{"title":"The role of endogenous opiates in the pathophysiology of hypovolemic shock and their interrelationship with the pituitary-adrenal axis.","authors":"T Vargish","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"57-61"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17410042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Spinal shock and injury: experimental therapeutic approaches.","authors":"J W Holaday, A I Faden","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"95-8"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17931012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L C Casey, H K Ballantyne, J R Fletcher, B Chernow, C R Lake
{"title":"Development of a primate model of exposure hypothermia.","authors":"L C Casey, H K Ballantyne, J R Fletcher, B Chernow, C R Lake","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A nonhuman primate model of exposure-induced hypothermia was developed and the hemodynamic effects of hypothermia were evaluated in five animals. With decreasing core temperature from 37 degrees C to 33 degrees C there was a 47% increase in heart rate, a 23% increase in mean arterial pressure, a 48% increase in cardiac output, a 260% increase in oxygen consumption, and a 237% increase in minute ventilation. As the core temperature decreased from 33 degrees C to 29 degrees C there were decreases in the heart rate, blood pressure, and cardiac output such that at 29 degrees C these values were not significantly different from the values obtained at 37 degrees C. However, the oxygen consumption was still 180% increased and the minute ventilation 40% higher at 29 degrees C than at 37 degrees C. This model will allow the evaluation of the physiology of hypothermia and the effectiveness of different rewarming techniques.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"9 ","pages":"233-7"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17931689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The benefits of corticosteroid given after the onset of hypotension during endotoxin shock in the conscious rat.","authors":"C F Schaefer, D J Brackett, M F Wilson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We have shown that prophylactic treatment with a high dose of corticosteroid stabilizes the cardiovascular system, prevents hemorrhage of the small intestine, and improves survival. In this study we evaluated the effect of corticosteroid administered early after the manifestation of shock induced by endotoxin on blood pressure, heart rate, respiration rate, hematocrit, blood glucose, acid-base parameters, small-intestinal hemorrhage, and survival in the conscious rat. Male Sprague-Dawley rats were anesthetized with 2% enflurane and cannulae were placed in the carotid artery and jugular vein. Following recovery the animals were challenged with endotoxin (20 mg/kg). After the mean blood pressure had fallen to below 70 mm Hg the animals received corticosteroid (300 mg/kg) or an equivalent volume of saline. Supplemental doses of 30 mg/kg were given 90 min and 180 min after the initial dose. In groups other than those dealing with survival, rats were sacrificed after 4 h for pathological examination. When endotoxin was administered to untreated animals, 0/10 were alive at 15 h. In the treated group, 6/10 were alive at 24 h. Treatment shortened the early hypotensive period, but resulted in lower blood pressure from + 60 min to sacrifice. Heart rates in the treated animals were lower, pulse pressures were higher, and respiration rates were the same. Corticosteroid treatment prevented hypoglycemia, hemoconcentration, and acidemia, and markedly inhibited hemorrhage of the small intestine. Large-dose corticosteroid treatment is highly effective even when administered after the first evidence of shock induced by endotoxin in the conscious rat.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"183-94"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17410181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Interaction of supraspinal, serotonergic, and opiate systems during hemorrhage.","authors":"J A Spath, P S Blum","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Anesthetized cats were subjected to hemorrhage to a mean arterial blood pressure of 40 +/- 1 mmHg. After 60 min of oligemia pressure regulation was stopped, and naloxone hydrochloride or an equivalent volume of 0.9% saline was given intravenously as a bolus (2 mg x kg-1) followed by a continuous infusion (2 mg x kg-1 x hr-1). In other cats supraspinal systems were ablated by functional decapitation (FD) or serotonergic systems were ablated by IP injection of parachlorophenylalanine (pCPA, 300 mg/kg, 48 h prior to hemorrhage). Cats subjected to ablation of supraspinal or serotonergic neurons showed a distinct pressor response after naloxone. Although cats with intact neuronal systems failed to show a distinct pressor response to naloxone, the arterial pressures of these cats were significantly greater than hemorrhaged cats given saline (P less than 0.05, unpaired t). Our results suggest that a supraspinal system and a serotonergic system can interact to limit the pressor response to naloxone in hemorrhagic shock.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"111-20"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17931009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of vasopressin in the maintenance of cardiovascular function during early endotoxin shock.","authors":"D J Brackett, C F Schaefer, M F Wilson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This study was conducted as an initial step to elucidate the role of vasopressin in the events leading to irreversible shock. The influence of vasopressin on the maintenance of cardiovascular and respiratory function during early endotoxin shock was evaluated. Conscious, unrestrained male Sprague-Dawley rats (SD) and male homozygous Brattleboro rats (B) lacking vasopressin were anesthetized with 2% enflurane and cannulas were placed in the carotid artery and jugular vein. After recovery from anesthesia, endotoxin (20 mg/kg) was administered. Endotoxin in the B caused an immediate drop in blood pressure to below 40 mm Hg with no recovery. This resulted in death for all ten animals within 3 1/2 hours; eight of ten had expired within 90 min. In contrast, the blood pressure response of the SD dropped to 70 mm Hg but recovered to values near control until sacrificed 240 min after endotoxin. Corticosteroid treatment (300 mg/kg) administered 30 min before endotoxin in the B prevented the severe decrease in blood pressure with values falling to and remaining near 70 mm Hg for the 240-min observation period. All treated animals survived this period. Heart rates in the SD increased sharply after endotoxin and continued to rise, whereas both treated and untreated B increased slowly. Respiration rates for the untreated B were severely depressed until death after endotoxin, whereas the SD and treated B remained at or above control. The results implicate vasopressin in the maintenance of cardiovascular function during the early phase of shock induced by endotoxin, and demonstrate the ability of corticosteroid to substantially improve cardiovascular integrity in the absence of vasopressin.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"9 ","pages":"147-56"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17931684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T Sato, J Tanaka, J R Cottrell, R A Cowley, B F Trump
{"title":"The pathophysiology of septic shock: comparison of systemic hemodynamical responses in the rat following a sonicated, heat-killed, and live E coli injection.","authors":"T Sato, J Tanaka, J R Cottrell, R A Cowley, B F Trump","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Systemic hemodynamical responses in anesthetized rats subjected to a bolus IV injection of sonicated (50 watts, 3 min), heat-killed (100 degrees C, 15 min), or live E coli suspension (12-15 X 10(8) E coli organisms in 0.5 ml saline per kg body wt) were continuously monitored for 6 h. A transpulmonary thermodilution method was used for measurement of cardiac output. After injection of sonicated E coli suspension, there was a triphasic hemodynamical response: 1) a hypodynamic state immediately following treatment, 2) a recovery phase, and 3) a profound, progressive hypodynamic state in the late phase. In contrast, heat-killed E coli suspension induced a biphasic response: 1) an insignificant hyperdynamic state in the early phase, and 2) a progressive hypodynamic state in the late phase. An injection of live E coli suspension resulted in a biphasic response: 1) a hyperdynamic state in the early phase, and 2) a progressive hypodynamic state in the late phase.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"9 ","pages":"115-23"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17410045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Naloxone in endotoxic shock: experimental models and clinical perspective.","authors":"N Gurll","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Naloxone has been used as a pharmacological tool to investigate the role of endorphins and opiate receptors in the cardiovascular pathophysiology of shock. It would appear that endorphins act on opiate receptors to contribute to the abnormalities found and that naloxone improves survival as well as cardiovascular function in shock. Preliminary studies in humans and the subhuman primate create cautious optimism regarding the clinical application of this information. Naloxone has served us well as a key to unlock the involvement of endorphins and opiate receptors in shock. However, further advances in our understanding may depend on the development and use of opiate receptor agonists and antagonists specific for the different opiate receptors described, each subserving different functions. Naloxone's disadvantage of increasing pain awareness may limit its clinical usefulness but might be overcome by using drugs that reverse the behavioral and neuroendocrine changes produced by beta-endorphin without altering pain relief. Thyrotropin-releasing hormone (TRH) is just such a \"physiological\" opiate antagonist which has been shown to increase MAP in experimental endotoxic and hemorrhagic shock [32].</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"63-71"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17370340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Studies on a central site of action for naloxone in endotoxin shock.","authors":"H F Janssen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A complete understanding of naloxone's role in shock has not been well established; however, it has been accepted that naloxone applied specifically to the central nervous system can improve the course of the cardiovascular response. The currently available data would suggest that these central effects are mediated via nuclei that 1) are found in both the rostral and caudal regions of the brainstem, 2) contain opiate receptors, 3) interact with the fastigial nuclei of the cerebellum, and 4) possibly receive input from peripheral thermoreceptors. Recordings of neural activity from specific nuclei during shock as well as microinjections and iontophoresis of naloxone onto specific sites is needed to improve the current understanding of this apparently complex process.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"73-81"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17369623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R G Karanfilian, C R Spillert, G W Machiedo, B F Rush, E J Lazaro
{"title":"Effect of age and splenectomy in murine endotoxemia.","authors":"R G Karanfilian, C R Spillert, G W Machiedo, B F Rush, E J Lazaro","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The protective role of the spleen in gram-positive infections, particularly in infancy and childhood, is well established. Since it is not known whether the spleen is protective in gram-negative sepsis, particularly in elderly individuals as compared to young subjects, the following study was undertaken. Splenectomized and nonsplenectomized Swiss Webster mice, 3 months old (young), or 12 months old (elderly) were utilized. Splenectomy was performed 4 weeks prior to administration of E coli endotoxin. Mortality in elderly nonsplenectomized mice was significantly greater than that of young nonsplenectomized mice. Prior splenectomy significantly increased the mortality in young mice at 48 h, whereas the mortality of E coli endotoxemia (ECE) in elderly mice was not altered by prior splenectomy. The spleen, therefore, appears to have a protective role for young mice but does not protect elderly mice with ECE. It is postulated that this loss of splenic protection reflects deteriorating splenic function with age.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"9 ","pages":"125-32"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17410046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}