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This case report describes the inadvertent poisoning of a young man with "poppers" after having ingested an unknown amout of the drug. "Poppers" (alkyl nitrite) were made famous in the 1960s as a party drug, and during certain sexual practices, and are still in use today. The drug's inhalation leads to a short-lived rush, vasodilation and relaxtion of smooth muscles. An accidental ingestion can lead to a significant build-up of methemoglobin with dire consequences. The therapy consists of the intravenous administration of methylene blue.

While nitrates have been in clinical use for more than 100 years, their mode of action is of rather recent discovery. Nitrates act by the release of the free radical NO (nitric oxide) which stimulates the cyclic guanosine monophosphate as vasodilatator and as inhibitor of platelet function. The endogenous nitrate NO is derived from L-arginine catalyzed by nitric oxide synthase, a recently cloned enzyme. Nitrates and other nitro-vasodilatators act similarly to the endogenous nitrate, whereby a basal release of NO in the vascular wall reduces the effect of nitro-vasodilatators. Therefore, drugs are particularly effective in endothelium-free vessel segments and in veins, where the basal release of NO is low. A recently discovered effect of nitro-vasodilatators is the inhibition of thrombin and angiotensin II-induced production of endothelin. Insofar the L-arginine/NO metabolism acts as an important regulator in the vessel wall and has a protective role in the circulation by its antispastic and antithrombotic principle.

The effectiveness of organic nitrates in the therapy of angina pectoris can be explained from their direct relaxing action on vascular smooth muscle. At conventional dosage the most important action of nitrates is a pooling of blood in the large systemic venous capacitance vessels which leads to a decrease of central venous pressure and ventricular filling pressure. The resulting reduction in left ventricular volume lowers, at virtually constant arterial pressure, systolic wall tension and hence myocardial oxygen consumption. Only at higher dosage, is a distinct dilatation of systemic resistance vessels affected. The fundamental action of the "Ca antagonists", i.e. the inhibition of transmembrane calcium influx in the myocardium and the vascular smooth muscle, includes various beneficial effects for the treatment of angina pectoris. The lowering of myocardial oxygen consumption after application of calcium antagonist is mainly due 1. to the decrease in afterload of the left ventricle, caused by the relaxation of peripheral resistance vessels, 2. to the reduction in ventricular preload by a peripheral venodilation. By a direct inhibitory effect on the coronary vascular tone, coronary blood flow at rest in patients with angina pectoris increases. In addition, Ca antagonists are very efficacious in relieving angiospastic angina. The primary mode of action of beta-blocking drugs in angina pectoris affects, in contrast to the peripheral mechanisms of nitrates and Ca antagonists, is on the heart directly. By the reduction in the extent of exercise heart rate, the increase in cardiac output and, hence, the mean arterial pressure is also significantly lower during exercise under beta-blockade. Beta-blockers also depress the contractile state of myocardium. Therefore, the main factors of the myocardial oxygen consumption (mean arterial pressure, size of the left ventricle, contractility and heart rate) may be essentially influenced. By the decrease in heart rate and the longer diastolic period a better myocardial oxygen delivery results. Besides the immediate cardiac effects of beta-adrenergic blockade, a decline in peripheral resistance combined with a fall in blood pressure occur in hypertensive patients during long-term drug administration. Different hypotheses have been proposed in the last years to explain the antihypertensive mode of action of beta-blockers. Some possible mechanisms are discussed.

Directional Doppler-ultrasound has been found to be helpful in detecting disturbances of the left ventricular outflow tract, especially in aortic incompetence. Also in hypertrophic obstructive cardiomyopathy characteristic changes of flow in carotid artery have been demonstrated by directional Doppler-ultrasound, similar to those of the carotid pulse curve. These changes lead to diagnosis but usually do not allow an information about the hemodynamic status of hypertrophic obstructive cardiomyopathy. However, characteristic changes of the flow curve in the subclavian artery -- which are described in this paper -- seem to appear only in severe cases, when an intraventricular gradient was measurable, either at rest or under provocation test. So a combination of two non-invasive methods, echocardiography and directional Doppler-ultrasound of the carotid and the subclavian artery enables us to diagnose hypertrophic obstructive cardiomyopathy and at the same time informs us about hemodynamic conditions.