[A case of water intoxication during transcervical resection of the uterine myoma].

A 28-year-old woman underwent trans-cervical resection (TCR) of the uterine myoma. She had no history of complications except for anemia. Anesthesia was maintained with inhalation anesthesia. After 120 min from introducing the resectoscope, her serum sodium dropped to 86.1 mEq.l-1. But her heart rate and the systolic arterial pressure were stable. She was treated with steroid, mannitol, isotonic saline, and 7% NaHCO3. Soon after the end of the operation, she recovered consciousness. At two hours postoperatively, her serum sodium was 119.6 mEq.l-1. On the 1st postoperative day, her serum sodium returned to the normal range (137 mEq.l-1). We should be aware of asymptomatic water intoxication during TCR.

Developmental changes in histochemical properties of intrinsic laryngeal muscles in rats.

OBJECTIVE: Using neonatal rats, the developmental changes in muscle fiber type of the intrinsic laryngeal muscles were analyzed. The potential influence of two factors were also studied, that were predicted would influence developmental changes in muscle fiber type, denervation and hypothyroidism. METHODS: Using the histochemical technique of myosin ATPase staining, postnatal changes in the ratio of muscle fiber types of each intrinsic laryngeal muscle were determined. In addition, to clarify factors influencing the development of the intrinsic laryngeal muscles, the same technique was employed to study recurrent laryngeal nerve-denervated rats and rats with experimentally-induced hypothyroidism. RESULTS: In normal pups, type 2C fibers had almost disappeared by postnatal day (PND) 14. In denervated pups, differentiation to type 1 and 2A muscle fibers was not observed. In contrast, differentiation to type 2B muscle fibers was impaired in the hypothyroid pups. CONCLUSION: The differentiation of intrinsic laryngeal muscles occur earlier than that of hindlimb muscles. Each intrinsic laryngeal muscle exhibits a particular pattern of developmental changes in normal pups. The developmental changes in the intrinsic laryngeal muscles are affected by recurrent laryngeal nerve innervation and thyroid hormonal control. The findings suggest that both recurrent laryngeal nerve innervation and thyroid hormone play important roles in the differentiation of the intrinsic laryngeal muscles.

Continuous measurement of canine coronary blood volume change with alterations of heart rate.

OBJECTIVE: The aim was to examine the effects of heart rate on total coronary blood volume with pressure-type plethysmography in isolated and vasodilated canine hearts. METHODS: Nine hearts were excised from anaesthetised mongrel dogs (13.1-15.2 kg) and perfused with arterial blood of other dogs (17.0-29.0 kg). The venous blood returning to the right atrium and both ventricles was drained under constant negative pressure (-10 mm Hg). A thin latex balloon filled with water was inserted into the left ventricle to keep the intraventricular volume constant. The pressure difference between the cylinder into which the heart was placed and a compensation chamber was measured as a change in coronary blood volume while heart rate was altered from 120 beats.min-1 (control heart rate) to a target level (60, 90, 150, or 180 beats.min-1). RESULTS: The mean coronary blood volume change compared with that at control heart rate was 1.65(SEM 0.32) ml x 100 g-1 at 60 beats.min-1 (p < 0.005) and -0.74(0.20) ml x 100 g-1 at 180 beats.min-1 (p < 0.005) under the perfusion pressure of 70 mm Hg. The mean volume decreased with the increase in heart rate. Diastolic-systolic variations in coronary blood volume also decreased with an increase in heart rate, from 0.61(0.06) ml x 100 g-1 (60 beats.min-1) (p < 0.005) to 0.12 ml.100 g-1 (180 beats.min-1). Both mean change and variation were almost linear functions of R-R interval (r = 0.88 and r = 0.83). Lowering the perfusion pressure from 70 to 40 mm Hg diminished the changes in both mean and variation of the coronary blood volume. CONCLUSIONS: Tachycardia reduces the mean coronary blood volume and the diastolic-systolic variations in isolated vasodilated canine hearts.

alpha-Adrenergic augmentation of myogenic response in rat arterioles: role of protein kinase C.

We tested the hypothesis that protein kinase C (PKC) activation plays a major role in alpha-adrenergic augmentation of the myogenic response in rat isolated arterioles. Lumen diameter measured was with a video-monitored microscopic system. Lumen diameter did not change (131 +/- 5 vs. 126 +/- 6 microns) despite an increase in lumen pressure from 40 to 100 mmHg. Phenylephrine (Phe; 3 x 10(-7) M) augmented the myogenic response, since lumen diameter decreased significantly from 117 +/- 8 to 101 +/- 8 microns. High potassium (40 mM) failed to augment the myogenic response, while constricting the vessels to nearly the same extent as did Phe. PKC inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride (H-7, 5 x 10(-5) M, n = 7) and staurosporine (3 x 10(-9) M, n = 7) abolished the Phe-induced augmentation. H-7 and staurosporine depressed the myogenic response even without Phe. PKC activators phorbol 12,13-dibutyrate (3 x 10(-9) M; n = 7) and 4 beta-phorbol 12-myristate 13-acetate (6 x 10(-8) M; n = 6) constricted the vessels by 11 +/- 2 and 18 +/- 3%, respectively. However, PKC activators failed to augment the myogenic response. These results suggest that PKC activation does not play a major role in alpha-adrenergic augmentation of the myogenic response in rat skeletal arterioles.

Coronary zero flow pressure and intramyocardial pressure in transiently arrested heart.

STUDY OBJECTIVE: The aim of the study was to examine the relation between zero flow pressure and intramyocardial pressure in the inner and outer layers of the myocardium. DESIGN: Zero flow pressure was obtained in maximally vasodilated excised hearts by decreasing perfusion pressure (at 2 mm Hg.s-1) during transient heart arrest. Intramyocardial pressures in inner and outer myocardium were measured simultaneously with needle tip pressure transducers at depths of 8.0(SD 2.6) and 3.3(1.2) mm from the epicardium respectively. Ventricular and atrial pressure could be controlled at will. EXPERIMENTAL MATERIAL: The excised hearts of eight mongrel dogs, body weight 14.0(0.8) kg, were used. MEASUREMENTS AND MAIN RESULTS: During left ventricular pressure elevation (0, 15, 30 mm Hg), zero flow pressures were 9.1(2.4), 13.8(2.2), and 19.1(5.1) mm Hg, respectively. Corresponding values of intramyocardial pressure at the outer myocardium were in good agreement with the zero flow pressures, at 9.1(3.4), 13.4(2.8), and 20.8(5.4) mm Hg. Values at the inner myocardium increased from 7.4(2.4) to 18.9(8.6) and 32.9(13.0) mm Hg. The latter two values were significantly higher than the corresponding values of zero flow pressure and intramyocardial pressure at the outer myocardium (p less than 0.05, p less than 0.01). In isotransmural pressure elevation, the three pressures increased almost equally. CONCLUSIONS: The results show that zero flow pressure is strongly affected by intramyocardial tissue pressure, and if uneven intramyocardial pressure distribution is present the value of zero flow pressure depends on the lower values of intramyocardial pressure.

Effects of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate on the ventriculo-atrial conductivity of accessory pathways.

The purpose of this study was to examine the effects of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a newly developed antiarrhythmic agent belonging to class Ic, on the ventriculoatrial (VA) conductivity of accessory pathways and paroxysmal supra-ventricular tachycardia (PSVT). Twelve patients with accessory pathways were examined by standard electrophysiologic technique before and after a single oral dose of SUN 1165 (100 mg). 1 h after administration, SUN 1165 blocked VA conduction of the accessory pathway in six of twelve patients and prevented the induction of PSVT in six of seven cases. In the cases in which VA block did not occur, the VA interval prolonged (from 178 +/- 7 to 190 +/- 11 ms, p less than 0.05), and the effective refractory period of VA conduction was also increased (from 273 +/- 10 to 318 +/- 15 ms. p less than 0.05). SUN 1165 also prolonged the conduction time in normal conduction systems (AH and HV intervals and QRS duration), but the degree of the prolongation was moderate and not dangerous. There was no adverse effect. These results indicate that SUN 1165 is a potent and safe antiarrhythmic agent, and useful for preventing or stopping PSVT by blocking or depressing VA conduction through accessory pathways.