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Glutamate stimulation (Glu) may raise the excitability of medulla vasomotor neurons in stroke-prone hypertensive rats (SHRSP) and spontaneously hypertensive rats (SHR). L-Glutamate (Glu, 10mM, 30 nl) was used to find vasoactive sites. Hypertensive rats showed larger responses to blood pressure and renal sympathetic activity and lower threshold does of Glu as compared to Wistar-Kyoto rats (WKY).

A stimulation of the gigantocellular tegmental field (FTG) in the medulla oblongata often increases systemic arterial blood pressure (SAP) and decreases heart rate (HR). We investigated if the cardioinhibitory/depressor areas, including the nucleus ambiguus (NA), the dorsal motor nucleus of vagus (DMV) and the caudal ventrolateral medulla (CVLM), underlied the functional expression of FTG neurons in regulating cardiovascular responses. In 73 chloralose-urethane anesthetized cats, the HR, SAP and vertebral nerve activity (VNA) were recorded. Neurons in the FTG, NA, DMV and CVLM were stimulated by microinjection of sodium glutamate (25 mM Glu, 70 nl). To study if the NA, DMV, and CVLM relayed the cardioinhibitory messages from the FTG, 24 mM kainic acid (KA, 100 nl) was used as an excitotoxic agent to lesion neurons in the NA, DMV or CVLM. We found that the cardioinhibition induced by FTG stimulation was significantly reduced by KA lesioning of the ipsilateral NA or DMV. Subsequently, a bilateral KA lesion of NA or DMV abolished the cardioinhibitory responses of FTG. Compared to the consequence of KA lesion of the DMV, only a smaller bradycardia was induced by FTG stimulation after KA lesion of the NA. The pressor response induced by Glu stimulation of the FTG was reduced by the KA lesion of the CVLM. Such an effect was dominant ipsilaterally. Our findings suggested that both NA and DMV mediated the cardioinhibitory responses of FTG. The pressor message from the FTG neurons might be partly working via a disinhibitory mechanism through the depressor neurons located in the CVLM.

The aim of the present study was to examine the relationship between the lateral tegmental field (FTL), a cardioinhibitory area, with other cardioinhibitory areas, i.e., the ambiguus nucleus (NA) and the dorsal motor nucleus of vagus (DMV) and the caudal ventrolateral medulla (CVLM), a vasopressor inhibitory area. In 55 cats anesthetized with chloralose (40 mg/kg) and urethane (400 mg/kg), the cardiovascular responses of heart rate (HR), systemic arterial blood pressure (SAP) and vertebral nerve activity (VNA) were recorded. The FTL, NA, DMV and CVLM were identified first by stimulation (rectangular pulses in 80 Hz, 0.5 ms, 50-100 microA) and then confirmed by microinjection of sodium glutamate (Glu, 0.25M, 70 nl). In studying the influence of NA, DMV, or CVLM lesion on the Gluinduced responses in FTL, kainic acid (KA, 24 mM, 100 nl) was microinjected into the NA, DMV or CVLM. FTL stimulation produced an average decrease of HR by 55%. After KA lesioning of the ipsilateral NA or the DMV, the decreased HR induced by FTL was significantly diminished. After subsequent lesion of the contralateral DMV or NA, the bradycardia of FTL was abolished. The reduction of resting HR was more intense after lesioning the NA than DMV and with the left side more than that of the right side. These studies suggest that the cardioinhibitory responses of FTL are mediated through both NA and DMV with predominance of the former, while the hypotensive effect of FTL is mediated through CVLM. The precise pathway responsible for the FTL-induced bradycardia and hypotension is to be determined.

The purposes of the present study were to characterize and compare the mid-tail cortical and thalamic somatosensory evoked potentials (SEPs), and to examine how the depth of the barbiturate anesthesia affected them. After the tail representative locations of sacrococcygeal dorsal root (S2 or S3), thalamus (ventroposterior lateral nucleus, VPL) and primary somatosensory cortex (SI) were set up for recording, the rats were infused serially with diluted sodium pentobarbital solution beginning from light (5 to 10 mg/kg/hr) to deep (30 to 40 mg/kg/hr) and then stop infusion (recovery). The effects of anesthetic depth on SEPs were examined of dorsal root, thalamic and cortical field potentials evoked by mid-tail stimulation of various stimulation intensities (100 microA to 2mA, step 100 pA, at 2 Hz) and frequencies (0.5 to 11 Hz, step 0.5 to 1 Hz, at 3T). The depth of anesthesia did not affect the strength-response curves of the SEPs. In contrast, the depth of anesthesia differentially influenced the frequency following capabilities of different recording sites. Under light anesthesia, thalamic SEP was only significantly affected with stimulation frequencies higher than 8 Hz, whereas cortical SEP was significantly affected with 2 Hz or higher. Under deep anesthesia, thalamic SEP evoked by low frequency tail stimulation was not significantly changed. In contrast, cortical SEP was affected much strongly so that under 1 Hz stimulation, a significant difference could be observed. We concluded, therefore, that thalamus was only partially responsible for the limited frequency following capability of the SI, and that the main effect of pentobarbital was on the cortical level. From the data obtained, an exponentially decaying curve could be observed for the cortical SEP under different stimulation frequencies. The decay constant showed a 50% change with a change in anesthesia depth. We propose that the decay constant could be used as a sensitive index for the monitoring of anesthetic depth.

The effects of hypercapnia and hypocapnia on the activities of the cardiac and pulmonary vagal single fibers were examined in the decerebrated, unanesthetized, paralyzed, and vagotomized cats. The animals breathed 100% O2. Fractional end tidal CO2 concentration was raised to 9% by adding CO2 into the O2 inlet. Average discharge rate of efferent cardiac vagal units (n=10) increased from 1.0+/-0.3 to 2.2+/-0.3 Hz. Hypocapnia apnea was produced by hyperventilation. Activities of cardiac vagal units tested (n = 4) showed dramatic decrease (0.1+/-0.0 Hz). Mean arterial blood pressure did not change significantly under these conditions. In contrast, only instantaneous firing rate during inspiration was significantly increased for efferent pulmonary vagal units (n = 11) during hypercapnia. The activities of the 3 pulmonary vagal units tested with hypocapnia decreased significantly. We concluded that cardiac and pulmonary vagal neurons were excited by chemoreceptor input.

In 35 adult cats anesthetized with intraperitoneal chloralose and urethane, the ventrolateral medulla was explored by microinjection of kainic acid (KA, 24 mM, 200 nl) with metal electrode-tubing or glass micropipette to determine regions which elicit persistent apnea. Persistent apnea is defined as: (1) In spontaneously breathing cats, termination of respiration over 3 min with a decrease of the mean systemic arterial pressure (MSAP) to 25 mm Hg. (2) In animals under artificial ventilation and paralyzed by gallamine, cessation of bilateral phrenic nerve (PNA) activities over 25 min. The apnea producing area was located dorsal to the rostral pole of the lateral reticular nucleus, ventromedial to the ambiguous nucleus and immediately caudal to the retrofacial nucleus. Functionally, this region includes the rostral part of the ventral respiratory group (rVRG) encompassing the pre-BOtzinger area. We define this region as the VRG apnea producing area (VRG-Apa). Fatal apneusis was observed under following conditions: (1) Persistent apnea was produced after a single KA microinjection in one side of the VRG-Apa (5 animals). Microinjection of sodium glutamate (0.25 M, 70-200 nl) in the same area produced only brief apnea, while microinjection of kynurenic acid (0.1 M, 200 nl) showed little effect on the respiration but slightly increased the SAP. (2) Positioning an electrode nearby but not in the VRG-Apa with or without KA injection did not produce apnea. But when a second electrode insertion to the opposite VRG-Apa immediately produced persistent apnea even without KA injection (6 animals). (3) Midsagittal division of the medulla 0-5 mm rostral to the obex produced persistent silence of PNA on both sides in artificial ventilated animals (7 animals), while similar division 0-5 mm caudal to the obex (4 animals) produced a brief but reversible quiescence of PNA. In conclusion, findings of the present study support the existence of a restricted region of VRG-Apa. VRG-Apa on both sides are closely connected, and integrity of both VRG-Apa is essential for normal respiration.

The cardiac and vascular components of the baroreceptor reflex in spontaneously hypertensive rat (SHR) and stroke-prone spontaneously hypertensive rat (SHRSP) were compared against their counterparts in normotensive Wistar Kyoto rat (WKY). SHR, SHRSP and WKY of 12-16 weeks old were chronically instrumented for intra-arterial recording of blood pressure. Intravenous injections of phenylephrine and nitroprusside were used to challenge their baroreflex. The products of blood pressure change and the half time required for the pressure to return to the control value were used as the quantitative estimation of the blood pressure stabilizing capability. The cardiac component of the baroreflex was obtained from the change in the blood pressure stabilizing capability after blockade of beta and muscarinic receptors by atenolol and atropine, respectively. The vascular component was obtained by subtracting the cardiac component from the total stabilizing capability which was the difference after blockade with a ganglionic transmission blocker, hexamethonium. We found the cardiac component of the baroreflex of the hypertensive rats was significantly less sensitive than that of the WKY. In contrast, the vascular component of the baroreflex of the three strains did not differ significantly. Therefore, we concluded that the 12-16 week old SHRs were able to maintain a stable blood pressure due to the intact vascular component of the baroreflex.

The origin of medullary cells that form the cardiac vagal branch and the vagal branches in the lower thorax innervating the gastrointestinal (GI) tract was studied using horseradish peroxidase (HRP), a retrograde transport tracer in the cat. The distributions of parasympathetic postganglionic neurons of the heart were studied with acetylcholinesterase histochemistry. Intracardiac ganglionic neurons were found mainly in the connective tissue surrounding the base of the pulmonary arteries and in an area in and dorsal to the interatrial septum. Following injection of HRP into the subepicardum where most of the cardiac postganglionic neurons reside, 91% of the labelled neurons were found bilaterally distributed in the nucleus ambiguus (NA). A small population of labelled neurons was found in the dorsal motor nucleus of the vagus (DMV) and an intermediate zone (IZ) between the two nuclei. When HRP was injected into the left or right cardiopulmonary vagus branch, labelled neurons were found exclusively in the ipsilateral NA, DMV and IZ with a predominance in the NA. In the thorax, after they course around the heart, the left and right thoracic vagus nerves divides into a left and a right branch, respectively. The left branch of the left thoracic vagus joins the left branch of the right thoracic vagus to form the anterior vagus nerve at 3 cm above the diaphragm. The right branch of the right thoracic vagus nerve joins the right branch of the left thoracic vagus to form the posterior vagus nerve. After application of HRP into the right or the left branch of the left thoracic vagus, HRP labelled cells were found in the left DMV. Similarly, after application of HRP into the left or the right branch of the right thoracic vagus, labelled cells were found in the right DMV. On the other hand, when HRP was injected into the anterior vagus, labelled neurons were found bilaterally in the DMV. This suggests that all rostral branches of the thoracic vagus have their origin in the ipsilateral DMV, and intermixing occurs only at the caudal level near the diaphragm. Findings of the present experiments suggest that parasympathetic preganglionic neurons innervating the GI tract are located exclusively in the DMV while those of the heart are located mainly in the NA. Within the DMV, GI vagal neurons were found medially from the level 0-2.5 mm rostral to the obex. In contrast, cardiac vagal neurons were found in the lateral edge of the DMV at the level 0-1 mm rostral to the obex.

The functional correlation of the depressor caudal ventrolateral medulla (CVLM) with the two pressor regions, i.e. rostral ventrolateral medulla (RVLM) and dorsomedial medulla (DM), and with another inhibitory region, i.e. the paramedian reticular nucleus (PRN), were studied in cats anesthetized intraperitoneally with chloralose (40 mg/kg) and urethane (400 mg/kg). Systemic arterial pressure (SAP), heart rate (HR) and the sympathetic vertebral nerve activity (VNA) were recorded. The correct location of CVLM, RVLM or DM was determined by their specific responses, i.e. decreases of SAP, HR and VNA, for CVLM increases of these parameters for RVLM and DM, elicited first by electrical stimulation (80 Hz, 0.5 ms, 50-100 microA) then followed by microinjection of glutamate (Glu, 0.25 M, 70 nl). The depressor action of PRN was produced by electrical stimulation only. It was found that the depressor responses caused by the CVLM stimulation were greatly reduced 2 h after lesioning either the RVLM or DM by microinjection of kainic acid (KA, 24 mM, 200 nl) ipsilateral to the side of CVLM stimulation. The CVLM responses were further reduced after the remaining side of RVLM or DM was lesioned. The reduction of the CVLM-depressor responses was more apparent after the RVLM than DM lesioning. Data suggest that the CVLM-depressor responses are mediated through inhibition of the sympathetic-pressor neurons in both RVLM and DM with predominance of the former. Lesioning the PRN by KA and/or combination with DC electrolytic lesion reduced the CVLM-induced depressor responses. In turn, lesioning the CVLM by KA reduced the PRN-induced depressor responses. The reduction in the later manipulation was more apparent in the PRN-depressor responses than the CVLM-depressor responses. Data suggest that part of the PRN depressor action is mediated through activation of the CVLM.

The purpose of this survey is to study the sex knowledge of adolescents, and to analyze their need in sex consultation and related health problem in Kaohsiung city. A total of 1,000 study subjects were recruited from May 1991 to May 1994. A self-administered questionnaire and medical records were used to obtain related information. The results were as follows: 1. The male to female ratio of study subjects was 1:2. Half of them were students, 44.1% had sexual experience, and the mean +/- standard deviation of age at first sex experience was 19.1 +/- 2.8 years. 2. The average percentage of correct knowledge was as low as 67.6%. It indicated an inadequacy of sex knowledge in adolescents. Females had better knowledge than males. Subjects who had graduated from senior high schools had better knowledge than those graduated from middle schools. No association was found between the score of sex knowledge and occupation. 3. 12.5% of study subjects believed that "masturbation" might cause neurasthenia, kidney malfunction and loss of memory, while 11.9% recognized that "nocturnal emission" might result in abnormal ejaculation, mental aberration and guilty feelings. Furthermore, 3.8% considered that kissing, hugging or sleeping together might cause pregnancy. 4. Most adolescents felt that "guidance on sex knowledge" was the major reason for them to visit the adolescent clinic and "obstetric and gynecological problems" was the second most important. 5. Males and females have the same prevalence of sex experience, and 50.6% of them did not practice contraception. 88.9% subjects had a high risk of getting pregnancy. 6. Males had a higher percentage of more than one heterosexual partner than females did. There was a higher percentage of people with a high education level having a fixed heterosexual partner than that of those with a low education level.

Evoked potential methods were used to compare the patterns of responses to periaqueductal grey (PAG) stimulation in two major medullary sympathoexcitatory areas, namely, ventrolateral medulla (VLM) and dorsal medulla (DM). Adult cats were anesthestized with chloralose and urethane, paralyzed, ventilated and bilaterally vagotomized. Pressor points in the PAG were identified with rectangular pulses in 80 Hz, 200 microA, 0.1 ms and used as stimulation points. Pressor points in VLM and DM were identified by injection of 100 nl of 0.25 M glutamate solution. Adjacent points 1 mm away from these pressor points where injected the same amount of glutamate solution elicited very little blood pressure changes were used as control recording points. Stimulation of the PAG pressor points with rectangular pulse in 1 Hz, 0.1 ms, 200 microA elicited complex evoked field potentials in both VLM and DM. In 9 of the 13 pressor-control pairs tested, distinctive evoked potential of long latency were seen in the pressor point only. These evoked potentials, averaged 3.5 ms in the DM, and 5.6 ms in the VLM. Therefore, it was postulated that pressor points of PAG had separate and independent connections with DM and VLM.