[Role of central nervous system and sympathetic nervous system in essential hypertension].
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Biomedical subjects
Publications and source records attributed to S Sumita.
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BACKGROUND: Prolonged effects of non-depolarizing muscle relaxants in septic patients have been reported, although the influence of sepsis on neuromuscular transmission has not yet been clarified satisfactorily. These studies were intended to elucidate the influence of sepsis on neuromuscular transmission and on the action of drugs being utilized for regulation of muscle tone (a neuromuscular blocker and anti-cholinesterase (anti-ChE) drugs). METHODS: The effect of d-tubocurarine (dTc) on neuromuscular transmission and the antagonistic action of anti-ChE drugs (neostigmine and edrophonium) on dTc-induced twitch depression were estimated using sham control and septic rat nerve-hemidiaphragm preparations in vitro. Isometric twitch tension elicited by indirect (phrenic nerve) or direct (muscle) stimulation at 0.1 Hz was evaluated. RESULTS: Sepsis induced by panperitonitis attenuated the twitch tension elicited by indirect or direct stimulation (P < 0.01) without obvious morphological inflammatory damage to the diaphragm. dTc dose-dependently decreased twitch tension elicited by indirect stimulation (P < 0.01) less intensely in the septic group than in the sham group (P < 0.01). The antagonistic actions of the anti-ChE drugs on dTc (1 microM)-induced twitch depression were less intense in the septic group (P < 0.01 or 0.05). CONCLUSION: These results demonstrate that sepsis in the acute phase attenuates the effects of a neuromuscular blocker and anti-ChE drugs and depresses muscle contractility simultaneously.
QT interval may change when cardiac function is improved by optimizing the atrioventricular the (AV) delay. The relationship between AV delay, QT interval and cardiac function in patients with implanted DDD pacemakers was studied in 12 patients (aged 71+/-12 SD years) with complete or high degree AV block. Cardiac output (CO) was measured using a Swan-Ganz catheter or by continuous Doppler echocardiography. The pacing rate was fixed at 70-80/min to eliminate the influence of heart rate. The AV delay was prolonged stepwise by 30 ms starting from 90 ms. All measurements were performed after 5 min of pacing. When the AV delay was prolonged, the CO and QT interval gradually increased and reached a peak, and then decreased. When the CO was increased from the minimum to the maximum value by optimizing the AV delay, the QT interval was significantly prolonged from 440+/-40 to 456+/-39 ms (P<0.002). The CO increased from 5.5+/-2.5 to 6.0+/-2.5 l x min(-1) (P<0.002) when the AV delay was changed, during which the QT interval was prolonged from the minimum to the maximum value. There was a significant positive correlation between the optimal AV delay at which CO was maximal (161+/-33 ms) and the optimal AV delay predicted from the maximum QT interval (167+/-29 ms, r=0.85, P<0.001). In conclusion, the optimal AV delay can be predicted from the QT interval.
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In patients with an implanted DDD pacemaker (PM), the atrial contribution may be interrupted by too short an atrioventricular (AV) delay, and filling time may be shortened by too long an AV delay. The AV delay at which the end of the A wave on transmitral flow coincides with complete closure of the mitral valve may be optimal. The subjects were 15 patients [70.3+/-12.3 (SD) years old] with an implanted DDD PM. Cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) were measured by Swan-Ganz catheter. Transmitral flow was recorded by pulsed Doppler echocardiography. AV delay was prolonged stepwise by 25 msc. When the AV delay was set at 155+/-26 ms, the end of the A wave coincided with complete closure of the mitral valve. When the AV delay was prolonged 25, 50, 75, and 100 ms from this AV delay, the interval between the end of the A wave and complete closure of mitral the valve was prolonged 16+/-5, 39+/-6, 65+/-4 and 88+/-5 ms, respectively (r = 0.97, P<0.0001) and diastolic mitral regurgitation was observed during this period. Thus, the optimal AV delay may be predicted as follows: the slightly prolonged AV delay minus the interval between the end of the A wave and complete closure of the mitral valve. When the AV delay was set at 215 ms, there was a significant positive correlation between the predicted optimal AV delay (166+/-23 ms) and the optimal AV delay (CO: 161+/-26 msec, r = 0.93, P<0.0001, PCWP: 161+/-28 msec, r = 0.95, P<0.0001). In conclusion, optimal AV delay can be predicted by this simple formula: slightly prolonged AV delay minus the interval between end of A wave and complete closure of mitral valve at the AV delay setting.
BACKGROUND: Low-flow sevoflurane anesthesia is associated with increasing circuit concentrations of compound A, which is nephrotoxic in rats, but the effect of compound A and low-flow sevoflurane anesthesia on renal function in humans is unclear. The authors compared the effects of high- and low-flow sevoflurane and isoflurane anesthesia on renal function and on several possible markers of nephrotoxicity in humans. METHODS: Forty-two patients without preexisting renal disease underwent either low-flow isoflurane (1 l/min, n = 14), low-flow sevoflurane (1 l/min, n 14), or high-flow sevoflurane (6 l/min, n = 14) anesthesia for body-surface-area surgery scheduled to last at least 4 h. Twenty-four-hour urinary excretion of N-acetyl-beta-glucosaminidase (NAG), beta2-microglobulin, protein, glucose, blood urea nitrogen (BUN), and serum creatinine concentrations were measured before and after anesthesia. RESULTS: There were no differences in blood urea nitrogen, creatinine, and creatinine clearance among the three groups after anesthesia. Increased urinary N-acetyl-beta-glucosaminidase excretions were seen in the low-flow and high-flow sevoflurane groups, but not in the low-flow isoflurane group (P < 0.01). Ten patients in the low-flow sevoflurane group had 24-h urinary excretion of protein that exceeded the normal ranges after anesthesia, but only one patient in the isoflurane and none in the high-flow sevoflurane groups had this. CONCLUSIONS: Low-flow sevoflurane anesthesia was associated with mild and transient proteinuria. However, the observed proteinuria was not associated with any changes in blood urea nitrogen, creatinine, and creatinine clearance in these patients with no preexisting renal disease.
The utility of cytokeratin fragment (Cyfra) 21-1, a new tumor marker, was investigated in 100 patients with lung cancer. Sandwich enzyme immunoassay detected Cyfra 21-1 in the sera of 60% of patients. Sensitivity of this marker was especially high (86.4%) for squamous cell carcinoma, exceeding that of a similar marker, squamous cell carcinoma antigen (SCC, 54.5%). In contrast, sensitivity of Cyfra 21-1 was relatively low for adenocarcinoma (52.6%) and for small cell carcinoma (50%). We conclude that Cyfra 21-1 is of value in diagnosis of lung cancer, particularly squamous cell carcinoma.
Visual interpretation of iodine-123-beta-15-(p-iodophenyl)-3(R,S)-methyl-pentadecanoic acid (123I-BMIPP) myocardial images cannot easily detect mild reduction in tracer uptake. Objective assessment of myocardial 123I-BMIPP maldistributions at rest was attempted using a bull's-eye map and its normal data file for detecting myocardial damage in patients with mitochondrial encephalomyopathy. Six patients, two with Kearns-Sayre syndrome and four with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and 10 normal subjects were studied. Fractional myocardial uptake of 123I-BMIPP was also measured by dynamic static imaging to assess the global myocardial free fatty acid. These data were compared with the cardiothoracic ratio measured by chest radiography and left ventricular ejection fraction assessed by echocardiography. Abnormal cardiothoracic ratio and lower ejection fraction were detected in only one patient with Kearns-Sayre syndrome. Abnormal fractional myocardial uptake was detected in two patients (1.61%, 1.91%), whereas abnormal regional 123I-BMIPP uptake assessed by the bull's-eye map was detected in five patients (83%). All patients showed abnormal uptake in the anterior portion, and one showed progressive atrioventricular conduction abnormality and systolic dysfunction with extended 123I-BMIPP abnormal uptake. The results suggest that assessment based on the normal data file in a bull's-eye polar map is clinically useful for detection of myocardial damage in patients with mitochondrial encephalomyopathy.
BACKGROUND: In patients with mitral stenosis, reduced cardiac output or altered pulmonary hemodynamics may increase sympathetic nerve activity. However, the magnitude of the increase in sympathetic activity in such patients and the effect of valvuloplasty on this activity are unknown. METHODS AND RESULTS: We microneurographically measured muscle sympathetic nerve activity before and after mitral valvuloplasty in 10 patients (mean+/-SEM age, 48+/-2 years) with mitral stenosis and in 10 healthy volunteers (47+/-4 years); hemodynamic variables were also measured. Baroreflex sensitivity was assessed on the basis of the ratio of the change in heart rate or muscle sympathetic activity to the change in mean arterial pressure during intravenous infusion of sodium nitroprusside or phenylephrine. At baseline, muscle sympathetic activity was significantly higher in the patients with mitral stenosis than in the control subjects (42.1+/-3.2 versus 26.1+/-3.7 bursts/min, P<.05). However, there was no significant difference between the groups in sympathetic activity at 1 week after valvuloplasty. The reduction in sympathetic activity after valvuloplasty was maintained for > or = 6 months and correlated with the increase in cardiac index (r=.74, P<.05). Baroreflex sensitivity was significantly lower in the patients than in the control subjects, but after valvuloplasty there was no significant difference in baroreflex sensitivity between the groups. CONCLUSIONS: Sympathetic activity is increased in patients with mitral stenosis. Mitral valvuloplasty in such patients results in early and long-lasting normalization of sympathetic nerve activity, possibly because of an improvement in arterial baroreflex sensitivity.
To clarify whether plasma somatostatin affects thyrotropin secretion in critical illness, plasma somatostatin and thyrotropin responses to thyrotropin-releasing hormone were studied in forty-three critically ill patients. High somatostatin levels were associated with blunted thyrotropin secretion in critically ill patients. There was an inverse correlation between plasma somatostatin levels and the maximum increment of thyrotropin after stimulation by thyrotropin-releasing hormone. Decreased somatostatin and increased thyrotropin secretion before discharge from the intensive care unit were demonstrated in survivors. On the other hand, non-survivors maintained high somatostatin levels and had blunted thyrotropin secretion during their intensive care admission. These results suggest that high plasma somatostatin levels may play a role in the blunted thyrotropin secretion observed in critical illness.
Pentamidine isethionate induced torsades de pointes in a 33-year-old woman with acute myelogenous leukemia. This is the first report of Pentamidine-induced torsades de pointes in Japan for over ten years. On the 4th day of intravenous pentamidine for Pneumocystis carinii pneumonia, asymptomatic sinus bradycardia was noted with QT interval prolongation, and torsades de pointes were revealed on the 8th day. Although torsades de pointes was dissolved with discontinuation of the intravenous pentamidine and administration of magnesium sulfate, sinus bradycardia and prolonged QT interval persisted. Ventricular pacing resulted in no arrhythmia and normalization of the QT interval on the 10th day after discontinuation of pentamidine. Careful monitoring of the electrocardiogram should be carried out during intravenous pentamidine therapy.
The accuracy of auscultatory blood pressure (BP) determination was assessed in patients with chronic atrial fibrillation by performing simultaneous auscultatory BP determination on the upper arm and a direct BP determination on the contralateral arm. The subjects were three hospitalized patients, aged from 52 to 75 years. A Teflon catheter was introduced into the radial artery which was connected to a pressure transducer, and a cuff was twisted around the contralateral upper arm in the supine position. Simultaneous recording of directly determined BP and cuff pressure enabled the comparison of direct BP with auscultatory BP. The appearance of the Korotkoff I sound (systolic BP) and V sound (diastolic BP) was marked on the cuff pressure curve. This maneuver was repeated five times in each patient. The method of Bland and Altman was employed to assess the agreement between auscultatory and direct determinations. The auscultatory method estimated BP with differences of -14.3 to +27.3 mmHg in systolic BP and -12.1 to +11.9 mmHg (+/-2SD) in diastolic BP compared with the direct method. The difference in systolic BP between the auscultatory and the direct methods was greater than that in diastolic BP. Thus, there are unacceptable differences in systolic BP between auscultatory and direct methods that can be attributed to BP fluctuations. The auscultatory method in diastolic BP is more accurate than that in systolic BP and may be more useful in the clinical setting.
A 13-day-old infant with multiple teratisms of the oral cavity was scheduled for resection of the epignathus. Her oral cavity was occupied by large epignathus, submandibular tumor, congenital bifid tongue and cleft palate, but she had no other congenital abnormalities. We anticipated that an endotracheal intubation would be difficult because of the large size of the tumor in relation to the oral cavity. Initially, awake intubation using a standard laryngoscope was attempted. Although a large elastic epignathus did not interrupt the insertion of the curved laryngoscope blade, the hard submandibular tumors protruded from the submaxillary ramport interfered with mid-line management of the laryngoscope. After several attempts of intubation, a better exposure was obtained and she was successfully intubated using a stylet under deep sedation. We recognized that a careful observation of anatomical abnormalities in the oral cavity is important to keep airway in an infant with multiple abnormalities of the oral cavity.
We reported two patients who developed skin eruptions and severe hypotension immediately after scrubbing their wound in the leg using 4% chlorhexidine solution. Both patients were successfully treated by epinephrine administration. Patient-1 (a 42-year-old man) had his wound scrubbed using this antiseptic several times before the operation. He showed a positive skin scratch test for chlorhexidine. Patient-2 (a 74-year-old man) had no prior treatment with chlorhexidine. Positive lymphocyte transformation test was not demonstrated in these patients. It has been reported that more than 10% of patients with anaphylactic shock induced by chlorhexidine use had previous exposure to it and 80% of them had it used for mucosa or wound washing. From these results, we should keep it in mind that chlorhexidine is not likely to be a safe antiseptic and can possibly induce anaphylactic shock.
The effects of right ventricular outflow pacing were studied in 13 patients (mean [+/-SD] 69.8 +/- 8.2 years old). All patients received DDD pacemakers except two patients with implanted VVI pacemakers who had chronic atrial fibrillation. Cardiac output and pulmonary capillary wedge pressure were measured by Swan-Ganz catheter. Pacing rate was fixed at 70-80/min and atrioventricular delay was fixed at 165 msec. When the pacing site was changed from the right ventricular apex to the right ventricular outflow during right ventricular pacing in 11 patients, cardiac output increased from 3.3 +/- 0.6 to 3.4 +/- 0.5 l/min (p < 0.001), and wedge pressure decreased from 9.3 +/- 1.9 to 8.8 +/- 2.0 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow during atrioventricular pacing in eight patients, cardiac output increased from 3.9 +/- 0.4 to 4.0 +/- 0.4 l/min (p < 0.05), and wedge pressure decreased from 7.1 +/- 2.3 to 6.6 +/- 2.1 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow in seven patients with ejection fraction (EF) greater than 55%, cardiac output increased from 3.6 +/- 0.5 to 3.7 +/- 0.4 l/min (p < 0.05), and in four patients with EF less than 55%, it increased from 2.9 +/- 0.4 to 3.0 +/- 0.4 l/min (p < 0.01). Cardiac function was improved by right ventricular outflow pacing compared to right ventricular apex pacing regardless of the pacing mode or cardiac function.
Evoked spinal cord potential (ESCP) elicited by direct spinal cord stimulation has been applied to monitor the spinal cord function during spinal surgery. We report here two patients who showed excessive muscle contraction and developed severe metabolic acidosis as a result of the stimulation of spinal cord to measure ESCP. These changes were prevented by vecuronium administration prior to ESCP monitoring. These results suggest that excessive muscle contraction by direct spinal cord stimulation may lead to metabolic acidosis. In conclusion, the use of a non-depolarizing muscle relaxant is recommended to prevent the adverse effects of ESCP monitoring.
A 42-year-old woman with diabetes mellitus lost consciousness and was transferred to the Yokohama City University Hospital. Blood chemistry findings indicated low blood sugar levels and chest X-ray examination revealed cardiomegaly and bilateral pleural effusions. These clinical abnormalities were corrected by treatment with glucose, diuretics, angiotensin converting enzyme inhibitor and digitalis. Cardiological laboratory examinations were performed after admission. Electrocardiography revealed first degree atrioventricular block and incomplete right bundle branch block. Ultrasonography showed lower grade of ejection fraction and diffuse hypokinesis of the cardiac wall. After admission, sinus arrest suddenly occurred. The diagnosis was sick sinus syndrome. Scintigraphy using iodine-123 betamethyl-p-iodophenyl-pentadecanoic acid showed abnormal mottled defects. Coronary angiography found no significant stenosis of the coronary artery. Electron microscopy showed abnormally shaped mitochondrial accumulations in an endomyocardial biopsy specimen. Mitochondrial DNA amplification by polymerase chain reaction followed by restriction enzyme Apa I digestion revealed adenine-to-guanine transition at 3243 of the mitochondrial tRNA(LEU)(UUR) gene.
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