In an attempt to determine the mechanism by which hyaluronidase reduces myocardial injury following coronary artery occlusion, myocardial blood flow was studied in 20 open-chest dogs with occlusion of the left anterior descending coronary artery. Ten dogs served as controls, and 10 received hyaluronidase (500 NF units/kg) intravenously 20 minutes after occlusion. At 15 minutes and at 6 hours after occlusion, regional myocardial blood flow in the epicardial and endocardial halves of both ischemic and nonischemic zones were determined with radiolabeled microspheres. Mean arterial pressure, heart rate, and cardiac output were similar in the untreated and treated dogs through the 6 hours of the experiment. Moreover, regional blood flow to nonischemic myocardium (areas without epicardial S-T segment elevation 15 minutes after occlusion) was similar in the two groups 15 minutes and 6 hours after occlusion. Fifteen minutes after occlusion, the flow to the ischemic myocardium subjacent to sites with S-T segment elevation exceeding 2 mV) in the untreated group was: transmural, 28.1 +/- 2.2 (mean +/- SE) ml/min per 100 g; endocardial, 20.7 +/- 1.8; and epicardial, 38.5 +/- 3.1. The endocardial-epicardial flow ratio was 0.56 +/- 0.04. Six hours after occlusion, the untreated group demonstrated a further decrease in blood flow to the ischemic myocardium: transmural, 15.2 +/- 1.4 ml/min per 100 g; endocardial, 6.8 +/- 1.1; and epicardial, 24.3 +/- 1.9. The endocardial-epicardial flow ratio fell to 0.28 +/- 0.04. In contrast, the hyaluronidase-treated dogs showed no further reduction in blood flow to ischemic myocardium 6 hours after occlusion: transmural, 30.3 +/- 3.1 ml/min per 100 g; endocardial, 21.3 +/- 2.5; and epicardial, 38.8 +/- 3.8. These regional myocardial flows were significantly higher than those of the untreated dogs 6 hours after occlusion. Thus, salvage of damaged myocardium by hyaluronidase might be explained by its beneficial effect on collateral blood flow to the ischemic tissue, though this effect on collateral flow could be the consequence rather than the cause of this salvage.
Eight patients with mixed mitral stenosis and regurgitation underwent hemodynamic and angiographic study prior to mitral valve replacement. The stenotic orifice of the mitral valve was calculated employing the total left ventricular stroke volume by cineangiography as the numerator of the Gorlin Formula. Excellent agreement with the measured orifice of the mitral valve was obtained using a value of 37.9 (0.85 X 44.5) for the constant in the Gorlin formula as recommended by Cohen and Gorlin. Recalculation of this constant independently by our data yielded a value that was almost identical. Regurgitant flows and orifice sizes were calculated for each patient using the same constant as for calculation of the stenotic orifices.
The feasibility of double-labeling of acute myocardial infarcts with /sup 113m/In-EDTMP (ethylenediaminetetra(methylene phosphonic acid)) and /sup 99m/Tc-EDTMP was evaluated. The in vitro distributions of these tracers in acute myocardial infarcts in dogs and their selectivities for infarcted versus noninfarcted myocardium were compared. Both tracers concentrated in acutely infarcted myocardium, and there was excellent correlation between their uptakes (r = 0.88). They also provided complete separation between infarcted and uninfarcted tissue, as checked by histology. Accordingly, these agents show promise for the multiple-labeling of acute myocardial infarcts in experiments to determine the natural course of myocardial infarction and the efficacy of therapy aimed at limiting infarct size. In addition, /sup 113m/In-EDTMP may be useful for serial scintigraphy during the early phase of acute myocardial infarction when the damage may be, at least to some extent, reversible. (auth)
L-tryptophan (L-T) was added at a dose of 150–450 mg daily to eight Parkinsonian patients who developed visual hallucinations with paranoidal features under L-dopa (L-D) treatment (112.5–75 mg daily) in combination with α-methyldopa hydrazine (12.5–75 mg daily). In six patients L-T ameliorated the symptomatology by arresting the visual paranoidal hallucinations or diminishing their frequency and relieving the psychomotor agitation. As a ‘side effect’, L-T produced new ‘pleasurable’, ‘LSD-like’ visual images in three patients. In two patients, in whom L-T did not affect the mental disturbances, amelioration was obtained only by phenothiazines. Theoretical considerations on the role of dopamine in the genesis of visual hallucinations and mental disturbances emphasizes the benefit of L-T administration in this ‘organo-mental’ syndrome.
SUMMARY The study wasdesigned to examine effects of acute cellular injury on regional myocardial blood flow (RMBF)and cor- onary vascular reactivity. Before myocardial infarction in 14 dogs,RMBFwas measured using 7-lO,u microspheres during the hyper-emic response following a 60 sec transient ischemic stimulation(TIS). Myocardial infarction wasinducedbycomplete occlusion for two hours and then inflow to the injured area was re-established.RMBF was measured four hours later during basal conditions,following a 60 sec TIS and during infusion of adenosine, 1.0mg/kg/min. Effects ofacute cellular injury were examinedby mea- suring RMBFin multiple myocardial samples,grouped according to ISCHEMIA OFTHE MYOCARDIUM sufficient to ini-tiate acute myocardial injury effects local responses in thezone of ischemia which directly alter tissue perfusion.1-5 Studies from this laboratory6 have demonstrated that thealterations in regional myocardial perfusion which result from acutecellular injury are directly proportional
