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Cardiac ultrasound and upper gastrointestinal endoscopy are relatively old technologies. With the introduction of new ultrasound probes and by incorporating ultrasound technology into conventional endoscopes, 'new tricks' in cardiac imaging were discovered. Posterior structures of the heart are now able to be imaged clearly by the ultrasound probe from the oesophagus. Consequently, better resolution of cardiac anatomy allows more accurate diagnosis of cardiac pathologies which is not possible using conventional transthoracic (TT) approach. Over a period of two years, 1200 cases of transoesophageal echocardiography (TOE) were undertaken in our institution. The major indications were diseases of the aorta (10%), source of cardioembolism (28%), assessment of native and prosthetic valve function (20%), suspected endocarditis and its complication (17%), pre and post percutaneous transluminal mitral valvotomy (PTMV [13%], congenital heart disease (2%) and others (10%). The greatest impact with TOE is in the diagnosis of aortic dissection and transection. TOE is superior to conventional TT approach in detecting potential source of embolism, valvular vegetations and its complication, native and prosthetic valve dysfunction and LA thrombus prior to PTMV. Observations by TOE such as spontaneous echo contrast (SEC) in the left atrium open new challenges for further research in its role in the pathogenesis of LA thrombus and its association with cardioembolic event. Other areas of interest include; reclassification of distal aortic dissection and the use of TOE in intra-operative work.

Objective: To determine the value of transoesophageal echocardiography in the assessment of selected patients at risk of cardiogenic embolism or after it., Design: Prospective comparison of the results of transoesophageal and transthoracic echocardiography. Transoesophageal echocardiography was performed with a 5 MHz single plane phased array transducer., Setting: University teaching hospital., Patients: 100 patients referred for transoesophageal echocardiography after a cerebral ischaemic event or peripheral arterial embolism (n = 63), before percutaneous balloon dilatation of the mitral valve (n = 23), or before electrical cardioversion of atrial fibrillation (n = 14)., Results: Transthoracic echocardiography showed potential sources of embolism in four patients including left ventricular thrombus in two patients (with one false positive), left atrial appendage thrombus (n = 1), and patent foramen ovale (n = 1). Transoesophageal echocardiography showed 59 potential embolic sources in 45 patients including left atrial spontaneous echo contrast (n = 33), left atrial appendage thrombus (n = 13), left ventricular thrombus (n = 5), patent foramen ovale (n = 3), left ventricular spontaneous echo contrast (n = 2), mitral valve prosthesis thrombus (n = 1), mitral valve prolapse (n = 1), and pronounced aortic atheroma (n = 1). Transoesophagal echocardiography showed potential embolic sources in 36/53 (68%) patients with atrial fibrillation compared with 9/47 (19%) patients in sinus rhythm. Percutaneous balloon dilatation of the mitral valve was performed without embolic complications in 18 patients without left atrial thrombi and in three patients with small fixed thrombi in the left atrial appendage. It was cancelled in two patients with large thrombi in the left atrial appendage. Cardioversion was performed without embolic complications in 14 patients without left atrial thrombi., Conclusions: Transoesophageal echocardiography detects potential sources of embolism better than transthoracic echocardiography in selected patients at risk of cardiogenic embolism or after it.

The clinical and echocardiographic variables related to left atrial spontaneous echo contrast were prospectively evaluated in a consecutive series of 400 patients undergoing transesophageal echocardiography with a 5-MHz single plane transducer. Left atrial spontaneous echo contrast was found in 75 patients (19%) and was significantly associated with atrial fibrillation, mitral stenosis, absence of mitral regurgitation, increased left atrial dimension and a history of suspected embolism. Seventy-one (95%) of the patients with spontaneous echo contrast had atrial fibrillation or mitral stenosis. Anticoagulant therapy had no significant association with spontaneous echo contrast. Multivariate analysis in 89 patients with mitral stenosis or mitral valve replacement showed that spontaneous echo contrast was the only independent predictor (p = 0.03) of left atrial thrombus or suspected embolism, or both. In 60 patients with atrial fibrillation of nonvalvular origin, spontaneous echo contrast (p = 0.01) and age (p = 0.03) were the only independent predictors of left atrial thrombus or suspected embolism, or both. It is concluded that left atrial spontaneous echo contrast is 1) a common finding in patients undergoing transesophageal echocardiography, 2) associated with conditions favoring stasis of left atrial blood, and 3) a marker of previous thromboembolism in patients with nonvalvular atrial fibrillation and those with mitral stenosis or mitral valve replacement.

To investigate the effects of sodium-potassium activated adenosine triphosphatase inhibition on central cardiovascular regulation a microinjection of ouabain was given into the hypothalamus of urethane anaesthetised rats. Doses of 0.01-1.0 micrograms per rat injected into the posterior hypothalamus produced a rise in blood pressure within 1 min, the maximum rise occurring 15-20 min later in a dose dependent manner. Both heart rate and abdominal sympathetic nerve activity increased with the rise in blood pressure. Ouabain injected into either the anterior preoptic hypothalamus or the ventromedial hypothalamus produced no notable cardiovascular responses. These results suggest that an endogenous digitalis like substance produced in the hypothalamus as a result of sodium loading may participate in central cardiovascular regulation by increasing sympathetic outflow in the discrete area of the brain, as does ouabain.

To determine whether baroreflex can affect the norepinephrine system in the hypothalamus, the extracellular concentration of norepinephrine were measured by the brain dialysis technique in sinoaortic denervated rats (SAD). Twenty-four hours after sinoaortic denervation, systolic blood pressure and heart rate were significantly elevated, and norepinephrine concentration in perfusate of the posterior hypothalamus was significantly higher in SAD rats than in sham-operated rats. These results suggest that baroreflex could modify the activity of noradrenergic neuron projecting to the posterior hypothalamus.

Two children manifested EEG discharges which were triggered by blinking and/or eye closure in light and in darkness. The first case demonstrated single focal posterior discharges with eye blinks and repetitive focal posterior sharp wave discharges with eye closures. No photoparoxysmal responses were obtainable. Case 2 manifested generalized epileptic discharges triggered by eye closure which were sometimes associated with clinical seizures. In addition she showed photoconvulsive responses. Since the discharges triggered by eye blink and by eye closure occurred in both bright light and in darkness it is suggested that sensory afferents arising from contraction of the orbicularis oculi muscles may have been the epileptic trigger in Case 1 and could have contributed to the epileptic triggering mechanism in Case 2.

To determine whether the arterial baroreceptor reflex can act to oppose the development of hypertension, deoxycorticosterone acetate (DOCA)-salt hypertension was produced in sinoaortic-denervated and sham-operated rats. Systolic blood pressure measured by tail cuff started to increase in both sinoaortic-denervated and sham-operated rats 7 days after DOCA treatment, and the hypertension developed identically in both denervated and sham-operated rats. These findings suggest that the baroreceptor reflex cannot act against the development of hypertension. To determine whether the baroreceptor reflex is attenuated before the development of hypertension, bradycardiac and sympathoinhibitory responses to i.v. injections of norepinephrine were examined. Bradycardic and sympathoinhibitory responses were significantly smaller in DOCA-salt-treated rats in both prehypertensive (5th day after DOCA-salt treatment) and hypertensive stages (21st day after treatment). In urethane-anesthetized DOCA-loaded and control rats on the 5th day after treatment, aortic depressor nerve stimulation elicited frequency-dependent depressor and bradycardic responses accompanied by inhibition of sympathetic nerve activity in both DOCA-loaded and control rats. However, those responses were significantly smaller in DOCA-loaded rats than in control rats. These results suggest that the central component of the baroreceptor reflex mediated by the aortic depressor nerve is impaired before hypertension develops and that this impairment may contribute to the development of hypertension in DOCA-salt-treated rats.

To clarify the peripheral origin of plasma dopamine (DA), we studied the changes in plasma levels of free and conjugated catecholamines after nephrectomy, adrenalectomy, chemical sympathectomy and renal denervation. Nephrectomy markedly increased conjugated DA levels, indicating that plasma DA is rapidly excreted through the kidney and originates outside the kidney. Adrenalectomy reduced plasma total epinephrine (E) to undetectable limits, whereas total norepinephrine (NE) and DA levels remained unchanged. In addition, the subsequent immobilization stress significantly increased both total NE and DA, but not E. Chemical sympathectomy with 6-hydroxydopamine decreased both NE and DA by 66% and 72%, respectively. E level, however, was not affected by sympathectomy. Although the following immobilization stress significantly increased all catecholamines levels, the magnitude of increase in concentrations of NE and DA were much less than that of E. These results suggest that plasma DA is mainly derived from the peripheral sympathetic nerve terminals. However, the renal nerve, one of the sympathetic nerves, did not serve as a source of plasma DA because renal denervation had no effect on plasma DA levels in spite of the marked depletion of free DA in the kidney.

The present study was designed to investigate the short-term effects of intracerebroventricularly-administered taurine in DOCA-salt hypertensive (DOCA), spontaneously hypertensive (SHR) and their respective normotensive control rats anesthetized with urethane. Blood pressure, heart rate and sympathetic nerve activity were consistently decreased following the injection of taurine 150 micrograms per rat in hypertensive rats as well as in normotensive controls of the two groups. Percent changes from the baselines in blood pressure, heart rate and sympathetic nerve activity were significantly larger in DOCA-salt hypertensive rats than those in sham operated rats. In contrast, percent changes in blood pressure and sympathetic nerve activity were not significantly different between spontaneously hypertensive rats and normotensive wistar kyoto rats. These result show that the responses of blood pressure, heart rate and sympathetic nerve activity to intracerebroventricular taurine are different between spontaneously hypertensive rats and DOCA-salt hypertensive rats. It appears that augmented vasodepressor responses to taurine in DOCA-salt hypertensive rats, as compared to spontaneously hypertensive rats, are due to enhanced inhibition of the sympathetic outflow.

The effects of taurine on central cardiovascular regulation were investigated by intracerebroventricular (ICV) injection of taurine in urethane-anesthetized rats. Blood pressure fell gradually to attain the maximum level at 10 to 15 min after the injection of 50 micrograms taurine and returned to the basal level 20 min later. After injecting 200 micrograms of taurine, blood pressure began to fall within 30 seconds and attained the maximum level at 2 to 5 min and did not return to the basal level by 20 min. Both heart rate and abdominal sympathetic nerve activity decreased as the blood pressure fell, However, the similar amount of taurine injected intravenously did not affect the blood pressure, the heart rate or the abdominal sympathetic nerve activity. These results suggest that taurine causes the central nervous system to lower the blood pressure by decreasing the sympathetic nerve outflow.

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.

The concept of effective length (L) of the arterial system implies that it may be represented by a single viscoelastic tube terminated by an impedance, creating a single reflection site. Although the concept is straightforward, investigators for years have been unable to agree on the value of L. Proposed values range from a few millimeters to a few meters, confounding the identification of arterial reflection sites. This report shows analytically and illustrates with experimental data that the determination of the effective length leaves room for an infinite number of exact solutions for L and the corresponding terminal impedance if the input impedance of the tube is to match the measured input impedance of an arterial system. None of the possible values of L needs to bear any relationship to actual reflection sites.

In order to verify, whether baroreflex sensitivity is changed centrally in DOCA-salt hypertension, the left aortic depressor nerve (ADN) was electrically stimulated in DOCA-salt hypertensive rats. After 3 weeks, tail-cuff systolic pressure was significantly higher in DOCA-salt treated rats than in untreated rats (169 +/- 4 versus 130 +/- 4 mmHg, respectively; P less than 0.001). After cutting both ADN and the carotid sinus nerves, the central cut end of the left ADN was electrically stimulated and frequency dependent depressor, bradycardic and sympatho-inhibitory responses were elicited in both control and DOCA-salt hypertensive rats. However, these responses were significantly smaller in DOCA-salt hypertensive rats than in normotensive controls. Bradycardic and sympatho-inhibitory responses to i.v. injection of norepinephrine were also blunted in DOCA-salt hypertensive rats. These findings suggest that baroreflexes were centrally attenuated in DOCA-salt hypertensive rats and possibly contribute to overall baroreflex attenuation.

To study the antihypertensive effect of orally administered taurine in DOCA salt hypertension, urinary excretion of catecholamines, electrolytes, and arg-vasopressin was measured over four weeks in 20 taurine treated DOCA rats (group 1), 20 taurine untreated DOCA rats (group 2), and seven taurine untreated sham operated rats (group 3). Additional experiments were performed to determine whether or not the pressor and sympathetic responses to hypothalamic stimulation were altered after taurine treatment in DOCA rats. Systolic blood pressure decreased significantly in group 1 after the first week compared with that in group 2, and the differences became progressively more evident thereafter. At the fifth week the mean blood pressure was significantly lower in group 1 than in group 2, as was the heart rate. Although urinary excretion of adrenaline decreased significantly in group 1 at the first and fourth weeks, the difference in urinary excretion of noradrenaline between groups 1 and 2 was not significant. Urinary excretion of adrenaline and noradrenaline in group 3 was significantly lower than that in both hypertensive groups (groups 1 and 2). Urinary sodium excretion increased significantly in group 1 at the first and second week compared with group 2. With graded electrical stimulation of the ventromedial hypothalamus, resulting pressor and sympathetic responses were significantly smaller in group 1 than in group 2. These results suggest that the hypotensive effects of orally administered taurine in DOCA hypertensive rats are caused by suppression of the peripheral sympathetic nervous activity and by the resulting natriuresis.

When GABA (4-amino-n-butyric acid, 50-200 micrograms) was injected into the lateral ventricle of urethane-anaesthetized Wistar rats, sympathetic nerve activity, arterial pressure and heart rate were decreased dose-dependently. Graded electrical stimulation of the ventromedial hypothalamus (50, 100 and 150 microA) increased not only mean blood pressure but also the rate of sympathetic nerve firing, and both responses were attenuated by GABA pretreatment (100 and 200 micrograms, i.c.v.). In spontaneously hypertensive rats (SHR), i.c.v.-injected GABA also reduced sympatho-cardiovascular activity, but the magnitude of the depressor responses was significantly larger in SHR than in normotensive Wistar-Kyoto (WKY) control rats. Pressor and sympathetic nerve responses elicited by hypothalamic stimulation were initially larger in SHR than in WKY rats. However, upon subsequent i.c.v. injection of GABA, hypothalamic responsiveness in SHR was inhibited more prominently and became almost the same as that in WKY rats. These results suggest that, by depressing hypothalamic function, central GABA-ergic stimulation decreases sympathetic nerve activity thereby lowering blood pressure and heart rate. Because of the increased central sensitivity in SHR, GABA-ergic stimulation reversed hypothalamo-sympathetic hyperactivity and attenuated hypertension.

To determine whether baroreflex is changed centrally before the development of hypertension in DOCA-salt treated rats, aortic depressor nerve was stimulated electrically 5 days after DOCA-salt treatment in urethane-anesthetized rats: compared with those of sham-operated control rats, blood pressure was not elevated in either awake or anesthetized rats. Aortic depressor nerve (ADN) stimulation elicited frequency-dependent vasodepressor, bradycardiac, and sympatho-inhibitory responses in both DOCA-salt-treated and control rats. However, the responses to ADN stimulation were significantly smaller in DOCA-salt-treated rats. These findings suggest that baroreflex is attenuated centrally before the development of hypertension and this attenuation may contribute to the pathogenesis of DOCA-salt hypertension.

A 39-year-old woman with traumatic spinal paraplegia and chronic renal failure had peritoneal dialysis for acute renal failure precipitated by a bout of urinary tract infection. Two weeks after the dialysis she lapsed into coma for a few days. An electroencephalogram indicated petit mal stupor as it showed generalized epileptic discharges during the initial period of her coma.

To determine the central effects of 4-Amino-n-butyric acid (GABA), pressor and sympathetic nerve responses to electrical stimulation of the ventromedial hypothalamus were recorded following the intracerebroventricular (ICV) injection of GABA. In normotensive Wistar rats, anesthetized with urethane, ICV injections of GABA (50-200 micrograms) reduced sympathetic nerve activity, arterial blood pressure, and heart rate in a dose-dependent manner. Graded electrical stimulation of the ventromedial hypothalamus (50, 100, 150 microA) increased not only mean blood pressure but also the rate of sympathetic nerve firing, and both responses were attenuated by GABA pretreatment (100, 200 micrograms, ICV). In spontaneously hypertensive rats (SHR), ICV-injected GABA also reduced sympathetic and cardiovascular activity, but the magnitude of depressor responses was significantly larger in SHR than in normotensive Wister Kyoto controls (WKY). Pressor and sympathetic nerve responses elicited by ventromedial hypothalamic stimulation were initially larger in SHR than in WKY, but upon subsequent ICV injection of GABA, hypothalamic responsiveness in SHR was inhibited more prominently and became comparable to that in WKY. These results suggest that by depressing hypothalamic function, centrally injected GABA decreases sympathetic nerve activity to thereby lower blood pressure and heart rate, and in SHR, ICV-injected GABA reversed hypothalamo-sympathetic hyperactivity and thus attenuated hypertension.

Tail-cuff systolic pressures became elevated in male Wistar rats fed chow containing 8% NaCl for 4 weeks. After 4 weeks of salt loading, pressor and sympathetic responses to ventromedial hypothalamic stimulation were larger in salt-loaded rats. When similar experiments were done following sinoaortic denervation, all of the effects previously induced by dietary salt loading persisted. By contrast, after only 1 week of salt loading, pressor and sympathetic responses to hypothalamic stimulation were reduced, instead of being increased. Since circulating plasma volume was increased in week 1, it was considered possible that reduced hypothalamic responsiveness was due to enhanced cardiopulmonary baroreflexes. Supporting this interpretation, bilateral vagotomy reversed the hypothalamic inhibition occurring in week 1. Although neither the site nor mechanism causing sympathetic hyperactivity has been determined, our results indicate that chronic dietary salt loading has biphasic effects on the ventromedial hypothalamus: an initial inhibition in the first week followed by stimulation thereafter. These results could mean that dietary salt loading eventually increases sympathetic activity and thereby induces hypertension by stimulating the ventromedial hypothalamus.

To determine whether angiotensin II (A II) can modify baroreflex centrally and contribute to the central resetting of baroreflex in spontaneously hypertensive rats (SHRs), the aortic depressor nerve (ADN) was electrically stimulated following intracerebroventricular (ICV) administration of A II and/or A II analog in urethane-anesthetized normotensive Wistar rats (WKYs) and SHRs. Electric stimulation of the ADN elicited frequency-dependent depressor, bradycardic, and sympatho-inhibitory responses. Angiotensin II, administered ICV, dose-dependently attenuated these responses induced by ADN stimulation in normotensive rats. We found, however, these attenuations could be abolished by ICV pretreatment with A II analog. Vasopressin (ICV) did not change any responses to ADN stimulation. The vasopressor and sympatho-inhibitory responses to ADN stimulation were significantly less in SHRs when compared with those in WKYs: In SHRs, A II analog completely cancelled the A II-attenuated responses to ADN stimulation. These findings suggest that A II can centrally attenuate baroreflex, which might be independent from vasopressin, and in the brain A II can contribute to the central resetting of baroreflex in SHRs.

When captopril was injected intravenously in urethane anesthetized rats, a hypotensive effect accompanied by bradycardia was obtained, while an intravenous (i.v.) injection of prostaglandin I2 (PGI2), which induced hypotension of the same magnitude as the hypotensive effect obtained with captopril, caused a marked tachycardia. Simultaneously, sympathetic nerve activity recorded from abdominal sympathetic nerves was unchanged following injection of captopril, while it was significantly increased during hypotension induced by PGI2. The bradycardia, but not the hypotensive effects induced by captopril was abolished by i.v. pretreatment with atropine. Intracisternal injection of a small dose of captopril inhibited reflex tachycardia during hypotension induced by PGI2 and prolonged the hypotensive effect, while intravenous administration of this dose did not inhibit the reflex tachycardia induced by PGI2. In spontaneously hypertensive rats (SHR), the hypotensive effect of captopril was increased partly, however, the accompanying bradycardia was significantly reduced. These findings suggest that captopril inhibits the baroreflex and centrally activates the cardiac vagal nerve. Moreover in SHR, the effect of captopril on cardiac vagal activity was disturbed.

When tripamide was added to the food of spontaneously hypertensive rats (SHR), there were no appreciable effects on heart rate, body weight, or food intake. Tail-cuff systolic pressures measured weekly were also unaffected in normotensive control rats (WKY), but the elevation expected in SHR was significantly reduced. Pressor responses to hypothalamic stimulation were also reduced selectively only in SHR. A peripheral inhibition of cardiovascular reactivity was considered unlikely, since pressor responses to injected norepinephrine, tyramine, or vasopressin were unaltered. Diminished pressor responsiveness was considered to be due to concurrent reduction of central sympathetic vasomotor activity, because sympathetic nerve responses to hypothalamic stimulation were appreciably lessened in tripamide-treated SHR. Although neither the site nor the mechanism causing sympathetic inhibition was determined exactly, our results are in accord with the interpretation that antihypertensive effects of tripamide in SHR depend, at least partly, on sympathetic inhibition.

To analyze the conflicting data on the relationship between sodium intake and sympathetic activity, the effects of a chronically excessive intake of sodium on renal sympathetic activity and blood pressure were investigated in normotensive rats. Renal sympathetic activity was estimated by urinary excretion of free norepinephrine (NE) and the turnover of NE in the kidneys. Blood pressure increased in rats receiving a high sodium diet when compared with that of the basal sodium diet. Urinary-free NE, epinephrine (E) and dopamine (DA) excretions in rats receiving a high sodium diet were enhanced significantly from those in the basal sodium diet. The turnover of NE in the kidneys was more enhanced in the high sodium group than in the basal sodium group. By blocking the sympathetic tone with ganglionic blockade, hexamethonium, enhanced excretion of urinary NE and elevation of blood pressure in response to salt loading were blocked to the levels of the basal sodium diet. These results suggest that a chronically excessive intake of sodium enhances the renal sympathetic and adreno-medullary activities, leading to a rise in blood pressure in normotensive rats.