Physical characterization of litter and microplastic along the urban coast of Cagayan de Oro in Macajalar Bay, Philippines.

There are limited litter and microplastic (MP) studies in the Philippines despite the fact that is has one of the longest shorelines that is possibly threatened by waste disposal. This study was carried out to determine the litter and MP in surface sand samples in a highly urbanized coastal environment of Cagayan de Oro in Macajalar Bay, Philippines. The flotation and stereomicroscope identification methods were employed to study MP, while litters were counted to extrapolate the clean coast index (CCI). Overall, MP fibers were found ubiquitously with site-specific abundance. Particularly, the residential site adjacent to the river mouth had the highest litter and MP fiber counts. The built environment like the seaport showed fragmented forms of MP. Likewise, CCI analysis showed an extremely dirty beachfront (CCI = 85) which mainly caused by plastic litters. Overall, the highly urbanized coastal environment may accumulate a distinct form of plastics. This study is preliminary and may underestimate plastic analysis owing to the limited sampling.

Functional characterization of left ventricular segmental responses during the initial 24 h and 1 wk after experimental canine myocardial infarction.

Characterization of the temporal evolution of resting segmental function and inotropic reserve after coronary occlusion may be important in evaluating attempts to salvage ischemic but non-necrotic myocardium. Accordingly, we chronically implanted up to six pairs of pulse-transit piezoelectric crystals in the left ventricular myocardium of dogs to measure segmental wall thickness. Segments were separated into groups according to the loss of net systolic thickening (NET) at 5 min postocclusion of the left anterior descending coronary artery in awake, unsedated dogs. Group 1 included segments with NET values of 67--100+ (percent control); group 2 between 67 and 0; and group 3 less than 0 (paradoxical motion). 5 min after coronary occlusion, group 1 NET was 92 +/- 5% (SEM) although significant decreases occurred in NET in group 2 (36 +/- 4%) and group 3 segments (-33 +/- 5%). Between 5 min and 24 h after coronary occlusion, no further significant changes occurred in NET in groups 1, 2, and 3 crystals. Some segments underwent further functional deterioration between 24 h and 1 wk after left anterior descending coronary artery occlusion, although no overall change occurred in segments with mild to moderate ischemic dysfunction. Segments with NET less than 0 at 24 h, on the other hand, exhibited a reduction in aneurysmal bulging between 24 h and 1 wk from -41 +/- 10 to -23 +/- 11% (n = 12, P = 0.02). Inotropic reserve was assessed with postextrasystolic potentiation (PESP) in 14 dogs, and with infusions of dopamine (11 dogs), and isoproterenol (13 dogs). PESP was the most potent intervention and produced a significant augmentation in NET in group 2 crystals at 1, 2, 4, 6,8, and 24 h after coronary occlusion but only at 1 and 2 h in NET in group 3 crystals. Thus, following experimental coronary occlusion, the evolution of ischemic segmental dysfunction is dynamic and variable. A significant degree of inotropic reserve, as assessed by PESP, dopamine, and isoproterenol, exists in segments with moderate ischemic dysfunction for 24 h but for only 2 h after coronary occlusion in those segments with the most severe ischemic dysfunction. In addition, at least some segmental sites with mild to moderate ischemic dysfunction at 24 h deteriorate further between 24 h and 1 wk after experimental coronary occlusion.

Dissecting aortic aneurysm involving a right-sided aortic arch.

In this case, the first reported instance of aortic dissection involving a right-sided arch, an anomalous fourth arch vessel, the left subclavian artery, arose from a congenital aortic diverticulum. This report emphasizes the need for precise anatomic definition with aortography to permit appropriate therapy when congenital anomalies of the aortic arch are complicated by dissecting hematoma.

Effect of various degrees of systemic arterial hypertension on acute canine myocrdial ischemia.

There is continuing uncertainty about the effects of various degrees of systemic arterial hypertension on myocardial ischemia. In 46 open-chest anesthetized dogs, intramural carbon dioxide tension (PmCO2) was measured directly with a mass spectrometer during repetitive 10-min coronary artery occlusions separated by 45-min periods of reflow. During each occlusion, transmural regional myocardial blood flow (RMBF) in the ischemic area was quantitated with the injection of radioactive microspheres (7-10 micrometers diam). In all dogs the increase in PmCO2 from before to 10 min after the first occlusion (delta PmCO2) exceeded that during subsequent occlusions. In those dogs in which systemic arterial hypertension was not produced (controls), delta PmCO2 during the third occlusion was similar to that during the second occlusion. When phenylephrine was administered during the third occlusion to increase systemic arterial pressure mildly (diastolic pressure 95-115 mmHg), RMBF to the ischemic myocardium was unchanged, and the severity of myocardial ischemia was reduced, as reflected by a fall in delta PmCO2. When diastolic pressure was elevated moderately (116-140 mmHg), RMBF was augmented, but the extent of myocardial ischemia was neither diminished nor worsened. In contrast, when diastolic pressure was increased markedly (greater than 140 mmHg), myocardial ischemic injury was intensified (as reflected by an increase in delta PmCO2) even though RMBF rose significantly. Thus, in the dog with acute coronary artery occlusion, an increase of systemic arterial pressure exerts an influence on the severity of myocardial ischemic injury that is related directly to the magnitude of systemic arterial hypertension: a mild increase of pressure reduces ischemic injury, a moderate increase exerts no consistent effect on ischemia, and a marked increase worsens ischemic injury.

Interrelationships between regional left ventricular function, coronary blood flow, and myocellular necrosis during the initial 24 hours and 1 week after experimental coronary occlusion in awake, unsedated dogs.

This study examined the relationships between the left ventricular (LV) regional function, regional myocardial blood flow (RMBF), and myocellular necrosis after sudden proximal occlusion of the left anterior descending coronary artery (LAD) in 36 awake, unsedated dogs. Net wall thickening during systole (NET) was used to assess regional LV function, was expressed as percent control, and was measured with chronically implanted ultrasonic crystals. RMBF was measured with 8- to 10-micrometer radioactive microspheres. In regions with a moderate degree of functional loss, NET fell to 35.3 +/- 2.2% of control at 5 minutes when RMBF fell from 1.9 +/- 0.08 to .086 +/- 0.09 ml/g per min (P less than 0.05). No significant change occurred in midwall or epicardial RMBF. The relationship between endocardial flow and NET was non-linear (r = 0.69, P less than 0.0001). In these segments, subsequent changes in RMBF were unrelated to corresponding functional alterations through 24 hours. In segments with paradoxic systolic wall thinning RMBF fell in endocardial, midwall, and epicardial layers; endocardial ischemia was most severe (0.30 +/- 0.05 ml/g per min). Segmental myocellular necrosis was most severe in the endocardial layer and correlated significantly with both RMBF and segmental function. Myocellular necrosis increased in severity as flow was reduced below 70-75% of normal. Thus, in this model of LV ischemia, (1) regional LV functional loss is most sensitive to reductions in endocardial RMBF; (2) subsequent increases in RMBF are largely unassociated with functional recovery; (3) transmural ischemia results in paradoxical systolic wall thinning.

Effects of systemic hypertension on ischemic and nonischemic regional left ventricular function in awake, unsedated dogs after experimental coronary occlusion.

Hypertension and atherosclerotic coronary arterial obstruction frequently coexist in patients. However, the effect of increased aortic pressure on ischemic segmental dysfunction is not well understood. We studied the effects of aortic pressure increases on segmental left ventricular function during myocardial ischemia. Eighty-two dogs instrumented with three to six pairs of pulse-transit piezoelectric crystals were studied in an awake, unsedated state to measure segmental wall thickness. A pneumatic balloon occluder was positioned around the proximal left anterior descending artery (LAD). Thirty-three dogs underwent LAD occlusion and served as normotensive controls (group A). Group B dogs (n = 23) received a 6-hour infusion of phenylephrine (PE) beginning 5 minutes after LAD occlusion to increase aortic diastolic arterial pressure to 120-130 mm Hg; aortic pressure was then allowed to return to normal for the subsequent 18 hours. The eight dogs in group C received a 6-hour infusion of PE, but no coronary arterial occlusion was produced. In group D (n = 12), distal constriction of the thoracic aorta was maintained for 24 hours after LAD occlusion. Regional myocardial blood flow (RMBF) was measured with radioactive microspheres in six conscious dogs and both RMBF and intramyocardial PCO2 were measured in seven open-chest dogs to assess alterations in regional myocardial oxygen supply and demand. Segments of myocardium were arbitrarily grouped according to the amount of net systolic thickening (NET) present 5 minutes after LAD occlusion and before increasing aortic pressure: group 1 retained 67-100+% of control NET, group 2 0-67%, and group 3 less than 0% (paradoxic motion). In dogs receiving PE plus LAD occlusion and in dogs with aortic constriction and LAD occlusion, NET was transiently depressed in groups 1 and 2 compared with the normotensive cohort; 24 hours after occlusion, NET in groups 1, 2 and 3 did not differ significantly from that in the normotensive dogs. Systemic hypertension resulted in a significant increase in endocardial and midwall RMBF and, in seven open-chest dogs, decreased the intramyocardial accumulation of carbon dioxide after LAD occlusion. Increased aortic pressure in dogs without coronary occlusion produced reversible decreases in end-diastolic wall thickness, NET and LV dP/dt. Thus, the production of systemic hypertension with diastolic pressures of 110-120 mm Hg acutely or for 6 hours during evolving canine myocardial infarction does not appear to exert an important deleterious effect on myocardial oxygen supply and demand. However, 24 hours of mildly increased aortic pressure accentuates end-diastolic wall thinning in segments with paradoxic systolic motion and results in a failure of their return to control values at this period.