Abdominal accommodation induced by meal ingestion: differential responses to gastric and colonic volume loads.

BACKGROUND: Using an experimental model of colonic gas infusion, we previously showed that the abdominal walls adapt to its content by an active phenomenon of abdominal accommodation. We now hypothesized that abdominal accommodation is a physiological phenomenon, and aimed to confirm that it can be induced by ingestion of a meal; a secondary aim was to determine whether the response to gut filling is region-specific. METHODS: In healthy subjects (n = 24) a nutrient test meal was administered until tolerated at a rate of 50 mL min(-1). Electromyographic (EMG) activity of the anterior wall (upper and lower rectus, external and internal oblique) was measured via four pairs of surface electrodes, and EMG activity of the diaphragm via intraluminal electrodes on an esophageal tube. To address the secondary aim, the response to gastric filling was compared with that induced by colonic filling (1440 mL 30 min(-1) anal gas infusion; n = 8). KEY RESULTS: Participants tolerated 927 ± 66 mL of meal (450-1500 mL). Meal ingestion induced progressive diaphragmatic relaxation (EMG reduction by 16 ± 2%; P < 0.01) and selective contraction of the upper abdominal wall (24 ± 2% increase in activity of the upper rectus and external oblique; P < 0.01 for both), with no significant changes in the lower rectus (4 ± 2%) or internal oblique (5 ± 3%). Colonic gas infusion induced a similar response, but with an overall contraction of the anterior wall. CONCLUSIONS & INFERENCES: Meal ingestion induces a metered and region-specific response of the abdominal walls to accommodate the volume load. Abnormal abdominal accommodation could be involved in postprandial bloating.

Accommodation of the abdomen to its content: integrated abdomino-thoracic response.

BACKGROUND: We previously showed that changes in intra-abdominal content induce a volume-dependent muscular response of the anterior abdominal wall and the diaphragm. We aimed to determine the contribution of the thorax to abdominal accommodation and the influence of the intra-abdominal expansion rate. METHODS: Gas (1440 mL total load) was infused into the colon of nine healthy subjects, while abdomino-thoracic perimeters (by tape measure), electromyography (EMG) activity of the diaphragm (via six ring electrodes over an esophageal tube in the hiatus), intercostals and anterior abdominal wall (via five pairs of surface electrodes) and the position of the diaphragm by ultrasonography were measured. Infusion rates of 24, 48, and 96 mL min(-1) were tested on separate days. KEY RESULTS: Gas infusion induced anterior abdominal wall contraction (18 ± 1% EMG increment; P < 0.001) with relatively modest girth increment (4.9 ± 0.9 mm; P = 0.001), diaphragmatic relaxation (by 15 ± 1%; P < 0.001) with cephalad displacement (by 23 ± 6 mm; P = 0.005), and intercostal contraction (by 19 ± 2%; P < 0.001) with increased thoracic perimeter (by 2.0 ± 0.5 mm; P = 0.009). Responses were similar with the three infusion rates. CONCLUSIONS & INFERENCES: Accommodation of intra-abdominal loads involves a volume-related integrated abdomino-thoracic response regardless of the expansion rate.

N-Cyclopropylimine-1-pyrroline rearrangement. A novel photochemical reaction.

[reaction: see text] A novel aza-(vinylcyclopropane-cyclopentene) photochemical rearrangement is reported. 1-Pyrrolines are easily synthesized in good yields from N-cyclopropylimines. Hydrogen, alkyl, and aryl groups can be placed anywhere within the system, and the reaction proceeds regiospecifically.

The role of families in adolescent HIV prevention: a review.

Recent research has highlighted the significant contribution families make in the prevention of HIV risk behaviors among adolescents. As the most proximal and fundamental social system influencing child development, families provide many of the factors that protect adolescents from engaging in sexual risk behaviors. Among these are positive family relations, effective communication about sexuality and safer sexual behaviors, enhancement and support of academic functioning, and monitoring of peer activities. HIV risk behaviors occur in a social context, and it is becoming clear that the earliest and most effective way to intervene is in the context where one initially learns about relationships and behavior--the family. Both the Centers for Disease Control and Prevention and the National Institute for Mental Health have taken steps to support and emphasize research that will further elucidate our understanding of the role of families in HIV prevention. This article uses Ecodevelopmental Theory to guide and organize the findings of this promising research area. Within this context, and with special attention to the comorbidity of adolescent problem behaviors, this article reviews empirical research on the role of families in HIV prevention, discusses current intervention efforts that involve families and ecosystems, and addresses prospects and implications for future research and interventions.

Gastric wall tension determines perception of gastric distention.

BACKGROUND & AIMS: The primary mechanism that originates symptoms in response to gastric distention remains undefined. The aim of this study was to determine which factor, whether intragastric volume, pressure, or wall tension, determines perception of gastric distention. METHODS: Healthy subjects underwent increasing gastric distentions (2-minute duration at 5-minute intervals) either at fixed pressure levels using a conventional barostat (n = 10) or at fixed tension levels using a newly developed computerized tensostat (n = 12); perception was scored by a 0-6 scale. Distentions were performed during basal conditions (intravenous saline) and during gastric relaxation by glucagon administration (4.8 microgram/kg intravenous bolus plus 9.6 microgram. kg-1. h-1 infusion). RESULTS: Isobaric distentions with the conventional barostat produced more intense perception during glucagon (95% +/- 40% higher; P < 0.05). However, the factor that determined higher perception could not be ascertained, because at the same pressure levels both intragastric volume and wall tension were greater during glucagon administration (174% +/- 56% and 34% +/- 8% greater, respectively; P < 0.05 vs. saline for both). The tensostat evidenced that perception was selectively related to tension, not to elongation; during glucagon administration, intragastric volumes were significantly larger (80% +/- 28% larger increase; P < 0.05), but perception of isotonic distentions remained the same (27% +/- 22%; nonsignificant change). CONCLUSIONS: Gastric wall tension, but not intragastric volume, determines perception of gastric distention, at least below nociception.

ST segment elevation at the surface of a healed transmural myocardial infarction in pigs. Conditions for passive transmission from the ischemic peri-infarction zone.

BACKGROUND: Ischemia of the myocardium surviving an infarction induces ST segment elevation in infarct-related ECG leads. In cases with no viable tissues, ischemia adjacent to the infarction could induce a similar ECG pattern if there is ST segment potential transmission through the necrotic scar. We analyzed whether acute ischemia adjacent to a healed infarction with no viable tissue may induce ST segment elevation on the surface of the necrotic scar. METHODS AND RESULTS: Epicardial ST segment changes elicited during 30 minutes of acute reocclusion of the left anterior descending (LAD) coronary artery 2 cm above the first diagonal branch were analyzed by 32-channel mapping in 18 chloralose-anesthetized open-chest pigs with 1-month-old anterior infarctions induced by permanent ligature below the first diagonal branch (group 1). The effect of a previous infarction on the magnitude of ischemic ST segment changes was assessed by similar mapping in 21 control pigs submitted to a LAD ligature 2 cm above the first diagonal branch (group 2, n = 11) or just below this branch (group 3, n = 10). Myocardial perfusion after coronary ligature was estimated in 7 pigs with chronic infarction and in 3 control pigs by mapping of myocardial technetium-99m-methoxyisobutyl isonitrile (99mTc-MIBI) activity in transmural samples underlying each epicardial electrode. The width of cell layers surviving the infarction was measured and their viability after 60 minutes of coronary reocclusion was assessed by intracellular glycogen staining. Reocclusion of the LAD induced parallel ST segment elevation at the periinfarction zone and at the necrotic scar, although in the latter region the changes were less marked (maximal ST segment, 8.4 +/- 3.0 mV versus 2.7 +/- 1.8 mV, ANOVA, P < .001). ST segment elevation inside the scar was greater at the margins (3.9 +/- 1.8 mV) than at sites 20 mm toward the center (2.8 +/- 1.7 mV, P = .003). The necrotic area was virtually devoid of surviving cells except for a 0.22 +/- 0.04-mm-wide subendocardial band that continued to show a positive intracellular glycogen reaction after the second LAD ligature. Acute ischemia adjacent to the infarction (group 1) induced lower ST segment elevation than acute ischemia at a comparable cardiac region in noninfarcted pigs (group 2) (ANOVA, P = .02), despite the fact that these areas developed similar underperfusion after coronary occlusion (percent MIBI activity of that in normal myocardium, 7 +/- 8 versus 7 +/- 6, P = NS). ST segment changes in group 2 pigs were comparable to those induced in group 3 pigs with a 2-cm-lower coronary occlusion. CONCLUSIONS: Acute ischemia adjacent to a chronic infarction induces ST segment elevation at the surface of the scar despite the virtual absence of viable tissue within the infarction. Data suggest a passive ST segment potential transmission through the infarction. Moreover, ischemia adjacent to a chronic infarction induces lower ST segment elevation than ischemia not adjacent to a necrosis. The mechanisms accounting for these regional differences are probably independent of collateral myocardial perfusion and ischemia extension.

Low incidence of ventricular arrhythmias induced by ischaemia at the borders of a chronic infarct in a model with local postinfarction denervation.

OBJECTIVE: The aim was to assess the arrhythmogenic potential of acute ischaemia superimposed at the borders of a chronic myocardial infarct and to analyse the effects of myocardial necrosis on local autonomic innervation in pigs. METHODS: Ventricular arrhythmias were measured in alpha chloralose (100 mg.kg-1) anaesthetised open chest pigs during 60 min occlusion of the left anterior descending coronary artery 2 cm above the first diagonal branch (group I, n = 11) or just below this branch (group II, n = 12). These arrhythmias were compared with those induced in pigs with a one month old anteroseptal infarction (coronary ligature as in group II) submitted to a second occlusion 2 cm above the first (group III, n = 12). The area at risk after high or low ligature was measured in 12 control pigs using fluorescein. Sympathetic and parasympathetic innervation of the anteroseptal myocardium was studied in three pigs with a chronic anteroseptal infarction and in six pigs without infarction using adrenergic histofluorescence and acetylcholinesterase reaction. RESULTS: Compared with ischaemia alone, ischaemia at the borders of a chronic infarct induced a lower incidence of ventricular fibrillation (1/12 pigs v 11/11 in group I, p < 0.001, or 6/12 in group II, p < 0.05) and a tendency towards a lower occurrence of ventricular tachycardia (2/12 pigs v 8/11 in group I, p = 0.01, and 4/12 in group II) and fewer ventricular premature beats (mean number: 105 in group I v 30 in group III, p < 0.05). The mass of the ischaemic regions after low or high occlusion was 13.3(SD 3.0) g and 23.2(5.8) g, respectively. Adrenergic and cholinergic denervation was observed inside the necrotic area, along the subendocardium surviving the necrosis, and in a band of normal bordering myocardium [width: 3.2(2.0) mm for adrenergic and 2.1(1.2) mm for cholinergic denervation]. CONCLUSIONS: Acute ischaemia at the borders of a chronic anteroseptal infarct has a low arrhythmogenic potential in pigs. In this model the peri-infarction zone shows a band of sympathetic and parasympathetic denervation secondary to the necrosis.

T-Q, S-T segment mapping and hyperemia in reperfused pig heart with ischemic preconditioning.

The effects of ischemic preconditioning on epicardial T-Q and S-T segment mapping, local activation, and coronary blood flow were analyzed in nine barbiturate-anesthetized pigs during four coronary occlusion (5 min)-reperfusion (20 min) sequences. In seven sham pigs, one occlusion was performed after a control period of 75 min. The first reperfusion induced a marked coronary hyperemia [11 +/- 4 ml/min (baseline) to 33 +/- 16 ml/min, P < 0.005] and a rapid recovery (30 to 150 s) of epicardial activation delays, T-Q segment depression, and S-T segment elevation in the ischemia area. This recovery was transiently associated with enlargement of intersite T-Q potential variability (alpha: 2.5 +/- 0.6 to 3.4 +/- 0.7 mV, P < 0.05), T-Q segment overshoot to +1.4 +/- 0.9 mV, and S-T segment reelevation. A brief T-Q segment depression (-2.3 +/- 0.9 mV) occurred during early reperfusion in 60 of 91 electrodes overlying the normal myocardium. Compared with the first, the fourth occlusion induced lower S-T segment elevation (3.4 +/- 2.0 to 1.7 +/- 1.9 mV, P < 0.05), and the fourth reperfusion elicited a faster reversal of T-Q segment dispersion (53 +/- 21 to 43 +/- 16 s, P < 0.05), S-T segment elevation (149 +/- 101 to 81 +/- 45 s, P < 0.05), and coronary hyperemia (8 +/- 2 to 5 +/- 1 min, P < 0.05). This trend of changes was not observed during a fourth occlusion in sham pigs.(ABSTRACT TRUNCATED AT 250 WORDS)