Echocardiographic evaluation of right ventricular anterior wall motion in the Wolff-Parkinson-White syndrome.

Echocardiographic motions of right ventricular anterior wall (RVAW) were investigated in 71 patients with Wolff-Parkinson-White (WPW) syndrome. According to the criteria of Rosenbaum et al the electrocardiograms were classified as type A in 35 patients and type B in 36. Sixteen type B patients exhibited abnormal RVAW motion, which was characterized by an early onset of the posterior movement before S1 andl also by a premature peak formation before S2. A small step or hump nearly coincident with S1 was observed in 10 of these 16 patients. These findings seem to suggest that both contraction and relaxation of RVAW begin earlier than normal due to anterior right ventricular pre-excitation. RVAW motion was normal in all of type A patients. Echocardiographic investigation of RVAW motion appears to be useful in non-invasive estimation of the site of pre-excitation, especially in type B WPW patients.     

Rebamipide Attenuates Indomethacin-Induced Gastric Mucosal Lesion Formation by Inhibiting Activation of Leukocytes in Rats

Granulocyte elastase released from activatedleukocytes plays an important role in leukocyteinfiltration. Since activated leukocytes have been shownto be involved in the pathogenesis of gastric mucosal lesion formation induced by nonsteroidalantiinflammatory drugs, inhibition of granulocyteelastase release from activated leukocytes may be usefulin the prevention of these lesions. Rebamipide, a novel antiulcer agent, inhibited granulocyte elastaserelease from activated neutrophils in vitro. Rebamipideand ONO-5046, a granulocyte elastase inhibitor, markedlyinhibited gastric mucosal lesion formation in rats. Gastric myeloperoxidase activity wassignificantly increased 3 hr after indomethacinadministration. This increase was significantlyinhibited by rebamipide and ONO-5046. Cimetidine did notinhibit granulocyte elastase release from activatedneutrophils. Although cimetidine markedly prevented theindomethacin-induced gastric mucosal lesion formation,it did not reduce the gastric myeloperoxidase activity. Therefore, unlike cimetidine, rebamipide mayprevent indomethacin-induced gastric mucosal lesionformation by inhibiting neutrophil activation.     

Giant right atrial thrombus in Noonan syndrome combined with Eisenmenger's complex

A 54-year-old woman with the Noonan syndrome was admitted with congestive heart failure and a giant right atrial thrombus with atrial septal defect detected by two-dimensional echocardiography. The thrombus vanished on oral anticoagulant therapy with warfarin. The thrombus is considered to result from hemostasis in the right atrium due to congestive heart failure and to her specific skeletal characteristics. This report describes the first case of Noonan syndrome with right atrial thrombus.     

Tone-Inhibiting Insoles Enhance the Reciprocal Inhibition of Ankle Plantarflexors of Subjects With Hemiparesis After Stroke: An Electromyographic Study

Background

Spasticity is a common sequela of upper motor neuron pathology, such as cerebrovascular diseases and cerebral palsy. Intervention for spasticity of the ankle plantarflexors in physical therapy may include tone-inhibiting casting and/or orthoses for the ankle and foot. However, the physiological mechanism of tone reduction by such orthoses remains unclarified.

Changes in sodium-22 turnover and total body potassium in two-kidney, one-clip renovascular hypertension

Changes in sodium-22 turnover and total body potassium (TBK) were studied during acute (within 2 weeks after clipping) and chronic (12-14 weeks after clipping) phases in two-kidney, one-clip (2k, 1c) hypertensive rabbits by using a whole body counter. Sodium-22 injected intravenously was eliminated more rapidly in hypertensive rabbits than in controls. The biological half-life (BHL) of sodium-22 was shorter in hypertensive rabbits during both acute (p less than 0.05) and chronic phases (p less than 0.001). A significant negative correlation was obtained between the BHL of sodium-22 and blood pressure (r = -0.588, p less than 0.05) in hypertensive rabbits. TBK decreased significantly at the chronic phase in hypertensive rabbits (p less than 0.05), while TBK showed no significant change in controls. Serum sodium and potassium did not change during the observation period. Increased plasma aldosterone concentration was observed during the acute phase in hypertensive rabbits. These results suggested that sodium retention was not a major factor in the acute and chronic phases of 2k, 1c hypertension in rabbits and that pressure natriuresis could explain, at least in part, the lack of sodium retention. Furthermore, there appears to be a derangement in the intracellular potassium metabolism which may be associated with the maintenance rather than the development of hypertension.     

Renal denervation inhibits hypothalamo-sympathetic nerve system in normotensive and hypertensive rats

The role of the renal nerve in influencing the hypothalamo-sympathetic nerve system to regulate the cardiovascular system was studied in normotensive Wistar and spontaneously hypertensive rats (SHR). Renal denervation attenuated pressor and sympathetic nerve responses to electrical stimulation of the hypothalamus without lowering the basal blood pressure at 48 hours after denervated operation. These findings suggest that renal denervation could inhibit the hypothalamo-sympathetic nerve system in normotensive rats. The development of hypertension in SHR was completely inhibited by renal denervation during 2 weeks of observation (from 7 to 9 weeks of age) without increasing water intake and urine volume. Pressor responses to intravenous injection of norepinephrine were not affected by renal denervation. The results show that the antihypertensive effect of renal denervation was not due to the changing of vascular reactivity. Pressor and sympathetic nerve responses to hypothalamic stimulation were strongly diminished in renal denervated rats. These results suggest that renal denervation strongly inhibited they hypothalamo-sympathetic nerve system. It is also suggested that the renal afferent nerve may facilitate the hypothalamo-sympathetic nerve system in regulating blood pressure and that this facilitation may contribute to the development of hypertension in SHR.     

Augmented central cholinergic mechanisms in spontaneously hypertensive rats. Involvement of deranged noradrenergic mechanisms in the brain

Intracerebroventricular (ICV) injections of carbachol produced biphasic blood pressure responses consisting of initial vasodepression of short duration followed by a sustained pressor phase, which were accompanied by corresponding changes in sympathetic nerve activity in normotensive outbred-Wistar rats (NT) under urethane-anesthesia. In both normotensive Kyoto Wistar rats (WKY) and spontaneously hypertensive rats (SHR), on the other hand, carbachol elicited purely pressor responses, and accompanying sympathetic nerve activity was little affected. The magnitude of the pressor responses was larger in SHR than in WKY or NT rats. Spinal sectioning did not affect the magnitude of the pressor responses. Vasopressor responses to intravenous injections of arginine-vasopressin were not significantly different between WKY and SHR. These results indicate that carbachol injected intracerebroventricularly produces vasopressor effects mainly by releasing pituitary hormones, probably vasopressin, and that augmented pressor responses in SHR may be due to excessive release of vasopressin. When central noradrenergic neurons had been destroyed with ICV injections of 6-hydroxydopamine in both NT and WKY rats, carbachol-induced vasopressor responses were markedly augmented and resulted in responses similar to those of SHR. These findings indicate that central noradrenergic vasodepressive neurons are deficient and that the augmented vasopressor responses to carbachol resulted from deranged central noradrenergic mechanisms in SHR.