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Clinical and experimental observations prove that heparin-neutralizing doses of protamine increase pulmonary artery pressures and decrease systemic BP. Protamine also increases myocardial oxygen consumption, cardiac output, and heart rate, and decreases systemic vascular resistance. These cardiovascular effects have clinical consequences that have justified studies in this area. Protamine adverse reactions usually have three different categories: systemic hypotension, anaphylactoid reactions, and catastrophic pulmonary vasoconstriction. The precise mechanism that explains protamine-mediated systemic hypotension is unknown. Four experimental protocols performed at Mayo Clinic, Rochester, MN, studied the intrinsic mechanism of protamine vasodilation. The first study reported in vitro systemic and coronary vasodilation after protamine infusion. The second in vitro study suggested that the pulmonary circulation is extensively involved in the protamine-mediated effects on endothelial function. The third study, carried out in anesthetized dogs, reported the methylene blue and nitric oxide synthase blockers neutralization of the protamine vasodilatatory effects. The fourth study suggested that protamine also causes endothelium-dependent vasodilation in heart microvessels and conductance arteries by different mechanisms including hyperpolarization. Reviewing these experimental results and our clinical experience, we suggest methylene blue as a novel approach to prevent and treat hemodynamic complications caused by the use of protamine after cardiopulmonary bypass. In the absence of prospective clinical trials, a growing body of cumulative clinical evidence suggests that methylene blue may be strongly considered as a therapeutic approach in the treatment of distributive shock. [ABSTRACT FROM AUTHOR]

We describe the case of a 40-year-old woman, affected by episodic cluster headache, who presented with a cluster headache triggered by exposure to high altitude. Her attacks were refractory to sumatriptan, very effective at sea level, but responded to oxygen. A pathophysiological mechanism is proposed. [ABSTRACT FROM AUTHOR]

The article focuses on a 43 year old patient suffering from trigeminal neuralgia (TN), Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT), and cluster headache. Both cluster headache and SUNCT are classified as trigeminal-autonomic cephalalgias (TACs). After an angio-MRI the patient was diagnosed with compression of the right trigeminal root with an arterial structure. Combination of gabapentin and amitriptyline was given for treatment.