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Pulmonary Circulation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Both metabolic and respiratory acidosis augment HPV. Alveolar hypercapnia. Elevated alveolar Pco2 causes pulmonary vasoconstriction.Humoral factors. Catecholamines such as epinephrine cause, predominantly, vasoconstriction. Thromboxane and leukotrienes are all pulmonary vasoconstrictors whilst prostacyclin (PGI2) is a vasodilator. Serotonin released by activated platelets is a potent vasoconstrictor.Drugs. Inhaled nitric oxide is a potent pulmonary vasodilator. Nebulized prostacyclin is effective but its effects are due to systemic absorption. Phosphodiesterase inhibitors inhibit the breakdown of both cyclic guanosine monophosphate (cGMP) and cAMP. Milrinone, levosimendan and sildenafil are useful pulmonary vasodilators. Volatile anaesthetic agents also vasodilate the pulmonary vasculature.
Heart disease
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
PAH-targeted therapies should be continued in pregnancy. Specific therapies include: – Phosphodiesterase inhibitors (sildenafil, tadalafil). These can be safely continued or instigated in pregnancy.– Endothelin receptor antagonists (bosentan, ambrisentan). These are usually discontinued in pregnancy, as they are teratogenic in rats.– Prostanoid analogues (epoprostenol – intravenous [i.v.], iloprost – nebulized or i.v.) and nitric oxide – inhaled. These can be safely continued or instituted in pregnancy.
Death at High Altitude
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Clinically, HAPE is characterized by an increasing breathlessness accompanied by one or a combination of the above-mentioned symptoms of AMS beginning a few hours after arrival in high altitude. An initially dry cough turns productive with frothy white and later blood-tingled sputum [40]. Upon auscultation, crackles may be heard at the lung bases. In addition to tachycardia and tachypnoea, cyanosis and mild pyrexia may develop [25,38]. Reported incidences of HAPE vary substantially (due to varying subject populations, final altitude and rapidity of ascent) and range from 0.57 per cent [28] to 10 per cent [4]. Rapid deterioration and potentially death may be seen in those HAPE patients who do not descend or receive medical treatment. Optimal treatment depends on individual access to treatment facilities. HAPE patients should descend if there is no treatment possibility of receiving supplemental oxygen, entering a hyperbaric chamber and receiving a pulmonary vasodilator [25]. Furthermore, phosphodiesterase inhibitors may be useful, while diuretics are contraindicated [38].
Association between PRO 160/120 prescriptions and incidence of benign prostatic hyperplasia complications in Germany: a retrospective cohort study
Published in Postgraduate Medicine, 2023
S Madersbacher, M Rieken, K Reuber, K Kostev
The incidences of these study outcomes for PRO 160/120 were compared to those for finasteride and dutasteride (5ARIs), tamsulosin, and tamsulosin/dutasteride fixed-dose combination. Tadalafil was not considered as this drug occupies a special position in the German market. As a 5-phosphodiesterase inhibitor in the higher dosage of 10 mg or 20 mg, the application is erectile dysfunction. In these cases, tadalafil is considered a lifestyle preparation without public insurance reimbursement. After patent expiry in 2017, the active ingredient in a 5 mg dose for BPH treatment as a line extension was introduced. This time period however includes only a part of our study time period. Tamsulosin makes >90% of alpha-blocker prescriptions; finasteride and dutasteride makes >90% of 5α-reductases; other drugs were prescribed only rarely in Germany what is why we only investigated these drugs.
Second messengers and their importance for novel drug treatments of patients with bipolar disorder
Published in International Review of Psychiatry, 2022
Gabriele Sani, Georgios D. Kotzalidis, Federica Fiaschè, Giovanni Manfredi, S. Nassir Ghaemi
Further detail is provided on two studies. In one, a Canadian group used the Stanley Foundation Neuropathology Consortium to investigate the effects of drugs on the cAMP pathway in post-mortem tissue of patients with mood disorders. They found mood stabilizers to dampen the activity of the cascade in bipolar disorder, while patients with bipolar disorder who were on lithium at their time of death showed a trend towards lower levels of the stimulatory protein Gαs (Stewart et al., 2001). Abnormal cAMP-dependent responses were also found in lymphoblasts of patients with bipolar disorder, with down-regulation of cAMP binding on phosphokinase sites compared to healthy controls and increased PKA activity (Karege et al., 2004). Although the use of phosphodiesterase inhibitors has been advanced for mood disorders (Machado-Vieira et al., 2006), the evidence collected so far is too weak to suggest that targeting this system will obtain good translational results. It is rather possible that any new drug acting through alternative mechanisms will involve changes in this system.
Clinical pharmacology of antiplatelet drugs
Published in Expert Review of Clinical Pharmacology, 2022
Georg Gelbenegger, Bernd Jilma
Substances that increase the intraplatelet concentration of cAMP and cGMP inhibit platelet aggregation, regardless of the agonist employed [42,43]. Phosphodiesterases 3 and 5 degrade cAMP and cGMP to 5’-AMP and 5’-GMP, respectively, and thereby regulate two critical second messenger platelet signaling pathways, leading to increased concentrations of adenosine, cAMP and cGMP [44]. In addition to its inhibitory effect on phosphodiesterases, dipyridamole inhibits adenosine uptake of red blood cells, resulting in increased adenosine levels. Via A2 receptors, adenosine leads to cAMP-dependent inhibition of platelet aggregation. Cilostazol is a reversible phosphodiesterase 3 inhibitor. Phosphodiesterase inhibitors are used rarely and almost exclusively for secondary prevention of ischemic stroke [45].