Biomedical subjects
C J Shih
Publications and source records attributed to C J Shih.
Alterations in physiological functions and in brain monoamine content in the sympathectomized rats.
In the present study, we conducted pre-ganglionic decentralization (or sympathetic trunk resection) of the superior cervical ganglia and observed alterations in several physiological functions and in the monoamine content of different brain regions. Over an ambient temperature range of 8-30 degrees C, these sympathectomized rats maintained their rectal temperatures within a normal limit displayed by the intact controls. These sympathectomized animals, although showing no change in the level of spontaneous pain threshold or motor activity, did display an increased sensitivity of analgesic responses to morphine administration or locomotor stimulant responses to amphetamine administration. Biochemical examination revealed that these sympathectomized animals had a higher level of norepinephrine, dopamine or 5-hydroxytryptamine in the hypothalamus, as well as a higher level of dopamine in the corpus striatum. However, in the brainstem, these sympathectomized animals had a unaltered monoamine level. The data indicate that, in a sympathectomized condition, changes in the monoamine content of different brain regions may be correlated with the above-mentioned alterations in somatosensory and motor neural functions.
Malignant meningiomas--clinical and pathological study of 10 cases.
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Effects of brain epinephrine depletion on thermoregulation, reflex bradycardia, and motor activity in rats.
Two hours after i.p. administration of 2-cyclooctyl-2-hydroxyethylamine (CONH), 1-aminomethylcycloundecanol (CUNH), 2,3-dichloro-alpha-methylbenzylamine (DCMB), or 7,8-dichloro-1,2,3,4-tetrahydroisoquinoline (SKF64139), the hypothalamic and brain stem epinephrine (EPI) contents of rat brain were decreased. Depletions of brain EPI with these phenylethanolamine N-methyltransferase (PNMT) inhibitors reduced the rectal temperatures of rats at ambient temperatures of 8 and 22 degrees C. The hypothermia in response to these PNMT inhibitors was due to decreased metabolism and cutaneous vasodilatation. The locomotor stimulant responses induced by thyrotropin-releasing hormone were also reduced by administration of any one of these PNMT inhibitors. On the other hand, acute administration of any of these PNMT inhibitors enhanced the reflex bradycardia induced by i.v. infusion of EPI. The data suggest that brain (particularly the hypothalamus and brain stem) EPI-containing neurons are involved in the regulation of body temperature, reflex bradycardia, and motor performance in the rat.
Horseradish peroxidase localization of the sympathetic postganglionic neurons innervating the cat heart.
The localization of the sympathetic postganglionic neurons innervating the cat heart has been investigated by using retrograde axonal transport of horseradish peroxidase (HRP). HRP was injected into the subepicardial layers of 4 different cardiac regions. The animals were sacrificed 72-96 h later and fixed by perfusion via the left ventricle. The paravertebral sympathetic ganglia from the superior cervical, middle cervical and stellate ganglia to T10 ganglia were removed and processed for HRP identification. Following injections of HRP into the apex of the heart, the sinoatrial (SA) nodal region and the ventral wall of the right ventricle, we observed that HRP-labeled sympathetic neurons were localized predominantly in the right stellate ganglia, and to a lesser extent, in the right superior and middle cervical ganglia, and left stellate ganglia. Fewer labeled cells were found in the right T4-T6. T8 and T9. After HRP injection into the dorsal wall of the left ventricle, HRP-labeled cells were present mainly in the left stellate ganglia.
Traumatic intracavernous carotid aneurysm with massive epistaxis.
Five cases of traumatic intracavernous carotid aneurysm are presented. All of the patients were young men with a history of severe head injury. The clinical manifestations were massive epistaxis and an ipsilateral cavernous sinus syndrome. The diagnosis was made correctly by carotid angiography. All of the patients developed another episode of massive epistaxis after admission. Emergency trapping of the internal carotid artery was performed. An urgent rescue method was used in one of our patients to prevent exsanguination before definitive surgical treatment. One patient died of exsanguination in spite of emergency ligation of the internal carotid artery. In the other four patients, no epistaxis was experienced after the operation.
Retrograde localization of the innervation of the middle cerebral artery with horseradish peroxidase in cats.
The innervation of the middle cerebral artery (MCA) of the cat was studied by applying horseradish peroxidase (HRP) to the wall of the right MCA. After a survival period of 48 to 72 hours, the bilateral superior cervical ganglia, middle cervical ganglia, stellate ganglia, T-4 sympathetic paravertebral ganglia, geniculate ganglia, semilunar ganglia, nodose ganglia, and brain stem including midbrain, pons, and medulla oblongata were removed to be processed with tetramethyl benzidine. HRP-labeled neurons were found in the ipsilateral superior cervical ganglion, semilunar ganglion, and dorsal raphe nucleus. The other areas did not have HRP activity. The results suggest that the adrenergic nerves innervating the MCA originate in the ipsilateral superior cervical ganglion, the sensory nerves originate in the ipsilateral semilunar ganglion, and the serotonergic nerves originate in the ipsilateral dorsal raphe nucleus. Cerebral arterial constriction may relate to the intrinsic (intracerebral) neurogenic pathway involving the trigeminal nerve and the dorsal raphe nucleus.
Treatment of central diabetes insipidus with DDAVP.
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Intracranial aneurysms and arteriovenous malformations in Taiwan--brief report of a joint survey.
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Tachycardia, hypertension and decreased reflex bradycardia produced by striatal lesions induced by kainic acid.
The effects of intra-striatal injection of kainic acid on cardiovascular function were assessed in urethane-anesthetized rats. Intra-striatal administration of 2 micrograms of kainic acid (in a volume of 0.5 microliter) produced both tachycardia and hypertension. The tachycardia induced by intra-striatal injection of kainic acid was antagonized by either prior bilateral vagotomy or spinal transection of the animals (at C7). On the other hand, the hypertension induced by intra-striatal administration of kainic acid was antagonized by prior bilateral vagotomy, but not spinal transection. In addition, reflex bradycardia was produced by intravenous infusion of adrenaline in rats. Over the dose range (1.25-5.0 micrograms/kg, i.v.) of adrenaline used, a dose-dependent bradycardia was obtained. It was found that pretreatment of animals with intra-striatal injection of kainic acid, although causing no change in the adrenaline-induced pressor effect, did reduce the adrenaline-induced bradycardia. Intravenous administration of same dose of kainic acid had no effect on these cardiovascular responses. Thus, the data indicate that striatal neurones are involved in the central control of cardiovascular function.
Intracerebral hematoma simulating a new growth.
Three cases of organized intracerebral hematomas presented slowly progressive neurological deficits and hence mimicked brain tumors. Computed tomography scanning revealed ring enhancement of intracerebral mass lesions with midline shift. Angiographic studies showed avascular mass lesions. Soft, well-encapsulated, organized, large intracerebral hematomas with feeding arteries on their capsules were removed surgically. The lesions contained fresh and old hemorrhages. It is presumed that the feeding artery caused slowly continuous bleeding, thus causing these intracerebral hematomas to grow in a manner that made their clinical picture simulate that of intracerebral neoplasms. Their pathogenesis is discussed.
Experimental study on the pathogenesis of heat stroke.
A heat-balance study was carried out on conscious rabbits exposed to ambient temperatures (Ta) from 8 degrees to 40 degrees C. At Ta = 40 degrees C, heat gain exceeded heat loss and led to hyperthermia and heat stroke, and the latency for the onset of heat stroke was found to be around 87 minutes. At the onset of heat stroke, the comatose animals showed higher levels of rectal temperature, ear skin blood flow, respiratory evaporative heat loss, metabolic rate, intracranial pressure (ICP), and cerebral water content as compared to those of control animals (kept at an ambient temperature of 24 degrees C). Before the start of heat stress, the animals had an average mean arterial blood pressure (MABP) of 94 mm Hg and cerebral perfusion pressure (CPP) of 80 mm Hg. However, at the onset of heat stroke, the average MABP and CPP decreased to 67 and 19 mm Hg, respectively. The reduction in CPP at the onset of heat stroke was due to both a decrease in MABP and an increase in ICP. In addition, the comatose animals which received an intravenous infusion of 10% glycerol (3 ml/min) had a survival time (interval between onset of heat stroke and death) longer than that of the comatose animals which received the control-vehicle solution. The prolongation of survival time in the glycerol-treated animals may be due to lower rectal temperature, lower cerebral water content, or lower ICP during the development of heat stroke. The present data indicate that not only hyperthermia but also cerebral edema, intracranial hypertension, decreased MABP, and decreased CPP are the main causes of heat stroke. The therapeutic values of glycerol on heat stroke may be related to the depressant action on cerebral edema, intracranial hypertension, and body temperature.
Effects of pre-ganglionic decentralization or post-ganglionic excision of the superior cervical ganglia on brain edema and heat stroke in rats.
The preventive effect of pre-ganglionic decentralization (Sympathetic trunk resectioN) or postganglionic excision (ganglionectomy) of the superior cervical ganglia on thermal injury induced brain edema or the development of heat stroke was assessed in rats. Brain edema was induced by cold or heat injury to the cortex in 24 rats. The results showed that decentralization, but not excision, of the superior cervical ganglia greatly inhibited the formation of brain edema which was subsequently induced. When heat stroke was induced by exposing 24 rats to an ambient temperature of 41 degree C, the latency for the onset of the heat stroke and the survival time after the heat stroke were greatly prolonged by the former surgical procedure, but shortened by the later one. The present study demonstrates the potential benefit to brain edema and heat stroke of the pretreatment with decentralization of the superior cervical ganglia.
Autonomic dysfunction in palmar hyperhidrosis.
The autonomic (including sudomotor, baroreceptor, and vasomotor) functions were assessed in 3 groups of individuals, comprising normal, hyperhidrotic, and denervated subjects. The normal group had no palmar hyperhidrosis, with intact T2-3 ganglia, the hyperhidrotic group had palmar hyperhidrosis with intact T2-3 ganglia, and the denervated group had palmar hyperhidrosis treated with T2-3 ganglionectomy. Compared with both the normal and hyperhidrotic subjects, the denervated subjects had a much smaller sweating response of both the forehead, the upper chest region and the upper extremities, and a much greater sweating response of both the lateral lumbar and ventral thigh regions in response to body exercise. In addition, cardiovascular responses to either the Valsalva manoeuver, face immersion, or finger immersion were evaluated in these groups of subjects. When compared with those of either the normal or the denervated subjects, the hyperhidrotic subjects had less reflex bradycardia in response to either Valsalva manoeuver or face immersion. In contrast, when compared with those of either the normal or the denervated subjects, the hyperhidrotic subjects had a higher degree of cutaneous vasoconstriction in response to finger (or cold) immersion. The data indicate that the sympathetic fibers passing through the T2-3 ganglia play an important role in the elaboration or modulation of autonomic function elsewhere. Probably, the hyperhidrotic subjects have an over-functioning of the sympathetic nervous fibers which pass through the T2-3 ganglia, which leads to autonomic dysfunction. The autonomic dysfunctions observed in the hyperhidrotic subjects could be eliminated after the interruption of the excessive sympathetic activities passing through the T2-3 ganglia level. A preliminary report of this work was delivered at the 15th Congress of the Pan-Pacific Surgical Association, January 12-18, 1980 and the 12th World Congress of Neurology, September 20-25, 1981.
Unusual penetrating injury of the superior sagittal sinus.
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Primary osteogenic sarcoma of the skull: case report.
A case of primary osteogenic sarcoma of the skull with metastases to the lungs, left diaphragm, 2nd lumbar and 1st sacral vertebral bodies, and both femoral heads was presented. A young man with a lump over his right parieto-occipital region since the age of 14 had noticed rapid growth of the mass after having experienced definite head trauma. The tumor was surgically removed and the bony defect was repaired with a stainless stell plate. The recurrence of the tumor mass was suppressed by 60Co irradiation, but a necrotic lesion developed over the right temporal scalp. Twenty-two months after the surgical removal of the tumor, the patient died of respiratory failure and septicemia.
Recovery of vasomotor response in human spinal cord transection.
Vasomotor responses of the skin of the thumb and the big toe were measured in normal subjects and patients with spinal transection at a neutral ambient temperature of 22.0 +/- 0.5 degrees C, and in a cool (12.0 +/- 0.5 degrees C) and warm (32.0 +/- 0.5 degrees C) environment. The vasomotor response of the hand and foot to the cooling and warming of part of the opposite upper or lower extremity was also recorded. Spinal transection at T5-11 abolishes acutely all vasomotor responses in the paraplegic lower extremities, but does not alter the responses in the upper extremities. By 4 months, the vasomotor tone in the lower extremities at a neutral ambient temperature returned to normal values as did the response to a cool and warm environment. The crossed vasomotor reflex to cooling and warming one lower extremity recovers more slowly, requiring a period of 18 months for complete recovery. The slower recovery of the vasomotor reflex in spinally transected man than in similarly treated dogs is though to be due to the greater spinal shock in the former. The recovery of vasomotor responses in the paraplegic limbs to cooling and warming after thoracic transections suggests that these responses are primitive and powerful thermoregulatory mechanisms.
Effects of cholinomimetic drugs on sudomotor, metabolic, respiratory, vasomotor, and temperature response in palmar hyperhidrosis.
The effects of cholinomimetic drugs such as mecholyl (methacholine) and pilocarpine on autonomic functions (including sudomotor, metabolic, respiratory, vasomotor, and temperature responses) were assessed at room temperature (24 degrees C) in three groups of individuals, including normal, hyperhidrotic, and denervated subjects. The normal group had no palmar hyperhidrosis, with intact T2-3 ganglia, the hyperhidrotic group had palmar hyperhidrosis with intact T2-3 ganglia, and the denervated group had palmar hyperhidrosis treated with T2-3 ganglionectomy. Subcutaneous administration of mecholyl and pilocarpine each produced a fall in oral temperature in the normal group. The hypothermia was brought about by a decrease in metabolic rate, an increase in local sweating rate (mainly of the upper limb and trunk), and an increase in cutaneous circulation (estimated by an increase in the upper limb and trunk skin temperatures). The autonomic functions induced by these cholinomimetic drugs were antagonized by pretreatment with atropine sulfate (an antagonist of cholinergic receptors). Moreover, the hypothermia induced by mecholyl or pilocarpine was greatly reduced in the hyperhidrotic group. The reduction in the cholinomimetic-induced hypothermia in the hyperhidrotic group was due to the reduced sudomotor and metabolic responses after the injections of these cholinomimetic drugs, as compared to those of the normal group. However, neither the excessive sweating of the palms nor the reduced cholinergic responses in the hyperhidrotic group was observed after T2-3 ganglionectomy. The data indicate that the T2-3 ganglia play a role in the elaboration or modulation of the sudomotor and metabolic responses induced by activation of certain cholinergic receptors in humans.