Ratio of tritiated water and hydrogen generated in mercury through a nuclear reaction.

Tritium generated in a mercury target is a source of potential exposure of personnel at high-energy accelerator facilities. Knowledge of the chemical form of tritium is necessary to estimate the internal doses. We studied the tritium generation upon thermal neutron irradiation of a mercury target modified into liquid lithium amalgam to examine the ratio of tritiated water ([3H]H2O) and tritiated hydrogen ([3H]H2). The ratio between [3H]H2O and [3H]H2 generated in lithium amalgam was 4:6 under these experimental conditions.

Ratio of aerosol and gases of radioactive chlorine and particle size distribution of aerosol formed by high-energy proton irradiation.

To estimate internal doses due to the inhalation of radionuclides produced by the nuclear spallation of the air nuclei in high-energy proton accelerator facilities, the physicochemical properties of radionuclides are very important. Thus, the ratio of aerosol and gases of 38Cl and 39Cl formed by irradiating argon gas-added air with a 48 MeV proton beam has been measured. Radionuclides of 38Cl and 39Cl exist as aerosol, acid gas and non-acid gas. The percentages of activity of 38Cl and 39Cl aerosols are about 80%. The number size distributions of non-radioactive aerosol were characterised by two peaks with diameters of 10-20 nm and larger than 20 nm. As a result predicted by a simple surface model, it was found that the activity size distribution of 38Cl aerosols can be regarded as that having a single peak at 120 nm.

Disulfide-linked peptides in the chloroplast thylakoid membrane.

Two peptides move out from the diagonal when dodecyl sulfate gels of pea leaf chloroplast thylakoid membrane proteins are treated with a reducing agent and electrophoresed in the second dimension. Apparently two of the proteins in the thylakoid membrane are disulfide linked dimers. Additional changes in the electrophoretic mobility of certian peptides occur when thylakoid membranes are denatured in the presence of reducing agents: these peptides probably contain intrapeptide disulfide bonds or prosthetic groups covalently attached to the peptide through disulfide bonds.

Genesis of the Austin Flint murmur: relation to mitral inflow and aortic regurgitant flow dynamics.

OBJECTIVES: This study was designed to elucidate the genesis of the Austin Flint murmur. BACKGROUND: The Austin Flint murmur is an apical diastolic rumble associated with significant aortic regurgitation. The precise mechanism of the murmur remains unclear. METHODS: The relation between the Austin Flint murmur and mitral inflow and aortic regurgitant flow dynamics was evaluated nonivasively in 13 patients with moderate to severe aortic regurgitation and 15 control subjects using phonocardiographic and pulsed and color-coded Doppler echocardiographic techniques. The severity of aortic regurgitation was determined by color-coded Doppler echocardiography on the basis of the maximal distance of the regurgitant signal. RESULTS: The direction of aortic regurgitant flow was unrelated to the presence of the Austin Flint murmur. The severity of aortic regurgitation was greater in patients with than in those without this murmur. The peak mitral inflow velocity during early diastole (E) was significantly increased, and both peak mitral inflow velocity at atrial contraction (A) and the A/E ratio were significantly decreased in patients with the Austin Flint murmur compared with values in those without this murmur or in control subjects. However, the maximal amplitude of the Austin Flint murmur did not coincide temporally with the peak mitral inflow velocity. The murmur continued both after rapid mitral inflow had ended and during diastolic mitral regurgitation. CONCLUSIONS: The increased velocity of early diastolic mitral inflow in patients with the Austin Flint murmur is due to aortic regurgitation, but rapid mitral inflow is not an essential requirement for production of the murmur. In some cases, the Austin Flint murmur may be generated by aortic regurgitant flow alone.

High incidence of pneumonia in elderly patients with basal ganglia infarction.

BACKGROUND: Pneumonia is a major cause of death in patients with cerebral infarction. We assessed morbidity associated with pneumonia in 276 patients 65 years of age or older who were admitted to a long-term care facility. Furthermore, we studied the swallowing reflex during the day and at night and monitored the occurrence of silent aspiration during sleep. OBJECTIVES: To examine the possible relationship between the location of cerebral hemispheric infarctions and the incidence of pneumonia and to evaluate the role of silent aspiration in the development of pneumonia. METHODS: The incidence of pneumonia was analyzed in 4 groups of patients who were assigned to a group on the basis of the following computed tomographic findings: no infarct (group A); 1 or more unilateral basal ganglia infarcts (group B); bilateral basal ganglia infarcts (group C); and 1 or more cerebral hemispheric infarcts outside the basal ganglia (group D). Criteria for diagnosis of pneumonia were (1) a new pulmonary infiltrate seen on a chest radiograph and (2) 1 or more of the following features: cough, temperature greater than 37.8 degrees C, or subjective dyspnea. Before the study, the patients with stroke were followed up for more than 1 year after their ictus and were monitored to determine if they sustained affecting cerebral hemispheric structures. The average duration of observation for incidence of pneumonia was 22 months. To study the swallowing reflex and to monitor for the occurrence of silent aspiration during sleep, 15 of the patients who were confined to bed or chair were randomly selected from each of groups A through C. The swallowing reflex was examined at both 1 PM and 1 AM and was evaluated according to latency of response, which was timed from the injection of 1 mL of distilled water into the pharynx through a nasal catheter to the onset of swallowing. The incidence of silent aspiration during sleep was examined using indium-111 chloride as a radioactive tracer attached to the teeth, and scanning of the thorax was performed the next morning. RESULTS: The incidence of pneumonia was 2.12 times higher in the patients of group B (27.4%; P < .01) and 3.64 times higher in the patients of group C (47.0%; P < .001) than in the patients of group A (12.9%). The latency of response was longer in the patients of groups B (P < .05) and C (P < .001) than in those of group A at 1 AM. The percentage of positive scans was also higher in the patients of groups B (P < .01) and C (P < .001) than in those of group A. CONCLUSION: Basal ganglia strokes might predispose these patients to develop pneumonia owing to frequent aspiration during sleep.

Progesterone metabolism in recombinant yeast simultaneously expressing bovine cytochromes P450c17 (CYP17A1) and P450c21 (CYP21B1) and yeast NADPH-P450 oxidoreductase.

Simultaneous expression plasmids were constructed for bovine adrenal cytochromes P450c17 and P450c21 (pA gamma alpha) and for both P450s together with NADPH-cytochrome P450 reductase (pAR gamma alpha). On introduction of each of the plasmids into Saccharomyces cerevisiae AH22 cells, the transformed yeast strains AH22/pA gamma alpha and AH22/pAR gamma alpha produced about 10(5) molecules per cell of P450c17 and 2 x 10(3) molecules per cell of P450c21. The expression levels of NADPH-cytochrome P450 reductase was about 3 x 10(4) and 6 x 10(5) molecules per cell in the strains AH22/pA gamma alpha and AH22/pAR gamma alpha, respectively. When progesterone was added to growing cell cultures of the transformed yeast strains, the substrate was metabolized more rapidly in the AH22/pAR gamma alpha cells than AH22/pA gamma alpha cells, probably due to overproduction of the reductase. In the AH22/pAR gamma alpha cells, progesterone was first converted into 17 alpha-hydroxyprogesterone to the extent of 82% by the catalysis of P450c17. 17 alpha-hydroxyprogesterone was further converted into 11-deoxycortisol by P450c21 to the extent of 60% of the added substrate. The conversion of progesterone into androstenedione through 17 alpha-hydroxyprogesterone was estimated to be less than 3%, suggesting very low C17,20-lyase activity of P450c17, although other hydroxylation products were detected. Androstenedione was further converted into testosterone by an unknown pathway present in S. cerevisiae cells.

Comparison of the kinetic disposition and metabolism of E3810, a new proton pump inhibitor, and omeprazole in relation to S-mephenytoin 4'-hydroxylation status.

We studied the kinetic disposition and metabolism of E3810 [(+/-)-sodium 2-[[4-(3-methoxypropoxy)-3-methylpyridin-2-yl]methylsulfinyl ]-1H- benzimidazole], a new proton pump inhibitor, and omeprazole in 15 Japanese male volunteers, six of whom were poor metabolizers and nine of whom were extensive metabolizers of S-mephenytoin. All received once-daily 20 mg doses of E3810 or omeprazole for 7 days in a randomized crossover manner, with a 3-week washout period between the two trial phases. The parent drugs and their principal metabolites in plasma and urine were measured on days 1 and 7 after drug administration. The mean values for area under the plasma concentration-time curve (AUC) of omeprazole were 6.3- and 4.4-fold greater, whereas those of E3810 were 1.8- and 1.9-fold greater in poor metabolizers than in extensive metabolizers after the first and final doses, respectively. Although the mean AUC values for both drugs were significantly (p < 0.01 or p < 0.05) greater in poor metabolizers than in extensive metabolizers, the difference in the AUC between the two groups was smaller after E3810 than after omeprazole administration. The AUC of omeprazole tended to increase with the repeated doses in extensive metabolizers, whereas no such change was observed for E3810. The urinary excretions of the principal metabolite(s) of two proton pump inhibitors also reflected the data derived from plasma samples in relation to S-mephenytoin 4'-hydroxylation status. We conclude that the metabolism of two proton pump inhibitors is under coregulatory control of S-mephenytoin 4'-hydroxylase (CYP2C19), but that the magnitude of CYP2C19-mediated metabolism appears to differ between the two drugs. In contrast to omeprazole, the metabolism of E3810 is less saturable in extensive metabolizers during the repetitive dosings.

Comparison of the interaction potential of a new proton pump inhibitor, E3810, versus omeprazole with diazepam in extensive and poor metabolizers of S-mephenytoin 4'-hydroxylation.

OBJECTIVE: To compare the interaction potential of E3810, [(+/-)-sodium 2-[[4-(3-methoxpropoxy)-3-methylpyridin-2-yl]methylsulfinyl] -1H-benzimidazole] a new proton pump inhibitor, and omeprazole with diazepam in relation to S-mephenytoin 4'-hydroxylation status. STUDY DESIGN: Fifteen healthy male volunteers consisting of six poor metabolizers and nine extensive metabolizers of S-mephenytoin 4'-hydroxylation participated in the study, where two poor and three extensive metabolizers each as a group were randomly allocated to one of the three different treatment sequences with a 3-week washout period among the three trial phases. Each volunteer received an oral once-daily dose of E3810 (20 mg), omeprazole (20 mg), or placebo for 23 days and an intravenous dose (0.1 mg/kg) of diazepam on posttreatment day 8. Plasma concentrations of diazepam and demethyldiazepam were measured up to 16 days after the administration of diazepam. RESULTS: Diazepam was more slowly metabolized in the poor metabolizers than in the extensive metabolizers. No significant effects of E3810 and omeprazole on any kinetic parameters of diazepam were observed in the poor metabolizers. In the extensive metabolizers, omeprazole significantly decreased the mean clearance of diazepam and increased its half-life, area under the plasma concentration-time curve, and mean residence time compared with E3810 and placebo (p < 0.05 or 0.01), whereas no changes in these kinetic parameters were observed during the treatment with E3810. Omeprazole significantly increased the mean area under the plasma concentration-time curve (0-16 days) of demethyldiazepam in the extensive metabolizers compared with placebo (p < 0.01), whereas E3810 significantly increased it in the poor metabolizers compared with omeprazole or placebo (p < 0.05). CONCLUSION: The results indicate that E3810 as a substrate goes less toward S-mephenytoin 4'-hydroxylase (CYP2C19) and has a much weaker, if any, potential to interact with diazepam compared with omeprazole.

1alpha,25-dihydroxyvitamin D(3)-26,23-lactone analogs antagonize differentiation of human leukemia cells (HL-60 cells) but not of human acute promyelocytic leukemia cells (NB4 cells).

We examined the effects of two novel 1alpha,25-dihydroxyvitamin D(3)-26,23-lactone (1alpha,25-(OH)(2)D(3)-26,23-lactone) analogs on 1alpha,25(OH)(2)D(3)-induced differentiation of human leukemia HL-60 cells thought to be mediated by the genomic action of 1alpha, 25-dihydroxyvitamin D(3) (1alpha,25-(OH)(2)D(3)) and of acute promyelocytic leukemia NB4 cells thought to be mediated by non-genomic actions of 1alpha,25-(OH)(2)D(3). We found that the 1alpha,25-(OH)(2)D(3)-26,23-lactone analogs, (23S)-25-dehydro-1alpha-hydroxyvitamin D(3)-26,23-lactone (TEI-9647) and (23R)-25-dehydro-1alpha-hydroxyvitamin D(3)-26,23-lactone (TEI-9648), inhibited differentiation of HL-60 cells induced by 1alpha,25-(OH)(2)D(3). However, 1beta-hydroxyl diastereomers of these analogs, i.e. (23S)-25-dehydro-1beta-hydroxyvitamin D(3)-26, 23-lactone (1beta-TEI-9647) and (23R)-25-dehydro-1beta-hydroxyvitamin D(3)-26,23-lactone (1beta-TEI-9648), did not inhibit differentiation of HL-60 cells caused by 1alpha,25-(OH)(2)D(3). A separate study showed that the nuclear vitamin D receptor (VDR) binding affinities of the 1-hydroxyl diastereomers were about 200 and 90 times weaker than that of 1alpha-hydroxyl diastereomers, respectively. Moreover, none of these lactone analogs inhibited NB4 cell differentiation induced by 1alpha,25-(OH)(2)D(3). In contrast, 1beta,25-dihydroxyvitamin D(3) (1beta,25-(OH)(2)D(3)) and 1beta,24R-dihydroxyvitamin D(3) (1beta,24R-(OH)(2)D(3)) inhibited NB4 cell differentiation but not HL-60 cell differentiation. Collectively, the results suggested that 1-hydroxyl lactone analogs, i.e. TEI-9647 and TEI-9648, are antagonists of 1alpha,25-(OH)(2)D(3), specifically for the nuclear VDR-mediated genomic actions, but not for non-genomic actions.

Relationship between the angiotensin converting enzyme gene polymorphism and the effects of enalapril on left ventricular hypertrophy and impaired diastolic filling in essential hypertension: M-mode and pulsed Doppler echocardiographic studies.

OBJECTIVE: To investigate the relationship between the angiotensin converting enzyme (ACE) gene polymorphism and the effects of the ACE inhibitor enalapril on left ventricular hypertrophy and impaired diastolic filling. DESIGN AND METHODS: Enalapril (5-10 mg/day) was administered for 12 months to 60 previously untreated patients with essential hypertension. M-mode and pulsed Doppler echocardiography were performed before and after treatment, and changes in various parameters after treatment with enalapril were examined. ACE gene polymorphism was examined by the polymerase chain reaction method and the patients were classified as having the 190 bp deletion homozygous (DD) genotype, the 490 bp insertion homozygous (II) genotype or the 490 bp insertion 190 bp deletion heterozygous (ID) genotype. RESULTS: The DD genotype was observed in 10 patients (17%), the ID genotype in 24 patients (40%) and the II genotype in 26 patients (43%). Plasma ACE activity before treatment with enalapril was significantly higher in seven patients with DD genotype than it was in 18 patients with ID genotype and in 14 patients with II genotype. In all of the 60 patients, the left ventricular mass index, the peak atrial systolic velocity:early diastolic velocity ratio and the deceleration time from the peak of the early diastolic wave to the baseline in transmitral flow velocity were decreased significantly after treatment with enalapril. The changes in left ventricular mass index and atrial systolic velocity:early diastolic velocity ratio after enalapril administration were significantly greater in the DD genotype group than they were in the other two genotype groups. CONCLUSION: Enalapril-induced regression of left ventricular hypertrophy and improvement in left ventricular impaired diastolic filling were significantly greater in the DD genotype group than they were in the ID and II genotype groups, suggesting that the circulating and tissue renin-angiotensin systems, particularly the former system, are most active in hypertensive patients with the DD genotype.

Evaluation of left atrial appendage function by measurement of changes in flow velocity patterns after electrical cardioversion in patients with isolated atrial fibrillation.

We investigated temporary changes in left atrial appendage (LAA) flow velocity patterns in patients undergoing electrical cardioversion for chronic isolated atrial fibrillation, and evaluated the role of active LAA contraction in directing blood flow to the left atrial main chamber and left ventricle. The study consisted of 26 patients with chronic isolated atrial fibrillation treated with electrical cardioversion and 20 normal controls in sinus rhythm. Using transthoracic and transesophageal Doppler echocardiography, we recorded transmitral, pulmonary venous, and LAA flow velocity patterns before, 24 hours, and 1 week after cardioversion in all subjects. In the 15 patients who underwent successful cardioversion, the maximal LAA area 24 hours after cardioversion was smaller than the area before cardioversion, whereas LAA ejection fraction during atrial systole and peak atrial systolic emptying velocity of the LAA flow were lower 24 hours after cardioversion than those in the control group. One week after cardioversion, maximal LAA area and LAA peak atrial systolic emptying velocity were restored to levels approximately equivalent to those in the control group, although LAA ejection fraction was lower than in the control group. Maximal LAA area and LAA peak atrial systolic emptying velocity correlated negatively and positively with LAA ejection fraction, respectively, 24 hours and 1 week after cardioversion. These results suggest that LAA and the left atrial main chamber show stunning 24 hours after cardioversion, and the atrial systolic emptying wave of LAA flow is generated by active LAA contraction.

Pulmonary and systemic venous flow patterns assessed by transesophageal Doppler echocardiography in congenital absence of the pericardium.

In conclusion, alterations in venous return are more marked in the right side of the heart than in the left side of the heart in patients with complete absence of the left pericardium.

Predisposing factors for severe mitral regurgitation in idiopathic mitral valve prolapse.

To elucidate predisposing factors for severe mitral regurgitation (MR) in idiopathic mitral valve prolapse (MVP), 124 MVP patients were classified into the following categories: 55 with isolated clicks (click group), 35 with a late-systolic murmur (late-SM group), and 34 with a holosystolic murmur (holo-SM group). Their clinical and echocardiographic findings were compared with those of 26 patients with spontaneous chordal rupture (rupture group). In 22 patients in the click group, 24 in the late-SM group, and 22 in the holo-SM group, follow-up studies were performed for a mean of 4.5 years (range 1 to 13.5). The mean age was youngest in the click group and oldest in the rupture group. The click and late-SM groups showed a female predominance, but the holo-SM and rupture groups showed a male predominance. There was no difference in the incidence of systemic hypertension among the 4 groups. Most patients in the click and late-SM groups had anterior leaflet prolapse. In the holo-SM and rupture groups, however, the incidence of posterior leaflet involvement was significantly increased. The incidence of thickened mitral valve increased in order of the click (8%), late-SM (21%), holo-SM (38%), and rupture (50%) groups. Six patients in the holo-SM group developed chordal rupture with severe MR during the follow-up period. In the click and late-SM groups, however, there were no complications and no development into a holo-SM. Thus, aging, male sex, posterior leaflet prolapse, thickened mitral valve, and holo-SM were found to be important predisposing factors for severe MR in idiopathic MVP.

Polymorphism in the human complement C4 genes and genetic susceptibility to autoimmune hepatitis.

Susceptibility to autoimmune hepatitis is associated with the HLA-DR3 and DR4 haplotypes, but which genes are directly involved in the pathogenesis, has not been established. Low levels of complement component C4 and elevated frequencies of C4 null allotypes have been described in patients, suggesting that the C4 genes, which are closely linked with the HLA loci, may play a role. We therefore examined restriction fragment length polymorphisms in the C4 and 21-hydroxylase genes, and determined HLA-A and B phenotypes, and HLA-DR, DQ and DP genotypes in a large series of Caucasoid patients with autoimmune hepatitis and matched controls. A DNA deletion of the C4A gene and the 21-hydroxylase A pseudogene was found to be present in 50% of patients compared to 23% of controls (Pc < 0.005, relative risk = 3.3). This increase, however, appears to be due to linkage disequilibrium with HLA-DR52a which was most strongly associated with the disease. Complete C4A deficiency, determined by homozygosity for the deletion increased the risk to 18.1 (16% versus 1%, Pc < 0.005), suggesting an additional role for C4 in disease susceptibility. C4 deletions were associated with an increased mortality and tendency to relapse whilst on treatment but did not correlate with age of onset of disease. Our data suggest that MHC-encoded susceptibility to autoimmune hepatitis is polygenic, involving the HLA-DR genes plus other loci, and C4 deficiency may be a marker of disease susceptibility and/or severity.

Asymmetry in the nonmesonic weak decay of polarized (5)(Lambda)He hypernuclei

We have measured the asymmetric emission of protons from the nonmesonic decay of polarized (5)(Lambda)He produced by the (pi(+), K+) reaction. (5)(Lambda)He is an s-shell hypernucleus and its polarization is due to the Lambda. One expects to obtain direct information on the elementary weak Lambda-->p-->np process. The asymmetry parameter has been determined to be 0.24+/-0.22. The implication of the result is discussed.

Lanthanide trifluoromethanesulfonate-catalyzed asymmetric aldol reactions in aqueous media.

[figure: see text] Catalytic asymmetric aldol reactions catalyzed by lanthanide trifluoromethanesulfonates in aqueous media have been realized for the first time using a chiral crown ether.

Supra- and juxtatrigeminal inhibitory premotor neurons with bifurcating axons projecting to masseter motoneurons on both sides.

Inhibitory neurons participating in the bilateral disynaptic inhibition of jaw-closing motoneurons by stimulation of unilateral trigeminal sensory branches were searched for in the reticular formation around the trigeminal motor nucleus in cats anaesthetized with pentobarbital. Extracellular recordings were made from neurons which responded orthodromically after a monosynaptic latency to single shock stimulation of the ipsilateral infraorbital and/or inferior alveolar nerves. Direct inhibitory connection with contralateral masseter motoneurons was demonstrated in reticular neurons by the spike-triggered averaging technique, i.e., by averaging the intracellular potentials of a contralateral masseter motoneuron with respect to spontaneously occurring spikes of a reticular interneuron. By intraaxonal injection of neurobiotin, electrophysiologically identified inhibitory premotor reticular neurons were found to project to and to terminate in the trigeminal motor nuclei on both sides. Termination in the contralateral motor nucleus was demonstrated for four neurons that showed the peripheral input pattern stated above. The results provide hard evidence for contralaterally projecting interneurons in the reticular formation, participating in peripherally evoked disynaptic inhibition of masseter motoneurons on the contralateral side. Given the previously reported findings that the supratrigeminal region contains neurons which project to the ipsilateral motor nucleus and mediate disynaptic inhibition of masseter motoneurons, it is suggested that the supratrigeminal region contains bilaterally projecting interneurons, mediating peripherally evoked disynaptic inhibition of masseter motoneurons on both sides.

Morphological analysis of cat masseteric motoneurons after intracellular staining with horseradish peroxidase.

Intracellular injection of horseradish peroxidase (HRP) into 58 masseteric motoneurons identified by antidromic activation was performed in cats under pentobarbital anesthesia. Monosynaptic EPSPs were evoked by masseteric nerve stimuli in 52 cells, and were absent in the remaining six cells. The antidromic nature of the evoked spikes was confirmed by IS-SD separation observed at high frequency (50 Hz) stimulation. Motoneurons with monosynaptic excitation from masseter afferents showed IPSPs following stimulation of lingual and inferior alveolar nerves. Motoneurons which did not show monosynaptic excitation from masseter afferents showed no IPSPs from the above nerves. There were no differences in cell size or the number of stem dendrites between motoneurons with and without monosynaptic EPSPs. No recurrent collaterals were observed in any motor axons. Motoneurons with monosynaptic EPSPs were located at all rostrocaudal levels throughout the trigeminal motor nucleus, whereas motoneurons without such EPSPs were encountered only at the middle level. Dendrites of motoneurons with monosynaptic EPSPs did not extend into the medial portion of the nucleus where motoneurons innervating the anterior belly of the digastric muscle were located. In contrast, motoneurons without monosynaptic EPSPs had dendrite branches extending well into the medial part. The results show that there are two subpopulations of masseteric motoneurons that differ in peripheral inputs as well as dendritic morphology.

Pre-penile arteries are dominant in the regulation of penile vascular resistance in the rat.

The amount of blood flow into the penis that will produce an erection is dependent on the sum of inflow resistance from the feeder arteries, arterioles and the intra-penile vasculature. In the present study, our objective was to determine quantitatively the contribution to inflow resistance of these different components of the rat penile vasculature. Using methods developed previously, we determined the resistance properties of the isolated perfused whole penis in situ, both in an intact system and after serial transactions of the vessels. These cuts eliminated progressively larger distal segments of the vascular bed. Perfusion pressures were recorded at different flow rates (0.5-3 ml/min/kg body weight) under conditions of maximal dilatation and maximal vasoconstriction induced by methoxamine (MXA, 40 microg/ml). Regardless of the level of vascular tone, the pudendal artery contributes approximately 70% of the total resistance of the penile vasculature. In contrast, the vasculature within the penis (tip, shaft, crus) contributes only about one quarter of the resistance. Penile arterial inflow resistance properties both at maximal vasodilation and maximal alpha1-adrenergic constriction are dominated by the extra-penile vasculature in the rat. The implications of these findings are that alterations in the pudendal-artery (eg vasodilation, vasoconstriction, stenosis) would have primary control of arterial inflow and suggest an important role for pharmacological agents which can promote a more generalized vasodilation (eg phosphodiesterase inhibitors) in contrast to selective corpus cavernosal agents.

Cross sectional echocardiographic demonstration of the mechanisms of abnormal interventricular septal motion in congenital total absence of the left pericardium.

OBJECTIVE: To investigate the influence of the absence of the pericardium on the left ventricular wall, particularly on interventricular septal motion, using M mode and cross sectional short axis echocardiography in patients with congenital total absence of the left pericardium. METHODS: 21 patients with, congenital total absence of the left pericardium were divided into three groups according to the interventricular septal motion; systolic type (n = 6) with paradoxical motion during systole, diastolic type (n = 11) with abnormal posterior motion during mid to late diastole, and mixed type (n = 4) with paradoxical motion during systole and abnormal posterior motion during diastole. RESULTS: On cross sectional short axis echocardiograms of the left ventricle, in the diastolic type the degree of angular displacement of the papillary muscles during end diastole to end systole showed excessive anticlockwise rotation about the long axis of the left ventricle without marked anteroposterior displacement. In the systolic type, there was shift of the left ventricle towards the anteromedial portion in systole and towards the posterolateral portion in diastole without significant rotation. There was a significantly positive correlation between the degree of angular displacement and the amplitude of diastolic interventricular septal motion during mid to late diastole in all patients. CONCLUSIONS: There was abnormal interventricular septal motion during systole and diastole in patients with total absence of the left pericardium. Abnormal systolic motion was induced by anteroposterior displacement of the left ventricle, and abnormal diastolic motion by left ventricular rotation about the long axis of the heart during the cardiac cycle. Analysis using cross sectional echocardiography was useful for elucidating the mechanisms of abnormal interventricular septal motion.