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μμ© κΈ°μ : Organic nitrates act as prodrugs that donate nitric oxide (NO) to vascular smooth muscle, leading to profound vasodilation (predominantly venous, with some arterial effects at higher doses). **Mechanism Pathway:** Organic Nitrate β converted to **free radical Nitric Oxide (NO)** β activates **soluble guanylate cyclase (sGC)** β increases intracellular **cyclic GMP (cGMP)** β activates **Protein Kinase G (PKG)** β decreases intracellular calcium and dephosphorylates **myosin light chain** β **Vascular Smooth Muscle Relaxation**. * **Hemodynamic Effects:** By dilating the venous capacitance vessels, nitrates significantly decrease venous return to the heart (**reduced preload**), which lowers ventricular filling pressures and helps alleviate pulmonary edema in CHF. * **Additional Effects:** Nitrates functionally antagonize acetylcholine, norepinephrine, and histamine. They also relax non-vascular smooth muscle, including biliary, bronchial, gastrointestinal, ureteral, and uterine tissues.
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- Adjunctive treatment of heart failure associated with thyroid storm Β· Isosorbide dinitrate at 0.5-2 mg/kg PO q8-12h Β· PO Β· q8-12h Β· Start at lowest level and titrate upward.
- Refractory heart failure or in combination with hydralazine or amlodipine in patients unable to tolerate ACE inhibitors Β· Isosorbide dinitrate at 0.5-2 mg/kg PO twice daily OR isosorbide mononitrate at 0.25-2 mg/kg PO twice daily Β· PO Β· twice daily Β· Efficacy is unknown.
- Refractory heart failure or in combination with hydralazine or amlodipine in patients unable to tolerate ACE inhibitors Β· Isosorbide dinitrate at 0.5-2 mg/kg PO twice daily OR isosorbide mononitrate at 0.25-2 mg/kg PO twice daily Β· PO Β· twice daily Β· Efficacy is unknown. It is unknown if nitrate-free periods are required to prevent nitrate tolerance.
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κΈκΈ°
- Cardiogenic or hypovolemic shock
- Severe hypotension
- Hypovolemia
- Use as a sole agent for treating heart failure
- Concurrent use with selective phosphodiesterase inhibitors (e.g., sildenafil)
μ΄μλ°μ
- Postural hypotension
- Reflex tachycardia
- Lethargy or weakness (secondary to hypotension)
- Gastrointestinal upset
- Restlessness
- Headache (well-documented in humans, difficult to assess in animals)
- Hypersensitivity reactions (rare)
μ½λ¬Ό μνΈμμ©
- Antihypertensive Drugs (e.g., ACE inhibitors, amlodipine, beta-blockers) Β· Possible additive hypotensive effects; monitor blood pressure closely.
- Phenothiazines (e.g., acepromazine) Β· Possible additive hypotensive effects due to alpha-adrenergic blockade.
- Selective Phosphodiesterase Inhibitors (e.g., sildenafil, pimobendan) Β· Concurrent use with sildenafil can cause profound, life-threatening hypotension and is strictly contraindicated. Use with pimobendan (a PDE3 inhibitor) is common in vet med but requires monitoring for excessive vasodilation.
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- Clinical efficacy (improvement in respiratory rate/effort, resolution of pulmonary edema)
- Systemic blood pressure (monitor for hypotension)
- Heart rate (monitor for reflex tachycardia)
- Renal values and electrolytes (if used concurrently with diuretics and ACE inhibitors)
κ³Όμ©λ
**Toxicity Profile:** Isosorbide mononitrate caused significant lethality in rats and mice at massive dosages (2000 mg/kg and 3000 mg/kg, respectively). **Clinical Signs of Overdose:** * Profound venous pooling * Decreased cardiac output * Severe hypotension * Reflex tachycardia * Collapse or syncope **Treatment:** * Treatment is primarily **supportive**. * **Avoid Epinephrine:** Drug therapies with agents such as epinephrine are NOT recommended as they may exacerbate the cardiovascular collapse. * **Fluid Therapy:** Increasing central fluid volume may be useful to counteract venous pooling, but in patients with pre-existing congestive heart failure (CHF), IV fluids must be administered with **extreme caution** to avoid precipitating fulminant pulmonary edema.
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