The possible role of catecholamines in two forms of experimental hypertension in rats was investigated further. Inbred, spontaneously hypertensive (SH) Wistar rats had unchanged endogenous levels of norepinephrine (NE) in the three tissues studied, and a significantly (P<0.05) decreased rate of NE synthesis ( 14 C-tyrosine technique) in heart and brainstem but not in gut, in comparison to normotensive Wistar rats. Also, the levels of free fatty acids (FFA) and major urinary catecholamine metabolites in plasma revealed no evidence of increased catecholamine turnover or release. Sprague-Davvley rats rendered hypertensive by treatment with desoxycorticosterone acetate and 1% salt had decreased cardiac NE concentration and increased cardiac NE turnover (•''H-NE technique) and cardiomegaly, confirming the work of others. However, urinary normetanephrine and plasma FFA did not differ from those in normal rats. These and other results fail to support but do not completely exclude a primary role for catecholamines in either type of hypertension. MethodsExperiments were carried out on male SH rats and normotensive rats weighing 140 to 200 g and aged 11 to 14 weeks (8). Each hypertensive rat was carefully matched for age and weight with a normotensive control rat. Systolic blood pressure was measured weekly and on the day before each experiment in the unanesthetized state using a tail plethysmographic technique (9). The question of a suitable control for a genetic strain of rats is of fundamental importance (8). We use normotensive Wistar rats of the same strain, bred brother to sister and housed in the same animal house under the same conditions as the hypertensive rats. Both groups of rats are then treated identically, have similar growth rates, and accept skin grafts.In studies on the synthesis of NE from radioactive tyrosine, rats were given 0.5 ml 0.9% NaCl solution containing 20 fie of L-tyrosine-14 C (u.l., New England Nuclear Corporation, 370 mc/mmole) into a tail vein and were killed by decapitation at various times after injection. Blood samples were collected in heparin and centrifuged, and aliquots of plasma were analyzed for endogenous and labeled tyrosine. The heart, brainstem, and proximal ileum were removed rapidly, cooled on dry ice, homogenized in cold 0.4N perchloric acid, centrifuged, and analyzed for 14 C-labeled and endogenous NE.

The clinical courses of 100 patients with acute coronary insufficiency (ACI) were reviewed; ACI was defined as prolonged coronary pain without laboratory evidence of myocardial infarction (MI). Of these 100 patients, there was only a single hospital death. Six others developed later MI during hospitalization. Over an average follow-up period of 20 months after hospital discharge, 26 additional patients died, 8 from complications of MI, 13 suddenly, and 5 from other causes. The one-year survival was 85%. Patients who presented with deterioration of chronic angina had a significantly increased mortality over those with the recent new onset of coronary pain. All six hospital MIs and the single hospital death occurred in patients with recurrent pain after admission to the coronary care unit.Acute coronary insufficiency, coronary failure, immediate coronary syndrome, and preinfarction angina are some of the terms that have been used to describe patients who fall between angina and myocardial infarction in the spectrum of coronary disease.1-6 The previously reported overall incidence of progression to infarction has been high: 41% within three months,2 22% within two months,4 and 29% within six months.5There is no good generally accepted medical treatment for this syndrome. Recently, acute myocardial revascularization by the saphenous vein technique has been applied aggressively to a few patients with this clinical picture7,8 with the hope of averting myocardial infarction.The number of patients with this syndrome available to long term follow-up has been small and adequate data on mortality compared to other populations with ischemic heart disease are not available. To obtain this information, we reviewed all the cases of acute coronary insufficiency presenting to the coronary care unit of the Massachusetts General Hospi-tal over a 27-month period. An analysis of this data forms the basis of this report. Clinical Material and MethodsThe charts of all patients admitted to the coronary care unit of the Massachusetts General Hospital in the 27-month period from November 1967 to February 1970 were reviewed. Of these 705 patients, 523 (74%) presented with symptoms of ischemic heart disease, 115 (16%) had cardiovascular but nonischemic problems, and 67 (10%) received noncardiac diagnoses as an explanation for their presenting complaints.In the ischemic group, those patients who demonstrated electrocardiographic or enzymatic evidence of infarction, or both, in the first two days of hospitalization were excluded. One hundred and five of the remaining patients (19% of the ischemic group) satisfied our criteria for "acute coronary insufficiency" (ACI).These criteria were as follows: 1. Pain was consistent with a cardiac origin lasting at least 30 minutes and occurring within 24 hours prior to admission.2. The onset of pain was unrelated to obvious precipitating factors (eg, arrhythmias, anemia).3. The electrocardiogram on admission was not diagnostic of myocardial infarction (MI) and did not show evolution in the first 48 hours...

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