ABSTRACT
Polymyositis is characterized by symmetrical proximal muscle weakness, nonsuppurative inflammation of skeletal muscle, elevation of muscle enzyme levels, and abnormality of electromyographical change. Its pathogenesis is unclear. Paraneoplastic syndromes are caused by malignant tumors, although not through direct effects of the primary tumor or its metastases. Several paraneoplastic syndromes, including erythrocytosis, hypoglycemia, and hypercholesterolemia, have been reported in patients with hepatocellular carcinoma. A few cases of polymyositis associated with hepatocellular carcinoma and one case of combined hepatocellular-cholangiocarcinoma associated with polymyositis and chronic hepatitis B virus infection have been reported. Skeletal muscle injuries without trauma, including metabolic myopathy, effects of certain drugs and toxins, infection, electrolyte imbalances, and endocrine disorders, may cause rhabdomyolysis. We present here a case of primary liver cancer associated with polymyositis and rhabdomyolysis.
Subject(s)
Humans , Carcinoma, Hepatocellular , Hepatitis B, Chronic , Hypercholesterolemia , Hypoglycemia , Inflammation , Liver , Liver Neoplasms , Muscle Weakness , Muscle, Skeletal , Muscles , Muscular Diseases , Neoplasm Metastasis , Paraneoplastic Syndromes , Polycythemia , Polymyositis , Rhabdomyolysis , VirusesABSTRACT
Polymyositis is characterized by symmetrical proximal muscle weakness, nonsuppurative inflammation of skeletal muscle, elevation of muscle enzyme levels, and abnormality of electromyographical change. Its pathogenesis is unclear. Paraneoplastic syndromes are caused by malignant tumors, although not through direct effects of the primary tumor or its metastases. Several paraneoplastic syndromes, including erythrocytosis, hypoglycemia, and hypercholesterolemia, have been reported in patients with hepatocellular carcinoma. A few cases of polymyositis associated with hepatocellular carcinoma and one case of combined hepatocellular-cholangiocarcinoma associated with polymyositis and chronic hepatitis B virus infection have been reported. Skeletal muscle injuries without trauma, including metabolic myopathy, effects of certain drugs and toxins, infection, electrolyte imbalances, and endocrine disorders, may cause rhabdomyolysis. We present here a case of primary liver cancer associated with polymyositis and rhabdomyolysis.
Subject(s)
Humans , Carcinoma, Hepatocellular , Hepatitis B, Chronic , Hypercholesterolemia , Hypoglycemia , Inflammation , Liver , Liver Neoplasms , Muscle Weakness , Muscle, Skeletal , Muscles , Muscular Diseases , Neoplasm Metastasis , Paraneoplastic Syndromes , Polycythemia , Polymyositis , Rhabdomyolysis , VirusesABSTRACT
Coronary vasospasm plays an important role in the pathogenesis not only of variant angina, but also of ischemic heart disease in general, including other forms of angina pectoris, acute myocardial infarction, and sudden death. Vasoactive events leading to an acute reduction in regional myocardial flow in the presence of a normal or previously compromised circulation are a common cause of arrhythmias. However, coronary vasospasm-induced electrical and mechanical complications are rarely reported in patients with angiographically normal or near-normal coronary arteries. This paper presents our experience with a patient presenting with coronary vasospasm-associated ventricular fibrillation without findings of significant coronary artery disease.
Subject(s)
Humans , Angina Pectoris , Angina Pectoris, Variant , Arrhythmias, Cardiac , Coronary Artery Disease , Coronary Vasospasm , Coronary Vessels , Death, Sudden , Myocardial Infarction , Myocardial Ischemia , Ventricular FibrillationABSTRACT
Coronary vasospasm plays an important role in the pathogenesis not only of variant angina, but also of ischemic heart disease in general, including other forms of angina pectoris, acute myocardial infarction, and sudden death. Vasoactive events leading to an acute reduction in regional myocardial flow in the presence of a normal or previously compromised circulation are a common cause of arrhythmias. However, coronary vasospasm-induced electrical and mechanical complications are rarely reported in patients with angiographically normal or near-normal coronary arteries. This paper presents our experience with a patient presenting with coronary vasospasm-associated ventricular fibrillation without findings of significant coronary artery disease.
Subject(s)
Humans , Angina Pectoris , Angina Pectoris, Variant , Arrhythmias, Cardiac , Coronary Artery Disease , Coronary Vasospasm , Coronary Vessels , Death, Sudden , Myocardial Infarction , Myocardial Ischemia , Ventricular FibrillationABSTRACT
The arterial pressure is regulated by the nervous and humoral mechanisms. The neuronal regulation is mostly carried out by the autonomic nervous system through the rostral ventrolateral medulla (RVLM), a key area for the cardiovascular regulation, and the humoral regulation is mediated by a number of substances, including the angiotensin (Ang) II and vasopressin. Recent studies suggest that central interleukin-1 (IL-1) activates the sympathetic nervous system and produces hypertension. The present study was undertaken to elucidate whether IL-1 and Ang II interact in the regulation of cardiovascular responses to the stress of hemorrhage. Thus, Sprague-Dawley rats were anesthetized and both femoral arteries were cannulated for direct measurement of arterial pressure and heart rate (HR) and for inducing hemorrhage. A guide cannula was placed into the lateral ventricle for injection of IL-1 (0.1, 1, 10, 20 ng/2mul) or Ang II (600 ng/10mul). A glass microelectrode was inserted into the RVLM to record the single unit spike potential. Barosensitive neurons were identified by an increased number of single unit spikes in RVLM following intravenous injection of nitroprusside. I.c.v. IL-1beta increased mean arterial pressure (MAP) in a dose-dependent fashion, but HR in a dose-independent pattern. The baroreceptor reflex sensitivity was not affected by i.c.v. IL-1beta. Both i.c.v. IL-1alpha and beta produced similar increase in MAP and HR. When hemorrhage was induced after i.c.v. injection of IL-1beta, the magnitude of MAP fall was not different from the control. The IL-1beta group showed a smaller decrease in HR and a lower spike potential count in RVLM than the control. MAP fall in response to hemorrhage after i.c.v. injection of Ang II was not different from the control. When both IL-1 and Ang II were simultaneously injected i.c.v., however, MAP fall was significantly smaller than the control, and HR was increased rather than decreased. These data suggest that IL-1, a defense immune mediator, manifests a hypertensive action in the central nervous system and attenuates the hypotensive response to hemorrhage by interaction with Ang II.
Subject(s)
Animals , Rats , Action Potentials , Angiotensin II , Angiotensins , Arterial Pressure , Autonomic Nervous System , Baroreflex , Catheters , Central Nervous System , Femoral Artery , Glass , Heart Rate , Hemorrhage , Hypertension , Injections, Intravenous , Interleukin-1 , Lateral Ventricles , Microelectrodes , Neurons , Nitroprusside , Rats, Sprague-Dawley , Sympathetic Nervous System , VasopressinsABSTRACT
The blood pressure (BP) is regulated by the nervous system and humoral factors, such as renin- angiotensin system, vasopressin and others. In the present study, we examined the central effects of glutamate and GABA on the cardiovascular regulation by injection of these substances into the lateral ventricle and also investigated the relationship between these central effects and the action of angiotensin II (Ang). Male Sprague Dawley rats, 350~400 g, were anesthetized with urethane and instrumented with an arterial catheter for direct measurement of BP and heart rate (HR), and an guide cannula in the lateral ventricle for drug injection. A glass microelectode was inserted into the rostral ventrolateral medulla (RVLM) for recording single unit spikes. Barosensitive neurons were identified by changes of single unit spikes in RVLM following intravenous injection of nitroprusside and phenylephrine. The effects of GABA and glutamate injected into the lateral ventricle were studied in single neuronal activity of the RVLM in addition to changes in BP and heart rate, and compared the results before and after treatment with intravenous losartan, nonpeptide Ang II-type 1 receptor antagonist (1 mg/100 g BW). Intracerebroventricular administration of GABA decreased systolic blood pressure (SBP) and HR, but increased the firing rates in the RVLM. However, intracerebroventricular glutamate injection produced effects opposite to GABA. After pretreatment of intravenous losartan, the central effects of GABA on BP and firing rate in the RVLM were significantly attenuated and that of glutamate showed a tendency of attenuation. These results suggested that central GABA and glutamate regulated BP and firing rates in RVLM were inversely related to BP change. The central effects of GABA or glutamate on the autonomic nervous function were modulated by humoral factor, Ang II, by maintaining BP.
Subject(s)
Animals , Humans , Male , Rats , Angiotensin II , Angiotensins , Blood Pressure , Catheters , Fires , gamma-Aminobutyric Acid , Glass , Glutamic Acid , Heart Rate , Injections, Intravenous , Lateral Ventricles , Losartan , Nervous System , Neurons , Nitroprusside , Phenylephrine , Rats, Sprague-Dawley , Urethane , VasopressinsABSTRACT
The amygdala is known as a site for inducing analgesia, but its action on the trigeminal nucleus has not been known well. Little information is available on the effect of dynorphin on NMDA receptor-mediated electrophysiological events in the trigeminal nucleus. The purpose of this study was to investigate the changes in the single neuron spikes at the trigeminal nucleus caused by the amygdala and the action of dynorphin on the trigeminal nucleus. In the present study, extracellular single unit recordings were made in the dorsal horn of the medulla (trigeminal nucleus caudalis) and the effects of microiontophoretically applied compounds were examined. When (D-Ala2, N-Me-Phe4, Glys5-ol)enkephalin (DAMGO, 10-25 mM), a mu-opioid receptor agonist, was infused into the amygdala, the number of NMDA-evoked spikes at the trigeminal nucleus decreased. However, the application of naloxone into the trigeminal nucleus while DAMGO being infused into the amygdala increased the number of spikes. Low dose (1 mM) of dynorphin in the trigeminal nucleus produced a significant decrease in NMDA-evoked spikes of the trigeminal nucleus but the NMDA-evoked responses were facilitated by a high dose (5 mM) of dynorphin. After the kappa receptors were blocked with naloxone, dynorphin induced hyperalgesia. After the NMDA receptors were blocked with AP5, dynorphin induced analgesia. In conclusion, dynorphin A exerted dose-dependent dual effects (increased & decreased spike activity) on NMDA-evoked spikes in the trigeminal nucleus. The inhibitory effect of the dynorphin at a low concentration was due to the activation of kappa receptors and the excitatory effect at a high concentration was due to activation of NMDA receptors in the trigeminal neurons.