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Biomedical subjects

S Nosaka

Publications and source records attributed to S Nosaka.

At least 37 records · Page 2Linked to original sources

Is the aortic depressor nerve involved in arterial chemoreflexes in rats?

Recent anatomical and physiological studies showed that chemoreceptor afferent fibers are present in the rat aortic depressor nerve (ADN), which has been considered to contain exclusively baroreceptor afferent fibers. However, it remains to be proven whether the chemoreceptor afferents of the ADN are practically involved in chemoreflexes. The present study was performed in chloralose/urethane-anesthetized rats of either Sprague-Dawley (SD) or Wistar strain to examine whether the ADN carries sufficient information regarding arterial hypoxia and hypercapnia, and whether the ADN indeed participates in chemoreflexes, the circulatory and respiratory components. It was found in either strain that afferent discharges of the ADN were not affected at all by hypoxia or hypercapnia, whereas those of the carotid sinus nerve (CSN) markedly increased due to these stimuli. Hypoxia produced hypertension, transient bradycardia followed by tachycardia, and respiratory facilitation, which characterize the chemoreflexes. Any of these responses was not affected at all by the ADN section, but all were abolished by the CSN section. Intraaortic injection of cyanide also induced transient bradycardia and respiratory facilitation, but any of them was not affected by the ADN section while all were abolished by the CSN section. Furthermore, electrical stimulation of the ADN produced solely baroreflex responses, i.e. hypotension and respiratory suppression, whereas that of the CSN provoked chemoreflex responses, i.e. early, transient hypertension and respiratory facilitation. In conclusion, the rat ADN does not contain a functionally significant number of chemoreceptor afferent fibers, if at all, and does not appreciably contribute to generation of chemoreflexes.

Action Potentials↗

Left atrial endocardium and prostacyclin.

In patients with rheumatic mitral stenosis, intracardiac thrombi are found mostly, for reasons still unknown, in the left atrium. We compared the release of PGI2 from the endocardium of the left atrium with that of the right ventricle and from the endothelium of the pulmonary arteries. Endocardial endothelial cells (EECs) were isolated from right ventricles (RV) and left atrial appendages (LAA) of porcine hearts, and vascular endothelial cells (VECs) from pulmonary arteries (PA) were obtained from the same animals. Cultured EEC and PA-VEC monolayers were placed in a pressure loading apparatus and incubated for 30 min under various pressures. After incubation, the supernatants were sampled and the 6-keto-PGF1 alpha contents measured. PGI2 release from LAA-EEC was much less than from RV-EEC or from PA-VEC. Moreover, transmural pressure did not enhance PGI2 release from LAA-EEC, although it did from RV-EEC and PA-EEC in a pressure-dependent manner. These results may explain why the left atrium is a common site for intracardiac thrombus formation in patients with mitral valve disease.

6-Ketoprostaglandin F1 alpha↗

Hypoxia inhibits baroreflex vagal bradycardia via a central action in anaesthetized rats.

It is known that arterial baroreflexes are suppressed in stressful conditions. The present study was designed to determine whether and how hypoxia affects arterial baroreflexes, especially the heart rate component, baroreflex vagal bradycardia. In chloralose-urethane-anaesthetized rats, baroreflex vagal bradycardia was evoked by electrical stimulation of the aortic depressor nerve, and the effect of 15 s inhalation of hypoxic gas (4% O2) was studied. Inhalation of hypoxic gas was found to inhibit baroreflex vagal bradycardia. The inhibition persisted after bilateral transection of the carotid sinus nerve. Cervical vagus nerves were cut bilaterally and their peripheral cut ends were stimulated to provoke vagal bradycardia of peripheral origin so as to determine whether hypoxia could inhibit vagal bradycardia by acting on a peripheral site. In contrast to baroreflex vagal bradycardia, the vagus-induced bradycardia was not affected by hypoxic gas inhalation. It is concluded that baroreflex vagal bradycardia is inhibited by hypoxia and the inhibition is largely mediated by its direct central action.

Animals↗

Inhibition of baroreflex vagal bradycardia by nasal stimulation in rats.

Nasal stimulation provokes hypertension and bradycardia. We report here that such stimulation inhibits baroreflex vagal bradycardia (BVB). In chloralose- and urethan-anesthetized, beta-adrenergic receptor-blocked rats, the aortic depressor nerves were cut and electrically stimulated to induce BVB. Nasal application of smoke, warm distilled water, or cold or hot Ringer solution suppressed BVB, but application of warm Ringer solution did not. Smoke-induced inhibition was abolished by trigeminal but not olfactory denervation. Neither suprapontine decerebration nor C3 spinal cord transection affected the inhibition. Bradycardia induced by electrical stimulation of the peripheral cut end of the cervical vagus nerve (VIB) was suppressed by long-lasting smoke application. Intravenous prazosin, a proposed blocker of prejunctional inhibition of acetylcholine release from the vagus terminals, abolished VIB inhibition but attenuated BVB inhibition only slightly. Thus nasal stimulation inhibits BVB, and this inhibition is mediated exclusively by the trigeminal nerve and occurs principally at the pontomedullary level, although the potential exists for contribution of the prejunctional mechanism. The inhibition of BVB might contribute to cardiovascular regulation associated with protection from atmospheric hazards.

Animals↗

Acetylcholine-induced endothelium-derived contracting factor in hypoxic pulmonary hypertensive rats.

We determined the role of an endothelium-derived contracting factor in the impaired relaxation response to ACh of conduit pulmonary arteries (PAs) isolated from rats with hypoxic pulmonary hypertension (PH). A PGH2/thromboxane A2 (TxA2)-receptor antagonist (ONO-3708) partially restored the impairment of ACh-induced relaxation, whereas TxA2 synthase inhibitors (OKY-046 and CV-4151) did not affect the impaired relaxation in phenylephrine-precontracted hypertensive PAs. Endothelium-denuded hypertensive PA rings showed no difference in the response to ACh between preparations with and without ONO-3708. In both endothelium-denuded control and hypertensive PAs, exogenous PGH2 induced contractions, and the magnitude of the contractions was greater in the control than in hypoxic PH preparations. An endothelin A-receptor antagonist (BQ-485), an endothelin B-receptor antagonist (BQ-788), and a superoxide anion scavenger (superoxide dismutase) did not restore the impaired response to ACh in hypertensive PAs. These findings suggest that PGH2 produced from the conduit PAs of rats with chronic hypoxic PH may be the endothelium-derived contracting factor responsible for the impairment of ACh-mediated vasorelaxation.

Acetylcholine↗

Abdominal aortic aneurysm rupture in systemic lupus erythematosus.

Many cardiovascular complications have been described in systemic lupus erythematosus (SLE), however, aortic involvement is very rare. We are reporting abdominal aortic aneurysm rupture in a 47-year old woman with SLE. The patient was admitted to our hospital with severe abdominal pain. Emergency computed tomography of the abdomen demonstrated ruptured abdominal aortic aneurysm. The restoration of aortic flow with vascular prosthesis was performed in emergency. Postoperative course was uneventful.

Aneurysm, Ruptured↗

[Judicial judgements on anesthesia malpractice in Japan].

We reviewed 75 judicial precedents on anesthetic malpractice during surgical procedure which had appeared in legal journals in the period between 1963 and 1997. Anesthetic techniques employed were: general anesthesia (35 cases), spinal anesthesia (19 cases), local anesthesia (12 cases), and others (9 cases). Anesthesiologists were involved in 16 lawsuits, of which anesthesiologists lost 6 suits between 1986 and 1995. There were 8 cases classified as to be caused by respiratory problems including 2 cases of wrong gas supply. The defendants lost all the 8 cases. On the other hand, the plaintiff lost all the cases of malignant hyperthermia (n = 7). There is a tendency of increase in law suit with general anesthesia. Recent judgments suggested the importance of anesthetic managements, correct recording and appropriate monitoring by anesthesiologist during and immediately after surgery. Spinal anesthesia should be performed by anesthesiologist, and the frequency of anesthetic accident should be decreased. Japan is still in short of anesthesiologists and efforts should be paid to increase the number of anesthesia specialists.

Anesthesia↗

[Anesthetic management of patients with malignant pleural effusion undergoing hyperthermic perfusion under thoracoscopy].

Nine patients with malignant pleural effusion due to lung cancer had been scheduled for hyperthermic treatment with warmed distilled water (40 degrees C) under thoracoscopy. This treatment aims to produce adhesion of the lungs to reduce pleural effusion. To evaluate the risk of general anesthesia for patients with lung cancer at the end stage, we examined the problems of perioperative management. Seven out of nine patients were classified into ASA physical status > or = III and seven patients into Hugh Jones > or = III Shapiro's score was > or = 5 in four patients. The average %VC was 60 +/- 16 and % FEV1.0 was 41 +/- 18% (means +/- SE). A double lumen endotracheal tube was inserted and anesthesia was maintained with inhalational anesthetics. In two cases, one-lung ventilation could not be maintained because of severe hypoxemia during hyperthermic perfusion. Hypertension occurred in three cases and hypotension in one by direct heat stimulation of the cardiopulmonary system. Although their preoperative risk was poor, there were no major complications and the quality of life was improved. We stress that careful anesthetic management is important for avoiding hypoxemia and hemodynamic instability during this treatment.

Aged↗

Inhibition of baroreflex vagal bradycardia by selective stimulation of arterial chemoreceptors in rats.

We reported recently that hypoxia inhibits baroreflex vagal bradycardia (BVB) in rats and that this inhibition persists following chemoreceptor denervation. However, since it is possible that hypoxia also affects the central processing of chemoreceptive input, the existence of chemoreceptor-mediated inhibition of BVB cannot be ruled out. Therefore, we have studied whether selective chemoreceptor activation affects BVB in normoxic conditions. In pentobarbital-urethane-anaesthetized, succinylcholine-immobilized, artificially ventilated rats, BVB was provoked by electrical stimulation of the aortic depressor nerve. Arterial chemoreceptors were selectively activated by intracarotid injection of a minute amount of sodium cyanide. Cyanide injection consistently increased blood pressure while changing heart rate variably. BVB was inhibited in a dose-dependent manner. This inhibition, as well as changes in blood pressure and heart rate, was abolished following transection of the carotid sinus nerve (CSN) ipsilateral to the injection. Spinal cord transection at the C2 level did not affect the inhibition. On the other hand, intracarotid cyanide had no effect on bradycardia elicited by electrical stimulation of a peripheral cut end of the cervical vagus nerve. We conclude that chemoreceptor activation definitely inhibits BVB and that this inhibition is mediated by the CSN, and predominantly occurs in the central nervous system. The possibility is suggested that severe hypoxia suppresses not only BVB but also the chemoreceptor-mediated inhibition of BVB, both via the direct, central action.

Afferent Pathways↗

Hereditarily elongated carotid sinus nerve in a rat colony.

A specific colony of Wistar rats was found in which the common carotid artery bifurcates at an unusually caudal position, thereby the carotid sinus nerve that originates from the bifurcation is elongated. The present study was done to determine whether this elongated nerve carries baro- and chemosensations in the same manner as the carotid sinus nerve of conventional rats or of other species. In chloralose-urethane anesthetized rats of this specific colony, the afferent discharges were recorded from the elongated carotid sinus nerve in response to a phenylephrine-induced rise in blood pressure and a fall in oxygen tension, as well as an increase in carbon dioxide tension in the respiratory gas. Reflex effects of electrical stimulation of the nerve were also examined. In nerve recording, the afferent discharges of the elongated carotid sinus nerve were increased by any of the perturbations, hypertensive, hypoxic or hypercapnic. Electrical stimulation of the elongated carotid sinus nerve caused an initial rise and a subsequent fall in blood pressure, bradycardia, and an increase of respiratory volume and rate. These results confirmed that the elongated carotid sinus nerve of rats in this colony contains both baroreceptor and chemoreceptor afferent fibers. It seems that this colony of rats proffers a beneficial material which will facilitate the studies to analyze the features and reflex functions of carotid body chemoreceptors and/or carotid sinus baroreceptors.

Afferent Pathways↗

Protective effects of nicaraven, a new hydroxyl radical scavenger, on the endothelial dysfunction after exposure of pig coronary artery to hydroxyl radicals.

Recently, we have reported that a new synthetic compound, 1,2bis(nicotinamido)-propane (nicaraven), improved cardiac function following preservation and reperfusion. In this study, we investigated the efficacy of nicaraven as a radical scavenger by using an in vitro model of oxidative stress, to clarify mechanisms of the protective effect of this new compound on reperfusion injury in rat heart. Ring segments of epicardial right coronary arteries (RCA) of pig were suspended in organ chambers and exposed to hydroxyl radicals (.OH), generated (by two different systems) by 0.28 mM FeSO4/0.28 mM H2O2 and DHF/Fe3+-ADP (2.4 mM, 43 nM, and 1.56 uM, respectively) to the bathing solution for 60 min. Prior exposure of the coronary arteries to .OH significantly produced right-ward shift of the dose-response curves of the bradykinin-induced endothelium-dependent relaxations (an increase in the ED50 value for bradykinin by 4.37 and 1.98 times than control in two different .OH generating systems, respectively), but did not affect the maximum relaxation responses. The presence of nicaraven (10(-4) and 10(-5) M) in the .OH generating system, shifted the dose-response curves to bradykinin to the control level, suggesting a significant hydroxyl radical scavenging effect of the drug. These results indicate that nicaraven, a new hydroxyl radical scavenger, exhibits a protective effect on hydroxyl radical-induced endothelial dysfunctions of pig coronary artery.

Animals↗

Anaesthetic management for caesarean section combined with removal of phaeochromocytoma.

In this case report, the anaesthetic management for a removal of phaeochromocytoma undertaken immediately following Caesarean section is described. A 32-year-old female patients was given epidural anaesthesia for Caesarean section, and thereafter, general anaesthesia for a resection of phaeochromocytoma. During surgery, phentolamine, nitroglycerine and prostaglandin E1 were electively administered to decrease blood pressure and heart rate. A live infant was delivered and the supra-adrenal tumour was excised successfully. The patient's post-operative recovery was uneventful.

Adrenal Gland Neoplasms↗

Hepatic energy metabolism during ketamine and isoflurane anaesthesia in haemorrhagic shock.

The effects of ketamine and isoflurane on the phosphoenergetic state of the liver during haemorrhage were investigated using 31P nuclear magnetic resonance (NMR) spectroscopy. Male Wistar rats were anaesthetized with ketamine (1.0 mg kg-1 min-1 i.v., Ket 1.0 group, or 1.5 mg kg-1 min-1 i.v., Ket 1.5 group), or isoflurane 1.4% (Iso group). Haemorrhage was induced by withdrawing blood until the mean arterial pressure was reduced to 40 mm Hg, and this pressure level was then maintained for 45 min. Hepatic energy metabolism was evaluated from the changes in adenosine triphosphate (ATP) and inorganic phosphate (Pi). The beta-ATP decrease and the Pi increase were more marked in the two Ket groups than in the Iso group. At 20 min after haemorrhage, the beta-ATP peak areas were 34%, 32% and 76%, and the Pi peak areas were 257%, 260% and 160% of their initial values in the Ket 1.0, Ket 1.5 and Iso groups, respectively. NMR data were supported by chemical assessments. These results demonstrated that, in terms of phosphoenergetic levels, a continuous administration of 1.0 or 1.5 mg kg-1 min-1 ketamine markedly decreased hepatic metabolism during haemorrhagic shock, whereas inhalation of 1.4% isoflurane mitigates the metabolic damage.

Adenosine Triphosphate↗

Comparison of the effects of pancuronium and vecuronium in canine coronary and renal arteries.

BACKGROUND: Pancuronium has sympathomimetic actions but does not change or lowers systemic blood pressure in some studies of anesthetized humans and dogs. The present study was done to determine the actions and mechanisms of action of pancuronium on coronary and renal arteries other than those as a sympathomimetic agent. METHODS: Helical strips of coronary and renal arteries from mongrel dogs were suspended in oxygenated, warmed Ringer-Locke solution, and changes in the isometric tension were recorded. In some strips, transmural electrical stimulation (5 Hz for 40 s) was applied to activate perivascular adrenergic nerves. RESULTS: Pancuronium (10[-7] to 10[-5] M) caused dose-dependent relaxation in coronary and renal arteries contracted with prostaglandin (PG) F2alpha, whereas no significant response was induced with vecuronium. The relaxation was endothelium independent and abolished by indomethacin or tranylcypromine, a PGI2 synthase inhibitor. Transmural electrical stimulation caused coronary arterial relaxation, which was augmented by pancuronium and vecuronium. Desipramine also increased the response, and additional potentiation of the response was not elicited by pancuronium and vecuronium. In renal arteries, electrical stimulation caused contraction, which was also augmented by pancuronium and vecuronium. With desipramine treatment, these muscle relaxants did not potentiate the response. Endothelium-dependent coronary arterial relaxation caused by bradykinin was not affected by pancuronium. CONCLUSIONS: Pancuronium-induced relaxations in canine coronary and renal arteries appear to be mediated by PGI2 released from subendothelial tissues. Potentiations by pancuronium and vecuronium of the response to adrenergic nerve stimulation are expected to be due to an inhibition of the norepinephrine uptake but not to facilitated release of the amine.

Animals↗

[Mitral regurgitation due to mitral valve prolapse associated with epidermolysis bullosa: case report].

Mitral valve prolapse (MVP) has been associated with several connective tissue disorders, including Marfan's syndrome, Ehlers-Danlos syndrome, and pseudoxanthoma elasticum. We present a case of MVP in a patient with epidermolysis bullosa. The authors are aware of only one previously reported case of this association. A 49-year-old man with a history of epidermolysis bullosa since childhood was admitted to our institution due to dyspnea on effort. On general examination he was observed to have alopecia, deformities in his nails, and fusions of his fingers. Transesophageal echocardiography confirmed the presence of MVP. In addition, coronary angiography showed three-vessel disease. Mitral valve replacement (ATS valve 25 mm) and coronary artery bypass grafting (left internal thoracic artery-LAD) were performed. The resected mitral valve (anterior leaflet) contained the area of the myxomatous lesion histologically. The pathological mechanism of epidermolysis bullosa is thought to be the destruction of collagen fibers due to increased levels of enzyme collagenase. Therefore there may be a common cause of MVP and epidermolysis bullosa based upon an abnormality of collagen metabolism.

Coronary Artery Bypass↗

[A case of traumatic lung cyst].

Traumatic lung cyst is an uncommon lung injury due to closed chest trauma. A 5-year-old boy was admitted to our hospital after being run over by motor vehicle. Computed tomography of the chest demonstrated multiple cystic lesions. This case was diagnosed as traumatic lung cysts. Computed tomography taken 37 days after initial injury showed complete resolution of the cysts. Computed tomography was useful in diagnosing traumatic lung cyst and following its clinical course.

Accidents, Traffic↗

[Clinical study of synchronous double cancers of the lung and digestive tract].

Among 64 cases of surgically resected primary lung cancer from 1991 to 1997, there were 5 cases of synchronous double cancers of the lung and digestive tract. They were consisted of 4 males and 1 female and the patient age at the time of the lung resection ranged from 65 to 81 years (average: 74.6). One male was diagnosed as having lung cancer (squamous cell carcinoma) along with sigmoid colon cancer (adenocarcinoma) and others were lung cancer (adenocarcinoma) and gastric cancer (adenocarcinoma). In two patients with early gastric cancer, lobectomies were performed following endoscopic resection of gastric cancer. In three patients including two old man and woman (over 80 years old), lobectomies and gastrectomies (or sigmoidectomy) were performed at the same time. We omitted mediastinal lymph nodes dissections in two old patients and no operative complications occurred. All patients are alive now. It can be concluded that in cases of synchronous double cancers of the lung and digestive tract, we must select the best treatment that is not invasive for the patient and that simultaneous operation for double cancer can be safely performed.

Adenocarcinoma↗

[Perioperative management for nephrectomy in a long-term hemodialysis patient with anticoagulants for coronary stent].

A 53-year old man on long-term hemodialysis (HD) with anticoagulant therapy was scheduled for nephrectomy due to renal cell carcinoma. Two months before surgery, a coronary stent had been placed due to right coronary artery disease. One week before surgery, percutaneous transmural coronary angioplasty (PTCA) was performed for unstable angina. Aggressive oral antiplatelet therapy (aspirin and ticlopidine) was absolutely required to maintain patency. Following withdrawal of the antiplatelets, unfractionated heparin (UFH) was titrated to an activated partial thromboplastin time (APTT) of 1.5 times greater than the control value. Maintenance UFH (800 U.h-1) was continued until the time of arrival in the operation room (activated clotting time (ACT) was 166 seconds). One hour after arrival, reduced dose of UFH (200 U.h-1) was reinfused, and ACT was 121 140 seconds. Hemodynamic change was minimized using balanced general anesthesia (nitrous oxide-isoflurane, fentanyl, midazolam and vecuronium) accompanied by nitroglycerin and diltiazem. There was no ischemic change on ECG or transesophageal echocardiography. Following surgery, the UFH dose was augmented (400 U.h-1), and the maintenance dose was attained 11 hours after surgery. HD on the second postoperative day was performed uneventfully. This hemodynamic stability might be come from the no water removal. Fourteen days after surgery, the patient was discharged without hemorrhagic complications or clinical ischemic events. We conclude that perioperative UFH infusion is not contraindicated for dialysis patient if strict ACT control is maintained.

Anticoagulants↗