Methylene blue exhibits significant effects on blood pressure through multiple mechanisms. The drug primarily acts by inhibiting guanylate cyclase, reducing cGMP levels and nitric oxide release, leading to Vasoconstriction and increased vascular tone.
Administration typically induces a rapid elevation in mean arterial pressure within 30-60 seconds, with effects normalising in 90 seconds to 3 minutes at low to moderate doses (1-2 mg/kg). However, delayed hypertensive crises may occur 15-20 minutes post-administration, warranting careful monitoring.
The drug’s biphasic response pattern and complex interactions with over 270 medications necessitate thorough clinical assessment and precise dosing strategies. Understanding these mechanisms provides critical insights into optimal therapeutic management.
Key Takeaways
- Methylene blue immediately elevates mean arterial pressure within 30-60 seconds of administration through Vasoconstriction and increased vascular tone.
- Low to moderate doses (1-2 mg/kg) increase blood pressure, with normalisation occurring within 90 seconds to 3 minutes.
- The drug works by inhibiting guanylate cyclase, reducing cGMP levels and nitric oxide release, thereby elevating blood pressure.
- Delayed hypertensive crises can occur 15-20 minutes after administration, particularly in patients with underlying health conditions.
- Higher doses may paradoxically cause systemic hypotension, demonstrating a biphasic response pattern requiring careful dosing management.
What Is Methylene Blue
Methylene blue, a phenothiazine-derived basic dye with a molar mass of 319.85 g·mol−1, is synthesised through the oxidation of methylene and exhibits distinctive properties as both a chemical compound and therapeutic agent. The history of Methylene Blue spans multiple scientific disciplines, demonstrating remarkable versatility in medical and laboratory applications. This compound appears as a dark green powder and yields a characteristic blue solution upon dissolution in water. The solution exhibits a pH stability range of 3 to 12, making it suitable for a wide range of applications.
The Methylene Blue Synthesis involves a precise chemical process, specifically the oxidation of 4-aminodimethylaniline in the presence of sodium thiosulfate. This synthesis yields a compound with significant therapeutic potential, particularly for treating conditions such as methemoglobinemia, where it reduces ferric iron to ferrous iron in haemoglobin. Additionally, its reduction potential makes it an effective antidote for cyanide poisoning.
In clinical settings, methylene blue serves multiple purposes, from visualising complex anatomical structures during surgery to treating urinary tract infections. Recent research indicates promising applications in neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases. Laboratory applications include biological staining, cell viability assessment, and nucleic acid visualisation in agarose gel electrophoresis.
Despite its therapeutic benefits, methylene blue requires careful administration due to potential side effects and drug interactions, particularly its monoamine oxidase inhibitor activity. Its use requires precise dosing, as excessive doses can paradoxically induce methemoglobinemia, counteracting its intended therapeutic effect.
Immediate Effects On Blood Pressure
Methylene blue exerts rapid vasopressor effects by inhibiting guanylate cyclase, thereby increasing peripheral vascular tone and systemic blood pressure. The time course of blood pressure elevation correlates with the pharmacokinetics of methylene blue, with effects occurring within minutes of administration and lasting for up to 2 hours, depending on the dose. Low to moderate doses (1-2 mg/kg) typically induce measurable increases in pressure within 60 seconds, whereas higher doses may precipitate more pronounced and sustained hypertensive responses, particularly in pediatric populations. This mechanism is particularly effective in treating vasoplegic syndrome, in which excessive vasodilation leads to dangerous drops in blood pressure.
Rapid Pressure Rise Mechanism
Understanding the rapid pressure rise mechanism of methylene blue reveals a complex interplay of pharmacological actions that culminate in swift blood pressure elevation. The primary mechanism involves dual inhibition of nitric oxide synthase and guanylate cyclase, resulting in immediate Vasoconstriction and enhanced vascular tone. This pressure response is particularly evident in hypotensive conditions, where methylene blue’s ability to counteract excessive vasodilation proves therapeutically valuable. Research in The Annals of Thoracic Surgery has demonstrated significant success rates in treating vasoplegic syndrome.
The compound’s rapid action stems from its multifaceted mechanism of action on vascular regulation. By simultaneously supporting endothelial function and reducing oxidative stress, methylene blue maximises vascular smooth muscle responsiveness. The drug’s effect on cyclic guanosine monophosphate concentrations further contributes to immediate pressure stabilisation, especially in pulmonary circulation.
Notably, methylene blue’s neuroprotective properties complement its vascular effects, ensuring sustained blood pressure regulation through preserved autonomic function. This mechanism is particularly effective in critical conditions, such as septic and endotoxic shock, where the drug’s ability to restore normal tone and blood pressure rapidly is vital. The dependence of these effects on clinical context requires careful clinical monitoring to achieve optimal therapeutic outcomes while avoiding potential complications.
Dosage Impact Timeline
Upon administration, the rapid blood pressure effects of methylene blue follow a predictable temporal sequence characterised by distinct phases of cardiovascular response. Within 30-60 seconds post-administration, patients typically experience an immediate elevation in mean arterial pressure, followed by a normalisation phase occurring within 90 seconds to 3 minutes. This initial response pattern requires vigilant monitoring protocols, particularly during the critical first five minutes. Additionally, methylene blue’s mechanism of action operates through serotonin release from platelets, leading to Vasoconstriction.
Dosage variations greatly influence both the magnitude and duration of blood pressure alterations. Low to moderate doses (0.58-2 mg/kg) primarily induce transient increases, while doses exceeding 10 mg/kg may paradoxically result in systemic hypotension. A delayed hypertensive crisis can manifest approximately 20 minutes post-administration, potentially due to compromised hepatic catecholamine degradation. This delayed response necessitates extended cardiovascular monitoring, especially in patients with pre-existing hepatic dysfunction.
In cases of endotoxic shock, the temporal progression differs, presenting with an initial transient increase followed by a sustained elevation in blood pressure, accompanied by enhanced vascular responsiveness to norepinephrine. This temporal pattern underscores the importance of continuous hemodynamic assessment and individualised dosing strategies.
Understanding Delayed Hypertensive Crisis
While the pathophysiology of delayed hypertensive crisis involves multiple complex mechanisms, the condition’s development is greatly influenced by both underlying comorbidities and pharmacological interactions. Outpatient treatment is recommended in most cases since only 5% of severe asymptomatic cases show abnormal results. The presence of chronic kidney disease markedly elevates risk (OR 2.899), alongside hyperlipidemia (OR 2.028) and other cardiovascular comorbidities. These risk factors compound the risk of adverse outcomes when methylene blue is administered to affected patients.
The pharmacodynamic profile of methylene blue contributes to delayed hypertensive crisis through multiple pathways. Its inhibition of hepatic catecholamine degradation, combined with serotonin-mediated Vasoconstriction, creates a complex physiological response that may manifest as delayed blood pressure elevation. Remarkably, the magnitude of Vasoconstriction does not correlate directly with the administered dose, suggesting that other factors, such as surgical stimulation and sympathetic activation, also contribute.
Clinicians also contribute to the implications necessitating careful consideration of target organ damage when differentiating between hypertensive urgency and emergency. Disruption of vascular autoregulation can compromise endothelial function and increase vascular permeability, necessitating tailored therapeutic approaches for specific clinical scenarios. Management strategies must account for various patient populations, including pediatric and obstetric cases, where delayed recognition and treatment between 10 PM and 6 AM pose particular risks.
Immediate intervention becomes essential when a hypertensive emergency develops, with blood pressure reduction goals varying according to the underlying pathology, such as ischemic versus hemorrhagic stroke. This necessitates vigilant monitoring and prompt therapeutic response, especially in patients with pre-existing cardiovascular conditions.
Medical Uses And Applications
Methylene blue demonstrates remarkable versatility across diverse medical applications, thanks to its pharmacological properties, which enable critical interventions across multiple therapeutic domains. In cardiovascular medicine, its impact on blood pressure regulation is particularly significant, especially in the treatment of distributive shock and vasoplegia. The compound’s mechanism of action, primarily through inhibition of guanylate cyclase, increases systemic vascular resistance and stabilises blood pressure in post-cardiopulmonary bypass patients. Methylene blue administration can cause bluish-green urine discolouration as a common side effect.
Beyond its hemodynamic applications, methylene blue plays an essential role in various surgical and diagnostic procedures. During parathyroidectomy, intravenous administration aids surgical visualisation, whereas in sentinel lymph node dissections, it enables precise lymphatic mapping. The compound’s utility extends to treating methemoglobinemia through its reduction of ferric iron in haemoglobin, and it shows promise in managing ifosfamide-induced encephalopathy.
Precise dosing protocols have been established across these applications. For blood pressure management in vasoplegic syndrome, clinicians typically administer 2 mg/kg, while methemoglobinemia treatment requires 1 mg/kg. In malaria treatment, methylene blue demonstrates efficacy by enhancing the therapeutic response in patients, with dosing ranging from 100000 g daily in adults. Its integration into bone cement procedures and endoscopic interventions further exemplifies its broad therapeutic scope. The compound’s ability to prevent post-propofol pain and address calcium channel blocker toxicity underscores its significance in modern medical practice, particularly in scenarios requiring rapid blood pressure stabilisation.
How Methylene Blue Works
Intricate biochemical pathways underlie methylene blue‘s regulation of blood pressure via its primary mechanism of inhibiting guanylate cyclase. This molecular mechanism leads to decreased cyclic guanosine monophosphate (cGMP) production, thereby reducing nitric oxide release. Diminished nitric oxide activity results in Vasoconstriction, effectively increasing peripheral vascular tone and systemic blood pressure. This process is further enhanced by inhibiting both endothelial and inducible nitric oxide synthases. In clinical studies, a single dose of 2mg/kg has demonstrated effective hemodynamic stabilisation within 1 hour of administration.
The therapeutic applications of methylene blue extend beyond simple Vasoconstriction. It facilitates improved oxygen delivery by reducing methemoglobin to haemoglobin via an NADPH-dependent pathway. This conversion enhances oxygen-binding capacity, though the oxygen extraction ratio remains relatively unchanged. The compound demonstrates dose-dependent effects on the vascular system, with lower doses increasing systemic and pulmonary arterial pressure while selectively enhancing mesenteric blood flow.
At the cellular level, methylene blue modulates calcium homeostasis and influences vascular smooth muscle contractility. Its effects on hemodynamics are particularly notable in endotoxic shock conditions, where it can rapidly improve cardiovascular parameters. However, the dose-response relationship is critical, as higher concentrations may paradoxically worsen systemic hypotension and induce myocardial depression. This biphasic response pattern necessitates careful dosing considerations in clinical settings, particularly when treating vasoplegic syndrome or managing patients with compromised cardiovascular function.
Safety And Risk Factors
Close cardiovascular monitoring is essential during methylene blue administration, particularly given its propensity to induce transient hypertension and potential cardiac arrhythmias. Studies show that systemic vascular resistance increases significantly within one hour of infusion. Patients with pre-existing pulmonary hypertension, coronary artery disease, or cardiac rhythm disturbances represent high-risk populations requiring heightened vigilance and possible dosage modifications. The concurrent use of vasoactive medications or serotonergic agents requires careful consideration, as these agents may interact pharmacodynamically to amplify cardiovascular effects.
Monitoring Heart Health Carefully
Since monitoring cardiovascular health requires meticulous attention to multiple parameters, healthcare providers must implement thorough safety protocols when administering Methylene Blue treatments. Modern heart health monitoring techniques, ranging from portable electrocardiograms to advanced telemetry systems, enable extensive surveillance of patients’ cardiovascular responses during treatment. Integration of multiple monitoring modalities guarantees early detection of adverse reactions and facilitates prompt intervention when necessary. Discreet wireless chest patches provide continuous monitoring for up to 2 weeks, enabling comprehensive data collection during treatment.
Contemporary monitoring approaches incorporate both traditional and innovative technologies to maintain vigilant oversight:
- KardiaMobile devices for real-time arrhythmia detection and classification
- Continuous cardiac telemetry systems provide 99% accuracy in rhythm analysis
- Smart device integration utilising photoplethysmography for heart rate tracking
- Biomarker assessment through specialised test strips for heart failure markers
- Wireless monitoring systems for crucial sign trending and real-time data access
The complexity of Methylene Blue’s effects on blood pressure necessitates strong monitoring protocols. Healthcare providers should establish baseline measurements, implement regular assessment intervals, and maintain detailed documentation of cardiovascular parameters throughout treatment. This systematic approach enables early identification of potential complications and supports optimal patient outcomes through evidence-based interventions.
Identifying High-Risk Patients
While administering Methylene Blue therapy requires careful consideration for all patients, specific high-risk populations demand heightened vigilance and specialised protocols due to their elevated susceptibility to adverse effects. Cardiovascular concerns present a primary risk factor, particularly in patients with pre-existing hypertension or vasoplegic conditions. The medication’s hemodynamic effects necessitate stringent monitoring protocols. Historical evidence shows that increasing blood pressure during vasoplegic syndrome treatment has been a documented therapeutic effect since its early medical use.
| Patient Group | Primary Risks | Clinical Considerations |
|---|---|---|
| Cardiovascular | Hypertensive response, Vasoconstriction | Continuous BP monitoring, Dose adjustment |
| Serotonergic | Serotonin syndrome, MAOI interaction | SSRI discontinuation, Dose limitation <5mg/kg |
| Pediatric | Enhanced sensitivity, Crisis risk | Weight-based dosing, Enhanced monitoring |
Patients on serotonergic medications require particular attention due to methylene blue’s MAOI properties, necessitating medication discontinuation and careful timing of administration. Pediatric populations exhibit heightened sensitivity, as evidenced by documented cases of severe hypertensive responses even at low doses. Additionally, patients with renal dysfunction warrant modified protocols due to potential alterations in renal blood flow. These high-risk scenarios require individualised assessment and specialised management strategies to ensure optimal therapeutic outcomes while minimising adverse events.
Drug Interactions Matter
Understanding the complex network of drug interactions associated with methylene blue is essential for safe clinical practice, given its documented interactions with over 270 different medications across varying severity levels. Drug safety protocols mandate careful consideration of both immediate and delayed reactions, particularly regarding cardiovascular effects. The compound’s interaction with endothelin receptors and its inhibition of guanylyl cyclase necessitate heightened awareness of potential interactions when administered concurrently with other medications.
- Severe hypertensive crisis manifests within 30-60 seconds of administration.
- Vasoconstrictive reactions accompanied by dangerous reflex bradycardia
- Enhanced noradrenaline sensitivity leading to amplified sympathetic responses
- The compromised effectiveness of hormonal contraceptives requires alternative measures
- Potentially life-threatening interactions with antidepressants like fluoxetine
Critical interactions with commonly prescribed medications such as cyclosporine, rifampin, and warfarin require vigilant monitoring and potential therapeutic adjustments. The medication’s effects on soluble guanylyl cyclase and endothelin receptor pathways create a complex pharmacological profile that requires thorough pre-administration screening. Healthcare providers must maintain extensive documentation of concurrent medications and establish clear protocols for managing potential drug-drug interactions.
Drug Interactions And Precautions
Safety considerations for methylene blue encompass numerous critical drug interactions and precautions that require careful clinical evaluation. The medication exhibits 129 significant drug interactions, particularly with serotonergic psychiatric medications, including SSRIs, SNRIs, TCAs, and MAOIs. Additionally, 65 moderate interactions have been identified with medications such as artesunate and buprenorphine, necessitating thorough assessment before administration.
Of utmost importance is the contraindication in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency, given the risk of haemolytic anaemia. Precautionary measures must address severe hypersensitivity reactions, including anaphylaxis, angioedema, and bronchospasm, which require vigilant monitoring of crucial signs and ECG during treatment. The risk of serotonin syndrome is particularly significant when methylene blue is coadministered with serotonergic agents, demanding careful consideration of risk-benefit ratios.
Clinical monitoring is essential for several technical reasons. The presence of methemoglobin can lead to inaccurate pulse oximetry readings, potentially underestimating oxygen saturation. Moreover, hemolysis may occur during treatment of methemoglobinemia, necessitating monitoring for the development of anaemia. Healthcare providers must exercise particular caution in specific populations, including pregnant and lactating patients, where specialised precautions are required. The broad nature of these drug interactions and precautions underscores the importance of thorough patient evaluation and continuous monitoring throughout treatment to ensure optimal therapeutic outcomes while minimising adverse events.
Research In Animal Models
Research using animal models has yielded significant insights into methylene blue‘s effects on cardiovascular parameters, particularly blood pressure regulation. Animal model findings demonstrate that intravenous administration produces dose-dependent hypertensive responses, primarily by inhibiting soluble guanylyl cyclase. This mechanism prevents nitric oxide-mediated activation, thereby decreasing cyclic GMP levels and increasing vascular tone.
Studies in rats and rabbits have elucidated key mechanisms of hypertension, showing that methylene blue can restore normal arterial pressure in septic shock conditions while normalising total plasma NO content. The compound’s ability to modulate vascular smooth muscle responses is evidenced by its restoration of norepinephrine-induced pressor responses in lipopolysaccharide-treated subjects. However, it does not affect blood pressure in control animals.
Key observations from animal studies include:
- Transient blood pressure elevation following intravenous administration
- Normalisation of vascular tone in small femoral resistance arteries
- Reflex hypotension occurrence in intact but not pithed rats
- Restoration of normal arterial pressure in septic shock models
- Selective enhancement of norepinephrine responsiveness in disease states
These experimental findings have significant clinical implications, particularly for the treatment of conditions such as septic shock and vasoplegic syndrome. The research suggests therapeutic potential while highlighting important physiological mechanisms. However, careful consideration must be given to potential cardiotoxic effects, especially in scenarios involving cardiac ischemia and reperfusion, as indicated by preclinical studies.
Monitoring Blood Pressure Response
The monitoring of blood pressure responses to methylene blue administration reveals a biphasic pattern, with immediate vasoconstrictive effects manifesting within 30-60 seconds and potential delayed hypertensive complications occurring up to 20 minutes post-administration. Clinical vigilance must address both the initial pressure surge, often accompanied by reflex bradycardia, and the subsequent risk period where severe hypertensive episodes may develop, particularly in pediatric cases or with doses exceeding 2mg/kg. Implementation of continuous hemodynamic monitoring protocols, incorporating frequent blood pressure measurements and careful dose titration, remains essential for detecting and managing both immediate and delayed cardiovascular responses to methylene blue therapy.
Immediate Pressure Response Effects
While monitoring blood pressure responses to methylene blue administration, clinicians observe distinctive hemodynamic changes characterised by rapid-onset vasoactive effects. The mechanism primarily involves inhibition of nitric oxide synthase and guanylate cyclase, thereby increasing peripheral vascular tone. Clinical studies demonstrate normalisation of mean arterial pressure within 3 minutes of intravenous administration, with initial pressure changes occurring within seconds.
The immediate effects on blood pressure regulation are mediated by modulating vasoconstriction and vasodilation pathways, restoring vascular cyclic GMP levels, and pressor responses to norepinephrine. Experimental findings confirm dose-dependent hypertensive responses, particularly evident in LPS-treated subjects, in which both transient and sustained pressure increases are observed.
- Rapid elevation of systemic vascular resistance following intravenous administration
- Visible blanching of peripheral tissues as Vasoconstriction occurs
- Progressive normalisation of capillary refill times
- Restoration of pulse pressure amplitude
- Enhanced peripheral perfusion evidenced by warming of extremities
Given these potent hemodynamic effects, careful dose titration and continuous cardiovascular monitoring remain essential for safe clinical use, particularly in patients with compromised cardiovascular function.
Delayed Hypertensive Risk Signs
Despite initial hemodynamic stabilisation following methylene blue administration, clinicians must remain vigilant for delayed hypertensive responses, which typically manifest 15-20 minutes post-administration. Delayed hypertension awareness is vital, as these episodes can precipitate severe complications, including hypertensive encephalopathy and end-organ ischemia, even with low methylene blue doses.
The manifestation of delayed hypertensive crisis management requires understanding that systolic blood pressure may surge by over 100 mmHg, accompanied by reflex bradycardia, indicating vasoconstrictive phenomena. This response stems from complex mechanistic pathways involving serotonin release from platelets and altered hepatic catecholamine metabolism, enhancing noradrenaline sensitivity.
Clinical surveillance must extend beyond the immediate post-administration period, as the severity of delayed hypertensive responses does not correlate directly with dosage. The implementation of continuous hemodynamic monitoring protocols is essential, particularly in critically ill patients. Advanced monitoring of systemic vascular resistance and cardiac function may be warranted, given the unpredictable nature of individual responses. This all-encompassing approach enables early detection and prompt intervention for delayed hypertensive complications, potentially averting adverse outcomes.
Ongoing Measurement Best Practices
Accurate blood pressure measurement following methylene blue administration requires standardised monitoring protocols that incorporate both ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM). These evidence-based approaches facilitate comprehensive hypertension management by enabling continuous data collection and analysis. ABPM provides 24-48-hour measurements at predetermined intervals, whereas HBPM enables patient-directed monitoring, with a documented sensitivity of 90% and specificity of 84%.
- Patient wearing a compact ABPM device discretely under clothing during daily activities
- Digital display showing real-time blood pressure readings with trending data
- The electronic HBPM unit is positioned on a bedside table for morning measurements.
- Colour-coded measurement zones indicating ideal versus elevated readings
- Systematic documentation of readings in a patient monitoring log
Protocol implementation requires proper measurement techniques, including a 3-5-minute pre-measurement rest period and multiple readings at 1-2-minute intervals. Manual measurements serve as complementary validation points, using standardised cuff placement 1 inch above the elbow. This multimodal blood pressure monitoring approach enhances the detection of treatment-response variability and enables precise therapeutic adjustments based on comprehensive physiological data.
Treatment Guidelines And Protocols
Treatment guidelines for methylene blue administration specify protocols tailored to specific clinical conditions, with dosing regimens that vary considerably by therapeutic indication. Clinical trials throughout methylene blue’s history have established standardised dosing parameters, particularly for conditions affecting hemodynamic stability. For methemoglobinemia, the protocol specifies 1 mg/kg of a 1% solution administered intravenously over 5-30 minutes, whereas for vasoplegic syndrome, 2 mg/kg is infused over 20 minutes.
The therapeutic protocols emphasise careful consideration of potential complications, especially in patients receiving serotonergic medications, given methylene blue’s monoamine oxidase inhibitory properties. Implementation of these guidelines requires vigilant monitoring for hypertensive crisis, particularly during rapid administration. For specialised procedures such as lymph node mapping, practitioners must adhere to precise dosing of 2-5 mL of 1% solution administered intraparenchymally.
Critical protocol considerations include regular assessment of liver function and careful screening for contraindications, particularly in pregnancy. Treatment guidelines for ifosfamide-induced encephalopathy specify 50 mg administered intravenously every 4 hours until symptom resolution. In cases of Plasmodium falciparum infection, protocols dictate doses of 300-1000 mg daily in adults, with adjusted pediatric dosing of 20-300 mg daily for 3 days. These guidelines emphasise the importance of prophylactic measures against post-injection pain, including pre-emptive strategies such as administering propofol before procedures.
Frequently Asked Questions
Can Methylene Blue Be Used to Treat Chronic Low Blood Pressure?
While methylene blue demonstrates efficacy in acute hypotension, insufficient clinical evidence exists to support its use in the treatment of chronic hypotension. Long-term safety and efficacy studies remain necessary before recommending chronic administration.
Does Skin Colour Affect Methylene Blue’s Effectiveness on Blood Pressure?
Current evidence does not indicate that skin pigmentation influences methylene blue’s physiological effects on blood pressure regulation, as its mechanism operates through intravascular and cellular pathways independent of melanin content.
How Long Should Patients Avoid Certain Foods After Methylene Blue Treatment?
Like Orpheus’s cautionary period in the underworld, dietary restrictions after methylene blue treatment typically last 24-48 hours, and healthcare providers may adjust post-treatment guidelines based on individual clinical parameters.
Can Methylene Blue Cause Permanent Changes to Blood Pressure Regulation?
Methylene blue’s effects on blood pressure regulation are typically transient, with transient modulation of vascular tone via inhibition of guanylyl cyclase. No conclusive evidence indicates permanent alterations to cardiovascular regulatory mechanisms.
Do Genetic Factors Influence Individual Blood Pressure Responses to Methylene Blue?
Genetic polymorphisms substantially influence individual responses to methylene blue, with substantial interindividual variability in blood pressure attributed to hereditary factors that affect vascular reactivity and neurotransmitter metabolism.
Conclusion
Methylene blue exerts significant modulatory effects on blood pressure through interactions with nitric oxide synthase and monoamine oxidase inhibition pathways.
Like a master switch controlling multiple circuits, this versatile compound can both elevate and stabilise blood pressure in various clinical scenarios. Current evidence supports its therapeutic application in vasoplegic conditions, while necessitating careful monitoring due to potential delayed hypertensive responses and drug interactions, particularly with serotonergic agents.
