[Hemodynamic alterations in isolated right ventricular ischemia in anesthetized open-chest dogs].
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Publications and source records attributed to T Hyodo.
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Decreased cardiac performance during ventricular tachycardia or ventricular pacing has been ascribed to the lack of synchrony due to altered ventricular contraction. However, the direct effect of the pacemaking site on blood flow in the major coronary arterial branches and on regional contractile forces has not been adequately examined. In this investigation, twelve dogs were used to assess coronary flow in the left anterior descending (LAD) and circumflex coronary arteries (LCx) and the regional myocardial function in response to ectopic electrical pacing. The sites were the outflow tract of the right ventricle (RV pacing), the anterior left ventricular wall supplied by the LAD (LAD pacing), and the lateral wall perfused by the LCx (LCx pacing). Strain gauge arches were transmurally fixed to myocardial segments of the anterior and lateral walls of the left ventricle. The mechanical forces generated were measured while simultaneously recording blood flow in the LAD and LCx. RV pacing diminished developed-tension similarly in both areas. LAD flow was further decreased during anterior pacing as was the developed-tension in the LAD supplied area. A similar relationship was observed between LCx flow and developed-tension in the LCx area during lateral pacing. Compared to RV pacing, anterior pacing did not affect LCx flow and local myocardial force in the lateral wall of the left ventricle, and lateral pacing did not cause further changes in LAD flow and anterior myocardial function. The decrements in blood flow were closely related to decreased myocardial function (p less than 0.01). These findings indicate that ventricular pacing decreases ventricular performance with attenuated regional myocardial function at the pacing area, in addition to causing altered ventricular contraction sequence.
A simple modification of a commercially available gauge arch, namely the addition of pins to effect mechanical couplings to heart muscle rather than suturing, results in an isometric myocardial force sensor which is easy to insert, stable and relatively atraumatic to the myocardium. Compressing the pins by means of a machinist's vernier caliper which is removed after the sensor is implanted, insures controlled muscle stretch. Tests in open-chest dogs show that force sensed by this gauge is little affected by changes in heart rate, left ventricular end-diastolic pressure or aortic pressure, but faithfully reflects the inotropic effects of isoproterenol or propranolol. Thus, the modified strain gauge arch is sensitive to changes in contractility but not to changes in preload or afterload.
Utilizing an acid gel chromatography and insulin radioreceptor assay (RRA), serum levels of receptor assayable insulin-like activities were measured under various conditions. Acid gel filtration of sera on a Sephadex G-50 was adopted to separate small molecular ILAs from binding proteins before the assay by RRA. By employing 125I-pork insulin as the tracer, and pork insulin as the standard, an RRA for insulin was developed, in which kidneys of sacrificed pregnant guinea pigs were used as the source of the solubilized receptor. After gel-filtration of the sera, pooled fractions, which grossly corresponded to those of 125I-insulin marker, were assayed by RRA. The subjects consisted of fifty-nine cases: normal control subjects (n = 19), active acromegaly (6), Sheehan's syndrome (5), liver cirrhosis (7), chronic renal failure (10), non-insulin dependent diabetes mellitus (6), overt hyperthyroidism (5) and Nelson's syndrome (1). The average receptor assayable ILA of the normal control subjects was 40.2 +/- 12.2 ng/ml. As insulin RRA has a big interassay variation, receptor assayable ILA-ratio was used to minimize the variation, and each data was shown as the ratio to the average ILA of the normal controls. By this method, sera from normal adults had a mean (+/- SD) receptor assayable ILA ratio of 1.00 +/- 0.28. Four out of six cases of acromegaly revealed significantly high concentrations, and the average receptor assayable ILA-ratio of acromegaly was 1.30 +/- 0.28 (mean +/- SD, p less than 0.015). In the cases of Sheehan's syndrome, the ILA-ratio was 0.30 +/- 0.12, which was significantly low (p less than 0.001). Therefore, GH dependency was suspected from these two factors. However, the direct correlation was not indicated between GH and receptor assayable ILA. It was also considered that receptor assayable ILA was influenced not only by GH but also by some other factors. Furthermore, the subjects with liver cirrhosis indicated the low levels of receptor assayable ILA-ratio of 0.46 +/- 0.31, while the subjects with chronic renal failure showed the high ILA-ratio of 1.59 +/- 0.45 (p less than 0.05). No differences in ILA-ratio were found in the subjects with diabetes mellitus, hyperthyroidism and Nelson's syndrome, compared to the normal subjects.
Stress-induced changes in the resistance due to coronary arterial stenosis of a fixed diameter and in the myocardial blood flow distal to the stenosis were investigated in the open-chest dog. Myocardial blood flow in the inner and outer third of the left ventricular wall was continuously measured with heated cross-thermocouples. The circumflex coronary artery was constricted with a thick string so that myocardial reactive hyperemia was nearly eliminated. Without constriction, a 15-second occlusion of the artery produced no significant changes in the resistance of large coronary arteries. On the contrary, in the presence of coronary constriction, a brief coronary occlusion caused a sustained decrease in distal coronary pressure and subendocardial myocardial flow during reactive hyperemia, while coronary flow returned quickly to the pre-occlusion level with significant reactive hyperemia of subepicardial flow. This change resulted in a long-lasting increase in the stenosis resistance. These results suggest that stenosis resistance changes dynamically, resulting in additional myocardial ischemia especially in the subendocardial myocardial layers.
The effects of intravenous infusion of isoproterenol on stenosis resistance were studied in the anesthetized open-chest dog. The circumflex coronary artery (LCx) was isolated near its origin and an electromagnetic flow transducer was placed around the vessel for measuring coronary flow. A polyethylene catheter was inserted into the small branch of LCx for monitoring distal coronary pressure. LCx was constricted with a thick cotton string to a degree of obstruction that eliminated reactive hyperemia following a 20-second coronary occlusion. The coronary resistance across the stenotic segment (RL) was calculated as the pressure gradient across the stenosis divided by coronary flow. Isoproterenol was infused intravenously in a dose to keep the heart rate at a level 25-30% above the control with and without coronary constriction. For maintaining the ascending aortic pressure at the pre-isoproterenol level, the descending thoracic aorta was constricted with a tape. In the absence of coronary constriction, the vascular resistance of large coronary arteries was not affected by isoproterenol with a significant increase in coronary flow. In the presence of coronary stenosis, isoproterenol markedly increased RI regardless of additional aortic constriction. The magnitude of the increase in RL during aortic constriction varied directly with the percent increase in the pressure gradient across the coronary stenosis. Pacing-tachycardia essentially did not affect RL. These results suggest that isoproterenol increased the vascular resistance of the stenotic segment with fixed caliber.
Properties of Ca-dependent outward current were studied in bullfrog atrial muscle using double sucrose-gap techniques. Decreasing [Ca]o inhibited the instantaneous outward current (Ik1) and inward background current (Ib), and the reverse was noted with increases in [Ca]o. When gk1 was blocked with 0.3 mM Ba, there were no such effects. In the presence of Ba and TTX (1.5 X 10(-6)M), 3 mM Co abolished the slow inward current (Isi) and depressed the delayed outward current (Iout). The depression was confined to the voltage range of activation of Isi. Similar results were obtained by replacement of [Ca]o with Co in concentration of equal surface charge effects. Contrarily, isoproterenol (10(-7) M) increased the Isi and Iout at the same voltage range. The activation of Iout became more rapid in the presence of isoproterenol but slowed with Co. In the presence of Ba, TTX, and Co, Ca-free EGTA (approximately 0.3 mM) Ringer further depressed the Iout, eliminating any remaining tension response. The depression, however, was more extensive, the stronger the depolarization. The activation of Iout was markedly retarded and amplitude of the fully activated Iout diminished, yet the deactivation became more rapid. Thus, the Ca-sensitive outward current was classified into 1) Ca-linked Ik1, 2) Isi-dependent Iout, and 3) Isi-independent but [Ca]o-related Iout.
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A case of cough syncope due to A-V conduction block of the heart is reported in this paper. A-V conduction block and lightheadedness were induced by coughing but not by an Aschner test, carotid sinus massage, Valsalva maneuver, pharyngeal stimulation, and stimulation of systemic baroreceptors. Permanent right-ventricular pacing completely abolished the patient's symptoms. The results suggest that hypersensitivity of a broncho-pulmonary reflex to coughing was responsible for the A-V conduction block and resulting syncopes.
Changes in the stenotic resistance of a coronary artery following brief coronary occlusion were studied in the anesthetized open-chest dog. A critical coronary stenosis was constructed by tying a thick string around the circumflex coronary artery (LCx) near its origin. The LCx was occluded for 5, 10, 15, 20 and 30 seconds with and without coronary stenosis then the reactive hyperemia was observed. In the absence of the stenosis, resistance of the segment of the large coronary artery remained unchanged during the reactive hyperemia independent of the duration of occlusion. In the presence of the stenosis, however, stenotic resistance increased for a certain time after the release of occlusion. This increased resistance lasted longer with more severe stenosis and with longer duration of coronary occlusion. These results suggest that stenotic resistance can increase dynamically, and that the duration of increased resistance may reflect the severity of the stenosis.
Effects of Ca-free or Na-deficient Ringer solutions on the membrane currents of the bullfrog atrial muscle were studied using the double sucrose-gap method. Instantaneous outward current (Ik1) decreased in Ca-free and increased in Na-deficient conditions. The amplitude of nominal "fully activated delayed outward current" diminished under both sets of conditions. The diminution, however, was greater in Na-deficient medium (10 mM Na) and its activation curve shifted about 13.5 mV toward a more negative potential. In Ca-free Ringer, no such shift was observed, and the activation of the delayed outward current became slower and sigmoidal while the deactivation was faster than in the control. Contrarily, in Na-deficient Ringer, the activation became faster and exponential and the deactivation was slower. The current tail was composed of two exponentially declining components, and the slower, K-accumulation-related component (Ia) was suppressed in Ca-free and the faster component (Ixs) diminished in Na-deficient media. These findings may indicate that in the atrial muscle the instantaneous outward current is modified by a Na-Ca exchange mechanisms and that the delayed outward current consists of two components, Ixs and Ia, which are susceptible to Na and Ca ions, respectively.
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Bilateral ligation of both the submandibular and parotid ducts of adult normal and mutant hyperinsulinemic diabetic mice resulted in a significant hypoglycemic effect. Therefore, we postulated that duct ligation may result in the removal of hyperglycemic factor (Hoshino et al., 1976) rather than a change in insulin sensitivity. Indeed, no change in specific binding of 125I-insulin was observed in membrane fractions from several tissues obtained from mice of either sex or strains before and after duct ligation. After slices of the submandibular gland were incubated for 4 hr in Eagle's medium, an aliquot of the culture medium was injected i.p. into normal adult mice. A signigicant hyperglycemic effect was observed in 30 min in the injected animals. Eluates obtained by gel filtration of the crude extract of the submandibular gland were injected into normal adult mice, and hyperglycemia ensued. Thus, it is postulated that ligation of salivary ducts results in glandular atrophy and disappearance of the hyperglycemic factor which in turn leads to hypoglycemia and amelioration of diabetes mellitus, particularly of hyperinsulinemic type.
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Clinical features of epiretinal membranes were examined in 22 eyes of 13 patients with Terson syndrome who were treated with pars plana vitrectomy. The shape and localization of the epiretinal membranes were intraoperatively evaluated and correlated with the presence or absence of posterior vitreous detachment (PVD). Patients with complete PVD, but with no membrane found during surgery, were followed postoperatively. Membrane formation ultimately developed in 13 of the 22 eyes. In eight eyes, PVD was incomplete and the epiretinal membrane was found at the optic disc or along the temporal vascular arcades, displaying retinal folds and vascular tortuosity. Three eyes had massive tractional retinal detachment; five of those with complete PVD developed a thin epiretinal membrane around the posterior pole that became more apparent during long-term follow-up. From these observations, we can classify epiretinal membrane formation in Terson syndrome into two groups: with complete, or with incomplete, PVD. It also appears that multiple pathological processes involving the vitreoretinal interface were responsible for the formation of epiretinal membranes.