Patent foramen ovale (PFO) is implicated in platypnea-orthodeoxia, stroke and decompression sickness (DCS) in divers and astronauts. However, PFO size in relation to clinical illness is largely unknown since few studies evaluate PFO, either functionally or anatomically. The autopsy incidence of PFO is approximately 27% and 6% for a large defect (0.6 cm to 1.0 cm). A PFO is often associated with atrial septal aneurysm and Chiari network, although these anatomic variations are uncommon. Methodologies for diagnosis and anatomic and functional sizing of a PFO include transthoracic echocardiography (TTE), transesophageal echocardiography (TEE) and transcranial Doppler (TCD), with saline contrast. Saline injection via the right femoral vein appears to have a higher diagnostic yield for PFO than via the right antecubital vein. Saline contrast with TTE using native tissue harmonics or transmitral pulsed wave Doppler have quantitated PFO functional size, while TEE is presently the reference standard. The platypnea-orthodeoxia syndrome is associated with a large resting PFO shunt. Transthoracic echocardiography, TEE and TCD have been used in an attempt to quantitate PFO in patients with cryptogenic stroke. The larger PFOs (approximately > or =4 mm size) or those with significant resting shunts appear to be clinically significant. Approximately two-thirds of divers with unexplained DCS have a PFO that may be responsible and may be related to PFO size. Limited data are available on the incidence of PFO in high altitude aviators with DCS, but there appears to be a relationship. A large decompression stress is associated with extra vehicular activity (EVA) from spacecraft. After four cases of serious DCS in EVA simulations, a resting PFO was detected by contrast TTE in three cases. Patent foramen ovales vary in both anatomical and functional size, and the clinical impact of a particular PFO in various situations (platypnea-orthodeoxia, thromboembolism, DCS in underwater divers, DCS in high-altitude aviators and astronauts) may be different.

No abstract

ABSTRACT. This study was performed to determineOxygen is one of the major stimuli decreasing pulmonary whether prostaglandins play a role in the increase in pul-vascular resistance at birth (1,(13)(14)(15). Assali et al., (16) and monary blood flow in the fetal lamb caused by an increase Heymann et al., (17) isolated the effect of a rise in oxygen tension in oxygen tension similar to that occurring at birth. To from the effect of ventilation of the lungs with a gas in acutely increase fetal oxygen tension without ventilating the lungs, instrumented fetal lambs by placing pregnant ewes in a hypernine pregnant ewes with chronically instrumented fetuses baric chamber at several atmospheres of pressure. Morin et al.were exposed to 100% oxygen at 3 atmospheres absolute (18) adapted this technique to study chronically instrumented pressure for 20 min in a hyperbaric chamber. This expo-fetal lambs and found that the entire increase in pulmonary sure increased pulmonary arterial oxygen tension in the blood flow that normally occurs at birth could be produced by nine fetuses from 20 f 1 to 54 f 9 torr. It increased an increase in oxygen tension alone. pulmonary blood flow from fetal to newborn values, 31 fThe current study was performed to determine whether the 3 to 295 2 20 ml/kg/min. It did not change pulmonary response of the fetal pulmonary circulation to oxygen is mediated arterial pressure, 52 f 2 torr during normoxia and 50 f 2 by prostaglandins. We measured the ability of prostaglandin torr during hyperoxia. Treating five of these fetuses with synthesis blockade by indomethacin to diminish the increase in 3.2 f 0.4 mg/kg of indomethacin during hyperbaric oxy-fetal pulmonary blood flow caused by an increase in oxygen genation did not alter these effects (Po2 = 51 f 8 torr, tension. pulmonary blood flow = 283 f 13 ml/kg/min, and pulmonary arterial pressure = 48 f 2 torr). We conclude that gestation were prepared for study. A catheter was passed from the maternal jugular vein into the right atrium for sampling of Abbreviations blood and for induction of anesthesia with 700 mg of sodium thiamylal. Surgery was then performed with the pregnant ewe PGD2, prostaglandin D2 under halothane anesthesia. The uterus was exposed through an PGE2, prostaglandin Ez abdominal incision, and the fetal head and neck were delivered 6-keto-PGE2, prostaglandin E2 through a uterine incision. An incision was made in the fetal ATA, atmosphere absolute pressure neck, and catheters were inserted into the carotid artery for measurement of systemic pressure and via the jugular vein into the superior vena cava for injection of radioactive microspheres. A left thoracotomy was performed, and a catheter was inserted into the main pulmonary artery, proximal to the branching of At birth there is a dramatic decrease in pulmonary vascular the right and left pulmonary arteries and the ductus arteriosus, resistance and increase in pulmonary blood flow (1, 2). The for measurement of pressure; sampling of blood gases and withincrease in pulmonary blood f...

The inhibitory actions of somatostatin (100 ng./ml.) on insulin release, stimulated by high glucose (20 mM), and on glucagon release, stimulated by arginine (15 mM), were studied with two in vitro systems: the isolated perifused rat islets prepared by the collagenase procedure and the isolated perfused rat pancreas. Suppression of arginine-induced glucagon release by glucose (20 mM) and glyceraldehyde (5 mM) was also assessed in both systems. With the perfused pancreas, somatostatin caused 32 per cent inhibition of glucose-mediated insulin release and inhibited arginine-induced glucagon release by 72 per cent. In the same system, glucose and glyceraldehyde were similarly potent inhibitors of arginine-induced glucagon secretion. In contrast to the isolated perfused pancreas, there was no significant somatostation suppression of glucose-induced insulin release or arginine-induced glucagon release whether the inhibitor was present prior to or was added during stimulation by glucose or arginine. Furthermore, glucose was only minimally active and glyceraldehyde ineffective in inhibiting glucagon secretion due to arginine in the perifusion system. The most plausible explanation for the difference in the endocrine response of islet cells in the two types of widely used in vitro systems is that the alpha and beta cells have lost inhibitory receptors in the plasma membrane as a result of the collagenase isolation technic.

Public reporting burden for the collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden, to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to a penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number.

A B S T R A C T The effects of starvation and refeeding and of obesity on pancreatic a2-and 8-cell responses to glucose or tolbutamide were studied with the isolated rat or mouse pancreas perfused with an amino acid mixture in the presence and absence of glucose. It was observed that the physiological adaptation to a regimen of fasting and realimentation and to obesity differed greatly in the two types of endocrine cells. Whereas ,-cells of rats showed a dramatic reduction of glucose-and tolbutamide-stimulated insulin release during starvation that was reversed by refeeding, a2-cells preserved their response to stimulators and inhibitors during this experimental manipulation. Amino acid stimulation of glucagon release occurred equally well with the pancreas from fed and starved rats and was suppressed efficiently by glucose and tolbutamide in both nutritional states. Surprisingly, the rate of onset of glucose suppression of a2-cells was significantly higher in the fasted than in the fed state. This glucose hypersensitivity was apparent 2 d after food deprivation and had disappeared again on the 2nd d of refeeding. In the pancreas from animals starved for 3 d, glucose and tolbutamide suppression of a2-cells took place in the absence of demonstrable changes of insulin release.In the isolated perfused pancreas taken from the hyperphagic obese hyperglycemic mouse (C57 Black/ 6J; ob/ob), the observed rate of insulin secretion as a result of a combined stimulus of amino acids and gluDr.

No abstract

No abstract