Mechanisms of beneficial effects of vasodilators and inotropic stimulation in the experimental failing ischemic heart.

Both vasodilator and inotropic agents improve cardiac function in ischemic heart failure. However, since vasodilators may reduce coronary perfusion pressure and inotropic interventions may increase myocardial oxygen consumption (MVO2), both may increase myocardial ischemia. Accordingly, we determined myocardial blood flow and MVO2 in a canine model of failure induced by propranolol and volume load combined with acute coronary ligation. Both nitroprusside and digitalis reduced ventricular diastolic pressure (LVDP) and increased myocardial blood flow in the ischemic subendocardium. Decreased systolic wall tension also caused a significant reduction MVO2. The benefit of nitroprusside in failing hearts was obtained even with the addition of critical obstruction of the main left coronary artery (LCA). The role of preload reduction is emphasized by the contrasting results with nitroprusside in hearts with low LVDP: (1) decreased myocardial blood flow in ischemic subendocardium, and (2) left ventricular decompensation in animals with critical LCA obstruction. Thus, reduction of LVDP, which decreases subendocardial ischemia, is essential for the beneficial effects of vasodilators and inotropic interventions in ischemic heart failure. Decreased MVO2 caused by reduced heart size may also have a salutary role.

Ivermectin treatment of urinary capillariasis in a dog.

Eggs of Capillaria plica were found by microscopic examination of urine sediment from a 5-year-old female Border Terrier with signs of cystitis. Two courses of oral fenbendazole treatment failed to eliminate the infection or to alleviate clinical signs of cystitis; however, a single dose of ivermectin apparently resulted in complete parasitologic and clinical cure.

Effects of increased vertical dimension on size of constriction port and fricative sound intelligibility.

The effect of increased vertical bite dimension on fricative sound productions was studied in five adults who wore dentures. Oral port size and sound intelligibility were evaluated at different degrees of artificially induced open bite. The data demonstrate that rapid compensatory adjustments occurred and oral port size changed minimally at all degrees of opening tested. However, in three of the subjects, sound intelligibility declined at the 6-mm opening, and in all subjects, a four-fold increase in sound distortions occurred in the edentulous state. This finding suggests the possibility that either physiological parameters are controlled more successfully than acoustical parameters or that compensatory efforts to maintain constrictor size may, under certain circumstances, adversely affect sound intelligibility.

Prognosis in medically-treated coronary artery disease: influence of ejection fraction compared to other parameters.

The prognostic value of the left ventricular ejection fraction(EF) was compared to that of other commonly used indices--severity of coronary artery disease, left ventricular end-diastolic pressure, cardiac index, and abnormal ECG--in 144 patients with coronary artery disease followed for an average of 14 months on medical management. During this period, 14 patients (10%) died. Analysis of the mortality demonstrated that the EF was the most powerful predictor of short-term survival. Thus, patients with three-vessel coronary artery disease and anormal EF (greater than 0.50) had a significantly lower mortality (12%) than did patients with three-vessel CAD and a reduced EF (33%, P less than 0.001). Similar comparisons were observed within the subgroups with abnormal hemodynamics or an abnormal ECG. Therefore, the EF appears to be an important prognostic guide in the medical therapy of coronary artery disease, and is of significantly more discriminant value than other measurements when combined abnormalities exist.

Redistribution of collateral blood flow from necrotic to surviving myocardium following coronary occlusion in the dog.

Early changes in collateral blood flow after acute coronary occlusion may be critical for survival of ischemic myocardium. We used 15-mum radioactive microspheres to study myocardial blood flow in thoracotomized dogs 10 minutes and 24 hours after occlusion of the left anterior descending coronary artery (LAD). The ischemic area was delineated by dye injected into the distal artery, and indentification of potentially ischemic samples was confirmed by a newly developed technique in which microspheres were excluded from the normally perfused LAD. Layers were separated into necrotic or normal as defined by gross inspection and confirmed by histological examination and creatine phosphokinase assay. Infarction always involved endocardial layers and extended toward the epicardium. Average myocardial blood flow in 48 necrotic samples from 16 dogs either remained low (less than 0.05 ml/min g-1) or declined, falling from 0.11 +/-0.02(SE) at 10 minutes to 0.05 +/-0.01 ml/min g-1 at 24 hours (P less than 0.001). In contrast, in the 32 normal-appearing samples which were ischemic at 10 minutes, flow increased from 0.24 +/-0.03 to 0.39 +/-0.04 ml/min g-1 (P less than 0.001). Flow in control myocardium was 1.43 +/-0.12 and 1.04 +/-0.07 ml/min g-1, respectively. Peripheral mean coronary arterial pressure increased from 26 +/- 3 to 35 +/- 3 mm Hg, largely because of enlargement of collateral vessels; collateral conductance calculated from retrograde flow in 14 dogs increased from 0.023 +/- 0.005 after occlusion to 0.051 +/- 0.009 ml/min mm Hg-1 24 hours later (P less than 0.001). Thus, coronary collateral blood flow is redistributed from necrotic endocardial layers to surviving epicardial ones. In combination with a developing collateral supply this process may be essential for sparing myocardium after coronary occlusion.