine contraction to PGF mediated via the F prostanoid receptor (FP) was unaltered in TP/EP3 mice. These results demonstrate that the non-FP receptors TP and/or EP3 mediate the vasoconstrictor and pressor effects of PGF, which are still of concern under clinical conditions.-Liu, B., Li, J., Yan, H., Tian, D., Li, H., Zhang, Y., Guo, T., Wu, X., Luo, W., Zhou, Y. TP and/or EP3 receptors mediate the vasoconstrictor and pressor responses of prostaglandin F in mice and/or humans.
Topics: Animals; Blood Pressure; Cells, Cultured; Dinoprost; Female; Humans; Male; Mesenteric Arteries; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle, Skeletal; Receptors, Prostaglandin E, EP3 Subtype; Receptors, Thromboxane; Uterus; Vasoconstriction; Vasoconstrictor Agents
PubMed: 30277822
DOI: 10.1096/fj.201801064RR -
Future Cardiology Nov 2020Shock is an acute condition of circulatory failure resulting in life-threatening organ dysfunction, high morbidity and high mortality. Current management includes fluid... (Review)
Review
Shock is an acute condition of circulatory failure resulting in life-threatening organ dysfunction, high morbidity and high mortality. Current management includes fluid and catecholamine therapy to maintain adequate mean arterial pressure and organ perfusion. Norepinephrine is recommended as first-line vasopressor, but other agents are available. Angiotensin II is an alternative potent vasoconstrictor without chronotropic or inotropic properties. Several studies, including a large randomized controlled trial have demonstrated its ability to increase blood pressure with catecholamine-sparing effects. Angiotensin II was consequently approved by the US FDA in 2017 and the EU in 2019 as an add-on vasopressor in vasodilatory shock. This review aims to discuss its basic pharmacology, clinical efficacy, safety and future perspectives.
Topics: Angiotensin II; Blood Pressure; Humans; Randomized Controlled Trials as Topic; Shock; Vasoconstrictor Agents; Vasodilation
PubMed: 32462921
DOI: 10.2217/fca-2020-0019