From March 1986 to August 1992, 18 patients underwent diaphragmatic plication for the diaphragmatic paralyses complicating various pediatric cardiac procedures. Age at operation ranged from 16 day to 84 months with mean age of 11.8 months. In order of decreasing incidence, the primary cardiac procedures included modified Blalock-Taussig shunt [ 5 ], Arterial switch operation [ 4 ], modified Fontan operation [ 2 ], and others [ 7 ]. The suspicious causes of phrenic nerve injury included overzealous pericardial resection [ 7 ], direct trauma during the procedure [ 6 ], dissection of fibrous adhesion around the phrenic nerve [ 3 ] and unknown etiology [ 2 ]. The involved sides of diaphragm were right in 10, left in 7 and bilateral in one. The diagnosis was suspected by the elevation of hem-idiaphragm on chest x-ray and confirmed by fluoroscopy. The interval between primary operation and plication ranged from the day of operation to 38 postoperative days [mean : 14 days]. The method of plication were "Central pleating technique" described by Schwartz in 16 and other techniques in 2. Five patients expired after plication and the cause of death were not thought to be correlated directly with the plication itself. In the remaining 13 survivors, extubation or cessation of positive ventilation could be done between the periods of the day of plication and 14th postoperative days [mean; 3.8day]. We have made the following conclusions : 1] Phrenic nerve paralyses are relatively common complication after pediatric cardiac procedures and the causes of phrenic nerve injury are mostly preventable; 2] Phrenic nerve palsy is associated with corisiderable morbidity; 3] diaphragmatic plication is safe, reliable and can be applicable in patients who are younger age and require prolonged positive pressure ventilation.ntilation.
Choi, Chan Hun;Kim, Kyung Yoon;Jeong, Woo Sik;Jeon, Byung Guan;Jung, Jae Gon;Jung, Jong Gil;Lee, Sang Young;Jeong, Hyun Woo
Journal of Physiology & Pathology in Korean Medicine
/
v.26
no.5
/
pp.657-664
/
2012
The aim of this study is to investigate the effects of onion vinegar on the cerebral blood flow by measuring the changes of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) and by observing the recovery of focal ischemic brain injury in rats. Rats are divided into thee groups depending on the medication; control group (no medication), 8.8-OV group (vinegar using 8.8 brix onion medication), 14.6-OV group (vinegar using 14.6 brix onion medication). The medication of onion vinegar significantly increased rCBF but decreased MABP. This result suggests that onion vinegar significantly increased rCBF by dilating arterial diameter. In addition, focal ischemic brain injury is induced in rats by middle cerebral arterial occlusion. The recovery from focal ischemic brain injury is more significantly improved in the groups using onion vinegar compared to the control group. The amount of recovery is measured by the GAP-43 and the medication of onion vinegar significantly increased GAP-43. This result suggests that onion vinegar is effective on the nerve regeneration. After the medication, the change of body weight, outcomes of renal and liver function test, and outcomes of CBC are analysed for safety examination. There are no statistical differences among control group and all experimental groups in the body weight, renal and liver function test, and CBC. In conclusion, these results suggest that onion vinegar can increase rCBF in normal state, and improve the stability of rCBF in ischemic state.
Surgical procedures to relieve congenital right ventricular outflow tract[RVOT] obstruction of heart were performed on 125 patients from September 1985 to August 1992. There were 65 males and 60 females. Ages ranged from 7 months to 33 years with a mean age of 8 years. All the patients were divided into three main groups[I, II, III] depending on the presence or absence of cyanosis and combined anomalies. The patient were classified into two groups; A and B according to the outcome after surgical repair. Group A included the patients who had a good postoperative outcome with or without mild complications such as wound disruption, or hydrothorax. Group B included the patients who had a poor outcome including hospital death and significant postoperative complications such as heart failure, low output syndrome, respiratory failure, hepatic failure and others. And the results were summarized as follows. 1. There were no significant differences in age, body surface area and aortic dimension among the group I, II, and III, but there were significant differences among groups in pulmonary arterial dimension, ACT[aortic cross clamping time], TBT [total bypass time], preoperative and postoperative ratio of systolic pressure of right and left ventricles [pre PRV/RV and post PRV/LV], and the size of Hegar dilator which passed through the RVOT postoperatively [p<0.05]. 2. In the group A and B, there were significant differences in pulmonary arterial dimension [group A:1.6$\pm$0.5 cm, group B:1.9$\pm$0.6 cm], ACT [group A:102.3$\pm$ 46.0 minute, group B:76.1$\pm$46.1 minute], TBT [group A:133.9$\pm$56.6 minute, group B:94.9$\pm$51.9 minute], pre PRV/LV [group A:1.06$\pm$0.24, group B:0.8$\pm$0.32], post PRV/LV [group A:0.58$\pm$0.18, group B:0.43$\pm$0.16].It has been concluded that postoperative prognosis of RVOT obstruction was influenced by pulmonary arterial dimension, ACT, TBT, severity of RVOT obstruction [pre PRV/LV] and post PRV/LV.
The cardiopulmonary responses during total intravenous anesthesia (TIVA) between remifentanil/propofol infusion and remifentanil/ketamine infusion in dogs were compared. Fourteen healthy adult beagle dogs were premedicated with acepromazine (0.1 mg/kg, SC) and medetomidine (20 ${\mu}g$/kg, IV), and anesthetized for 3 hr with remifentanil (0.5 ${\mu}g$/kg/min)/propofol (loading dose: 1 mg/kg, CRI: 0.3 mg/kg/min) CRI (group 'P') or remifentanil/ ketamine (loading dose : 5 mg/kg, CRI: 0.1 mg/kg/min) CRI (group 'K'), respectively. Hemodynamics, blood gas analysis and behavioral changes during recovery were measured. The level of anesthesia was determined by toe-web clamping test. The level of surgical anesthesia was maintained throughout the experiment in both groups. Systolic arterial pressure, mean arterial pressure, $PaO_2$ and $SpO_2$ in group 'K' were significantly higher than in group 'P', and were maintained near the normal ranges. In addition, $PaO_2$ in group 'K' was significantly lower than in group 'P'. However, diastolic arterial pressure, heart rate and respiratory rate were not significantly differed. Mean extubation time from the end of infusion was significantly reduced in group 'K', but mean sitting time was significantly reduced in group 'P'. Mean head-up time and mean walking time were not significantly differed. In group 'K', brief muscle rigidity, head waving and licking during recovery were observed. In conclusion, infusion rate of ketamine (0.1 mg/ kg/min) with remifentanil (0.5 ${\mu}g$/kg/min) is an appropriate for obtaining the surgical plane of anesthesia. These results showed that group 'K' had better cardiopulmonary function than group 'P'. That is, remifentanil/ketamine CRI is better TIVA protocol than remifentanil/propofol CRI for 3 hr surgery.
Korean red ginseng (KRG) has been shown to enhance endothelium-dependent vasorelaxation in experimental animals; however, little is known about its pharmacological effects on vascular stiffness in patients with coronary artery disease (CAD). This randomized, double-blind, placebo-controlled crossover trial was carried out to determine whether KRG has beneficial effects on arterial stiffness, cardiovascular risk factors such as plasma lipid profiles and blood pressure (BP), and Rho-associated kinase (ROCK) activity. Twenty patients (mean age, 62.5 years) with stable angina pectoris were given KRG (2.7 g/day) and a placebo alternatively for 10 weeks. Blood biochemical analysis and pulse wave velocity (PWV) recording were performed on day 0 and after the completion of each treatment. ROCK activity was assessed based on the level of phospho-$Thr^{853}$ in the myosin-binding subunit of myosin light chain phosphatase, determined by Western blot analysis of peripheral blood mononuclear cells. KRG significantly decreased the systolic BP, brachial ankle PWV, and heart femoral PWV in the patients (all p<0.05), but did not significantly alter the serum lipid profiles, including triglycerides and total, high-density lipoprotein, and low-density lipoprotein cholesterol levels. The ROCK activity tended to decrease (p=0.068) following KRG treatment. The placebo did not significantly alter any of the variables. In conclusion, KRG decreased systolic BP and arterial stiffness, probably via the inhibition of ROCK activity, in patients with CAD, but had a neutral effect on serum lipid profiles. Our data suggest that KRG has a therapeutic effect on CAD.
Background: We evaluated the changes in mean arterial pressure (MAP) and heart rate (HR), and the anesthetic and hemostatic effects, after injection of 2% lidocaine containing various concentrations of epinephrine in rats and mice to determine the appropriate concentration of epinephrine in various anesthetic mixtures. Methods: Rats and mice were randomly allocated to experimental groups: 2% lidocaine without epinephrine (L0), 2% lidocaine with epinephrine 1:200,000 (L200), 1:100,000 (L100), and 1:80,000 (L80). Changes in MAP and HR after administration of the anesthetic mixture were evaluated using a physiological recording system in rats. Onset and duration of local anesthesia was evaluated by pricking the hind paw of mice. A spectrophotometric hemoglobin assay was used to quantify the hemostatic effect. Results: MAP increased in response to epinephrine in a dose-dependent manner; it was significantly higher in the L80 group than in the L0 group at 5 min post-administration. The HR was relatively lower in the L0 group than in the L80 group. The time required for onset of action was < 1 min in all evaluation groups. The duration of action and hemostatic effect of the local anesthetic were significantly better in the L200, L100, and L80 groups than in the L0 group. Conclusion: L200 demonstrated relatively stable MAP and HR values with satisfactory efficacy and hemostatic effect. L200 might be a better local anesthetic for dental patients in terms of anesthetic efficacy and safety.
The role of nitric oxide (NO) in the hemorrhagic hypotension was examined using a NO synthase inhibitor, $N^{\omega}-nitro-L-arginine$ methyl ester (L-NAME), in conscious rats. The rats were bled at a constant rate (2 ml/kg/min) through a femoral arterial catheter until the mean arterial pressure (MAP) was reduced by 50 mmHg. We studied the responses to hemorrhage under normal condition (Control) and after the pretreatment with 3 doses of L-NAME (1.6, 8, 40 mg/kg i.v. of NOX1.6, NOX8, and NOX40, respectively). Intravenous bolus injection of L-NAME produced a sustained increase in MAP and decrease in heart rate (HR). During hemorrhage, the MAP fell faster in the NOX8 and NOX40-treated groups than in Control group, but the control group showed same response to NOX1.6. HR greatly increased in NOX groups. The recovery from hemorrhagic hypotension was slowed in the control group, which was not treated with L-NAME. In comparison with the control group, NOX8 and NOX1.6-treated groups registered a significant recovery in MAP during the 15 min recovery period, but NOX40 brought about only a slight increase in MAP. NO precursor, L-arginine (150 mg/kg i.v.), produced significant bradycardic responses before and after hemorrhage and significant depressor response only after hemorrhagic hypotension regardless of pretreatment with L-NAME. These data suggest that the role of NO in blood pressure regulation is greater after hemorrhagic hypotension than basal condition, but the effect of NO can be detrimental to the recovery from hemorrhagic hypotension. In addition, the bradycardic response of L-arginine provides indirect evidence that NO may inhibit sympathetic activity, especially after hemorrhagic hypotension.
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 $(0.1,\;1,\;10,\;20\;ng/2\;{\mu}l)$ or Ang II $(600\;ng/10\;{\mu}l)$. 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. $IL-1\;{\beta}$ 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. $IL-1\;{\beta}$. Both i.c.v. $IL-1\;{\alpha}\;and\;{\beta}$ produced similar increase in MAP and HR. When hemorrhage was induced after i.c.v. injection of $IL-1\;{\beta}$, the magnitude of MAP fall was not different from the control. The $IL-1\;{\beta}$ 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.
Background: The authors studied the hemodynamic effect influent by using the novel high concentration of lidocaine HCl for surgical removal impacted lower third molar. The objective of this study was to evaluate the hemodynamic change when using different concentrations of lidocaine in impacted lower third molar surgery. Methods: Split mouth single blind study comprising 31 healthy patients with a mean age of 23 years (range 19-33 years). Subjects had symmetrically impacted lower third molars as observed on panoramic radiograph. Each participant required 2 surgical interventions by the same surgeon with a 3-week washout period washout period. The participants were alternately assigned one of two types of local anesthetic (left or right) for the first surgery, then the other type of anesthetic for the second surgery. One solution was 4% lidocaine with 1:100,000 epinephrine and the other was 2% lidocaine with 1:100,000 epinephrine. A standard IANB with 1.8 ml volume was used. Any requirement for additional anesthetic and patient pain intra-operation was recorded. Post-operatively, patient was instructed to fill in the patient report form for any adverse effect and local anesthetic preference in terms of intra-operative pain. This form was collected at the seven day follow up appointment. Results: In the 4% lidocaine group, the heart rate increased during the first minute post-injection (P < 0.05). However, there was no significant change in arterial blood pressure during the operation. In the 2% lidocaine group, there was a significant increase in arterial blood pressure and heart rate in the first minute following injection for every procedure. When the hemodynamic changes in each group were compared, the 4% lidocaine group had significantly lower arterial blood pressure compared to the 2% lidocaine group following injection. Post-operatively, no adverse effects were observed by the operator and patient in either local anesthetic group. Patients reported less pain intra-operation in the 4% lidocaine group compared with the 2% lidocaine group (P < .05). Conclusions: Our results suggest that a 4% concentration of lidocaine HCl with 1:100,000 epinephrine has better clinical efficacy than 2% lidocaine HCl with 1:100,000 epinephrine when used for surgical extraction of lower third molars. Neither drug had any clinical adverse effects.
As pointed out by many previous investigators, the cardio-pulmonary system of well trained athletes is so adapted that they can perform a given physical exercise more efficiently as compared to non-trained persons. However, the time course of the development of these cardio-pulmonary adaptations has not been extensively studied in the past. Although the development of these training effects is undoubtedly related to the magnitude of an exercise load which is repeatedly given, it would be practical if one could maintain a good physical fitness with a minimal daily exercise. Hence, the present investigation was undertaken to study the time course of the development of cardio-pulmonary adaptations while a group of non-athletes was subjected to a daily 6 to 10 minutes running exercise for a period of 4 weeks. Six healthy male medical students (22 to 24 years old) were randomly selected as experimental subjects, and were equally divided into two groups (A and B). Both groups were subjected to the same daily running exercise (approximately 1,000 kg-m). 6 days a week for 4 weeks, but the rate of exercise was such that the group A ran on treadmill with 8.6% grade for 10 min daily at a speed of 127 m/min while the group B ran for 6 min at a speed of 200 m/min. In order to assess the effects of these physical trainings on the cardio-pulmonary system, the minute volume, the $O_2$ consumption, the $CO_2$ output and the heart rate were determined weekly while the subject was engaged in a given running exercise on treadmill (8.6% grade and 127 m/min) for a period of 5 min. In addition, the arterial blood pressure, the cardiac output, the acid-base state of arterial blood and the gas composition of arterial blood were also determined every other week in 4 subjects (2 from each group) while they were engaged in exercise on a bicycle ergometer at a rate of approximately 900 kg m/min until exhaustion. The maximal work capacity was also determined by asking the subject to engage in exercise on treadmill and ergometer until exhaustion. For the measurement of minute volume, the expired gas was collected in a Douglas bag. The $O_2$ consumption and the $CO_2$ output were subsequently computed by analysing the expired gas with a Scholander micro gas analyzer. The heart rate was calculated from the R-R interval of ECG tracings recorded by an Offner RS Dynograph. A 19 gauge Cournand needle was inserted into a brachial artery, through which arterial blood samples were taken. A Statham $P_{23}AA$ pressure transducer and a PR-7 Research Recorder were used for recording instantaneous arterial pressure. The cardiac output was measured by indicator (Cardiogreen) dilution method. The results may be summarized as follows: (1) The maximal running time on treadmill increased linearly during the 4 week training period at the end of which it increased by 2.8 to 4.6 times. In general, an increase in the maximal running time was greater when the speed was fixed at a level at which the subject was trained. The mammal exercise time on bicycle ergometer also increased linearly during the training period. (2) In carrying out a given running exercise on treadmill (8.6%grade, 127 m/min), the following changes in cardio·pulmonary functions were observed during the training period: (a) The minute volume as well as the $O_2$ consumption during steady state exercise tended to decrease progressively and showed significant reductions after 3 weeks of training. (b) The $CO_2$ production during steady state exercise showed a significant reduction within 1 week of training. (c) The heart rate during steady state exercise tended to decrease progressively and showed a significant reduction after 2 weeks of training. The reduction of heart rate following a given exercise tended to become faster by training and showed a significant change after 3 weeks. Although the resting heart rate also tended to decrease by training, no significant change was observed. (3) In rallying out a given exercise (900 kg-m/min) on a bicycle ergometer, the following change in cardio-vascular functions were observed during the training period: (3) The systolic blood pressure during steady state exercise was not affected while the diastolic blood Pressure was significantly lowered after 4 weeks of training. The resting diastolic pressure was also significantly lowered by the end of 4 weeks. (b) The cardiac output and the stroke volume during steady state exercise increased maximally within 2 weeks of training. However, the resting cardiac output was not altered while the resting stroke volume tended to increase somewhat by training. (c) The total peripheral resistance during steady state exercise was greatly lowered within 2 weeks of training. The mean circulation time during exorcise was also considerably shortened while the left heart work output during exercise increased significantly within 2 weeks. However, these functions_at rest were not altered by training. (d) Although both pH, $P_{co2}\;and\;(HCO_3-)$ of arterial plasma decreased during exercise, the magnitude of reductions became less by training. On the other hand, the $O_2$ content of arterial blood decreased during exercise before training while it tended to increase slightly after training. There was no significant alteration in these values at rest. These results indicate that cardio-pulmonary adaptations to physical training can be acquired by subjecting non-athletes to brief daily exercise routine for certain period of time. Although the time of appearance of various adaptive phenomena is not identical, it may be stated that one has to engage in daily exercise routine for at least 2 weeks for the development of significant adaptive changes.
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