Severe lightning pain during spinal anesthesia

A 74-yr-old man was scheduled for the biopsy of prostatic tumor under spinal anesthesia. Preoperative serologic test for syphilis was highly positive. Spinal anesthesia was performed in the sitting position, and 2 ml of hyperbaric Neo-percamine S (a mixture of 0.24% dibucaine and 0.12% T-caine) was administered uneventfully with the onset of warm sensation on the perineal region. Ten minutes later, however, he began to complain of severe lightning sensation on the feet. After giving pentazocine intravenously, the short cystoscopic procedure was completed. As a cause of severe pain, an erroneous anesthetic solution or direct neuronal injury had been excluded because of rapid and complete recovery after anesthesia. Two weeks later, he was scheduled for TUR-P. He again complained of severe lightning pain after the successful spinal anesthesia with the same anesthetic solution. Because the pain was not relieved by analgesics, he was then anesthetized with enflurane and N2O in oxygen, and there were no neurological complications after anesthesia. Several cases of severe pain during spinal anesthesia have been reported in patients with tabes dorsalis. Although the patient lacks clear symptoms of neurosyphilis, positive serologic examination for syphilis without any other possible causes suggests altered sensitivity of the spinal cord to anesthetic solutions.     

Effects of vancomycin and ofloxacin on rabbit ERG in vivo

The retinal toxicity of vancomycin and ofloxacin was studied by electroretinogram (ERG) before and after intravitreal injection in rabbits. Vancomycin is known to be effective on methicillin-resistant Staphylococcus aureus. A dose of 1mg vancomycin caused no ERG change for at least eight weeks after injection. The feature that ERG became non-recordable during one to four weeks after an intravitreal injection of 10mg vancomycin, with recovery of only the c-wave was conspicuous. A dose of 200 micrograms ofloxacin did not cause deterioration of the b-wave, the c-wave or the oscillatory potentials throughout the follow-up period up to eight weeks. Judging from the susceptibility of each ERG component to antimicrobials and taking into account the difference of vitreous volume between rabbits and humans, clinical doses of intravitreal single-shot injection should be less than 1mg for vancomycin and 200 micrograms for ofloxacin.     

Transient Brain Ischaemia Provokes Ca2+, PIP2 and Calpain Responses Prior to Delayed Neuronal Death in Monkeys

To clarify the mechanism of postischaemic delayed cornu Ammonis (CA)-1 neuronal death, we studied correlations among calpain activation and its subcellular localization, the immunoreactivity of phosphatidylinositol 4,5-bisphosphate (PIP₂) and Ca²⁺ mobilization in the monkey hippocampus by two independent experimental approaches: in vivo transient brain ischaemia and in vitro hypoxia-hypoglycaemia of hippocampal acute slices. The CA-1 sector undergoing 20 min of ischaemia in vivo showed microscopically a small number of neuronal deaths on day 1 and almost global neuronal loss on day 5 after ischaemia. Immediately after ischaemia, CA-1 neurons ultrastructurally showed vacuolation and/or disruption of the lysosomes. Western blotting using antibodies against inactivated or activated μ-calpain demonstrated μ-calpain activation specifically in the CA-1 sector immediately after ischaemia. This finding was confirmed in the perikarya of CA-1 neurons by immunohistochemistry. CA-1 neurons on day 1 showed sustained activation of μ-calpain, and increased immunostaining for inactivated and activated forms of μ- and m-calpains and for PIP₂. Activated μ-calpain and PIP₂ were found to be localized at the vacuolated lysosomal membrane or endoplasmic reticulum and mitochondrial membrane respectively, by immunoelectron microscopy. Calcium imaging data using hippocampal acute slices showed that hypoxia-hypoglycaemia in vitro provoked intense Ca²⁺ mobilization with increased PIP₂ immunostaining specifically in CA-1 neurons. These data suggest that transient brain ischaemia increases intracellular Ca²⁺ and PIP₂ breakdown, which will activate calpain proteolytic activity. Therefore, we suggest that activated calpain at the lysosomal membrane, with the possible release of biodegrading enzyme, will cause postischaemic CA-1 neuronal death.     

Pseudopodia of capillary endothelium in ocular tissues

The frequencies of pseudopodia projecting from capillaries of various parts of the eye were observed in 16 human eyes with a transmission electron microscope. The pseudopodia were found mainly projecting from the choriocapillaris and rarely seen in the retina, iris or ciliary body. The frequencies of pseudopodia from the choriocapillaris were not correlated with the localization in the fundus (macular area or peripheral fundus), age, sex, time elapsed between death or enucleation and fixation. The significance of pseudopodia from the choriocapillaris is unknown. However, there is the possibility that pseudopodia are related to choroidal neovascularization or have other physiological functions.     

Effects of beta-adrenoceptor-related agents on hypoxic pulmonary vasoconstriction and relation with cyclic AMP and prostaglandins]

Effects of a beta-agonist (isoproterenol) and beta-antagonists (propranolol and pindolol) on hypoxic pulmonary vasoconstriction (HPV) and on changes in some chemical mediators were compared between HPV-responsive lobes and non-responsive lobes in which HPV was induced by aspirin DL-lysine (ASA groups). Hypoxic ventilation (4 min) was repeated in 56 of isolated, blood-perfused dog lung lobes. Each drug was administrated in a bolus dose of 0.2 mg in the intermittent period between hypoxia. In HPV-responsive lobes, the first hypoxia increased pulmonary vascular resistance by 33% or more in all groups. Both isoproterenol and pindolol inhibited the elicitation of HPV completely, but propranolol induced almost the same degree of HPV as control. In ASA groups, HPV was completely inhibited by isoproterenol, but was not influenced by propranolol. However, pindolol's inhibitory effect on HPV was less than that in HPV-responsive lobes. Isoproterenol significantly increased cyclic AMP from 17.0 to 76.7 pmol/ml in HPV-responsive lobes (n = 7). Pindolol increased prostaglandin E2 from 87.0 to 1015.4 pg/ml in HPV-responsive lobes (n = 7), and from 93.4 to 361.3 pg/ml when ASA was treated. Propranolol did not show the different results from the control group whether ASA was present or not. The different mechanisms among beta-adrenoceptor-related agents in HPV and pulmonary circulation were investigated.     

Antihypertensive effect of bopindolol on stroke-prone spontaneously hypertensive rats (SHRSP)

The antihypertensive effect of bopindolol, a long-acting beta-adrenoceptor blocking agent, was investigated in stroke-prone spontaneously hypertensive rats (SHRSP). One group received tap water during the period of 8 to 32 weeks of age. The average dose of bopindolol administered was calculated from water intake to be approximately 1.4 mg/kg/day. The lowering effect in blood pressure of bopindolol was apparent at the age of 14 weeks, and this continued up to the end of the experiment. Bopindolol significantly reduced the heart rate. Plasma levels of urea nitrogen (BUN), triglyceride, and phospholipid of SHRSP treated with bopindolol were lower than those of the control SHRSP. One of the 8 control SHRSP died, and no rats treated with bopindolol died during the experiment. The histopathological study revealed that three of the control SHRSP had cerebral apoplexy, whereas there was no evidence of cerebral apoplexy in the treated SHRSP. Chronic treatment of bopindolol clearly alleviated myocardial fibrosis and hypertrophic changes in the left ventricular wall of the heart. Decreases in the incidence of proliferative arteritis and malignant nephrosclerosis in the kidney and necrotizing arteritis of the mesenteric arteries were observed in SHRSP treated with bopindolol. The data presented indicate that bopindolol is a powerful antihypertensive agent.