Pub Date : 1992-05-01DOI: 10.1249/00005768-199205001-00671
J. Linderman, P. Dallman, R. E. Rodriguez, G. Brooks
To evaluate the hypothesis that lactate supply is essential to maintain euglycemia during iron deficiency, female Sprague-Dawley rats were assigned to iron-sufficient (50 mg Fe2+/kg diet, +Fe), or iron-deficient (15 mg Fe2+/kg diet, -Fe) dietary groups and were injected with a specific beta 2-adrenergic inhibitor, ICI 118,551 (1.0 mg/kg body wt). Rats were studied at rest or after 30 min of running at 13.4 m/min 0% grade. Dietary iron deficiency decreased hemoglobin concentration 38%, but resting arterial concentrations of glucose ([Glc]), lactate ([La]), or alanine ([Ala]) were unaffected. Administration of ICI 118,551 (beta 2-blockade) decreased [La] and [Glc] 52 and 32% in resting -Fe rats, respectively. beta 2-Blockade attenuated the exercise-induced rise in [La] and decreased [Glc] 31% in exercising -Fe rats. [Ala] were unaffected by iron deficiency or exercise but decreased 24 and 18% because of beta 2-blockade in resting and exercising +Fe rats. Iron deficiency depleted resting liver glycogen concentration 45%, with no additional effect of exercise or beta 2-blockade. beta-Blockade decreased arterial insulin and increased arterial glucagon concentrations in resting -Fe and +Fe rats. During exercise glucagon concentration increased significantly more in -Fe than +Fe rats. Decreased arterial [La] with a corresponding decrease in arterial [Glc] in response to beta 2-blockade support the contention that lactate supply is critical to maintenance of euglycemia in -Fe rats at rest and during exercise.
{"title":"Lactate is essential for maintenance of euglycemia in iron-deficient rats at rest and during exercise.","authors":"J. Linderman, P. Dallman, R. E. Rodriguez, G. Brooks","doi":"10.1249/00005768-199205001-00671","DOIUrl":"https://doi.org/10.1249/00005768-199205001-00671","url":null,"abstract":"To evaluate the hypothesis that lactate supply is essential to maintain euglycemia during iron deficiency, female Sprague-Dawley rats were assigned to iron-sufficient (50 mg Fe2+/kg diet, +Fe), or iron-deficient (15 mg Fe2+/kg diet, -Fe) dietary groups and were injected with a specific beta 2-adrenergic inhibitor, ICI 118,551 (1.0 mg/kg body wt). Rats were studied at rest or after 30 min of running at 13.4 m/min 0% grade. Dietary iron deficiency decreased hemoglobin concentration 38%, but resting arterial concentrations of glucose ([Glc]), lactate ([La]), or alanine ([Ala]) were unaffected. Administration of ICI 118,551 (beta 2-blockade) decreased [La] and [Glc] 52 and 32% in resting -Fe rats, respectively. beta 2-Blockade attenuated the exercise-induced rise in [La] and decreased [Glc] 31% in exercising -Fe rats. [Ala] were unaffected by iron deficiency or exercise but decreased 24 and 18% because of beta 2-blockade in resting and exercising +Fe rats. Iron deficiency depleted resting liver glycogen concentration 45%, with no additional effect of exercise or beta 2-blockade. beta-Blockade decreased arterial insulin and increased arterial glucagon concentrations in resting -Fe and +Fe rats. During exercise glucagon concentration increased significantly more in -Fe than +Fe rats. Decreased arterial [La] with a corresponding decrease in arterial [Glc] in response to beta 2-blockade support the contention that lactate supply is critical to maintenance of euglycemia in -Fe rats at rest and during exercise.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1992-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121502430","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}
Pub Date : 1992-04-01DOI: 10.1097/00003246-199204001-00028
S. Hollenberg, W. Tong, J. Shelhamer, M. Lawrence, R. Cunnion
Endothelial cells actively regulate their environment by secreting humoral substances, including endothelin-1 and a variety of eicosanoids, that have local actions. To elucidate interactions among these local mediators, we measured release of cyclooxygenase and lipoxygenase pathway products of arachidonate metabolism by human aortic endothelial cells after incubation with endothelin-1. Supernatants were collected, extracted, and fractionated using high-performance liquid chromatography. Radioimmunoassays for eicosanoids were performed on the appropriate fractions. After endothelin stimulation, production of the prostacyclin metabolite 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the thromboxane (Tx) metabolite TxB2, and prostaglandin E2 (PGE2) were increased (307 +/- 48, 320 +/- 91, and 315 +/- 74% of control, P < 0.05). Leukotriene B4 (LTB4) release was modestly increased (195 +/- 19% of control, P < 0.05). The release of 5-hydroxyeicosatetraenoic acid (5-HETE) was increased (300 +/- 57% of control, P < 0.05); production of 12-HETE and 15-HETE was unchanged. Production of eicosanoids peaked between 30 and 120 min. Preincubation with pertussis toxin prevented increased production of PGE2, LTB4, and 5-HETE after endothelin-1 stimulation; pretreatment with sphingosine had no effect. Interactions between endothelin and eicosanoids may be important components of the complex network that regulates vascular tone, coagulation, and inflammation at the local level.
{"title":"Eicosanoid production by human aortic endothelial cells in response to endothelin.","authors":"S. Hollenberg, W. Tong, J. Shelhamer, M. Lawrence, R. Cunnion","doi":"10.1097/00003246-199204001-00028","DOIUrl":"https://doi.org/10.1097/00003246-199204001-00028","url":null,"abstract":"Endothelial cells actively regulate their environment by secreting humoral substances, including endothelin-1 and a variety of eicosanoids, that have local actions. To elucidate interactions among these local mediators, we measured release of cyclooxygenase and lipoxygenase pathway products of arachidonate metabolism by human aortic endothelial cells after incubation with endothelin-1. Supernatants were collected, extracted, and fractionated using high-performance liquid chromatography. Radioimmunoassays for eicosanoids were performed on the appropriate fractions. After endothelin stimulation, production of the prostacyclin metabolite 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the thromboxane (Tx) metabolite TxB2, and prostaglandin E2 (PGE2) were increased (307 +/- 48, 320 +/- 91, and 315 +/- 74% of control, P < 0.05). Leukotriene B4 (LTB4) release was modestly increased (195 +/- 19% of control, P < 0.05). The release of 5-hydroxyeicosatetraenoic acid (5-HETE) was increased (300 +/- 57% of control, P < 0.05); production of 12-HETE and 15-HETE was unchanged. Production of eicosanoids peaked between 30 and 120 min. Preincubation with pertussis toxin prevented increased production of PGE2, LTB4, and 5-HETE after endothelin-1 stimulation; pretreatment with sphingosine had no effect. Interactions between endothelin and eicosanoids may be important components of the complex network that regulates vascular tone, coagulation, and inflammation at the local level.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"2012 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1992-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127409530","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}
Pub Date : 1992-03-01DOI: 10.1097/00132586-199306000-00021
P. Essén, M. Mcnurlan, J. Wernerman, E. Vinnars, P. Garlick
The impact of anesthesia and surgery on protein metabolism is not well characterized. The single effect of general anesthesia and the combined effects of surgery and general anesthesia on protein synthesis in skeletal muscle were studied in metabolically healthy patients (n = 14) undergoing elective abdominal surgery. The rate of muscle protein synthesis was calculated from the increase in enrichment of [1-13C]leucine in protein during 90 min after an intravenous infusion of [1-13C]leucine (0.05 g/kg, 20 atom percent excess). The 1-13C enrichments of plasma leucine and plasma alpha-ketoisocaproate were used to indicate the enrichment of muscle free leucine. The protein synthesis rate was unaffected by general anesthesia; however, at the end of surgery, a 31.5% decline was seen from 2.19(2.13,2.33)%/24 h before anesthesia to 1.50(1.21,1.77)%/24 h (P less than 0.05) immediately after cholecystectomy while the patients were still under general anesthesia.
{"title":"Uncomplicated surgery, but not general anesthesia, decreases muscle protein synthesis.","authors":"P. Essén, M. Mcnurlan, J. Wernerman, E. Vinnars, P. Garlick","doi":"10.1097/00132586-199306000-00021","DOIUrl":"https://doi.org/10.1097/00132586-199306000-00021","url":null,"abstract":"The impact of anesthesia and surgery on protein metabolism is not well characterized. The single effect of general anesthesia and the combined effects of surgery and general anesthesia on protein synthesis in skeletal muscle were studied in metabolically healthy patients (n = 14) undergoing elective abdominal surgery. The rate of muscle protein synthesis was calculated from the increase in enrichment of [1-13C]leucine in protein during 90 min after an intravenous infusion of [1-13C]leucine (0.05 g/kg, 20 atom percent excess). The 1-13C enrichments of plasma leucine and plasma alpha-ketoisocaproate were used to indicate the enrichment of muscle free leucine. The protein synthesis rate was unaffected by general anesthesia; however, at the end of surgery, a 31.5% decline was seen from 2.19(2.13,2.33)%/24 h before anesthesia to 1.50(1.21,1.77)%/24 h (P less than 0.05) immediately after cholecystectomy while the patients were still under general anesthesia.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1992-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126735686","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}
Pub Date : 1992-03-01DOI: 10.1152/AJPRENAL.1992.263.2.F351-R
E. Dafnis, M. Spohn, B. Lonis, N. Kurtzman, S. Sabatini
Considerable evidence supports the presence of an H(+)-K(+)-ATPase along the mammalian nephron. Inhibition of this enzyme might be expected to reduce acid excretion while increasing potassium excretion, thus causing hypokalemic distal renal tubular acidosis (RTA). In this study we administered vanadate at a dose of 5 mg/kg ip for 10 days to rats. These animals developed hypokalemic distal RTA with a blood pH of 7.22 +/- 0.01, a plasma bicarbonate of 15.2 +/- 0.6 meq/l, and a plasma potassium of 3.28 +/- 0.06 meq/l. The vanadate-treated animals had a urine pH of 6.70 +/- 0.09, a value significantly higher than NH4Cl-treated animals with the same degree of acidemia (urine pH = 5.25 +/- 0.04). When cortical collecting tubules (CCT) from these animals were microdissected and H(+)-K(+)-ATPase was measured, it was decreased by approximately 75% (P less than 0.001); but H(+)-ATPase was no different from control. In medullary collecting tubule, H(+)-K(+)-ATPase was also decreased but less than in CCT. Muscle potassium concentration in the vanadate-treated animals was significantly lower than in controls. These results demonstrate that vanadate causes hypokalemic distal RTA in association with inhibition of collecting tubule H(+)-K(+)-ATPase activity.
{"title":"Vanadate causes hypokalemic distal renal tubular acidosis.","authors":"E. Dafnis, M. Spohn, B. Lonis, N. Kurtzman, S. Sabatini","doi":"10.1152/AJPRENAL.1992.263.2.F351-R","DOIUrl":"https://doi.org/10.1152/AJPRENAL.1992.263.2.F351-R","url":null,"abstract":"Considerable evidence supports the presence of an H(+)-K(+)-ATPase along the mammalian nephron. Inhibition of this enzyme might be expected to reduce acid excretion while increasing potassium excretion, thus causing hypokalemic distal renal tubular acidosis (RTA). In this study we administered vanadate at a dose of 5 mg/kg ip for 10 days to rats. These animals developed hypokalemic distal RTA with a blood pH of 7.22 +/- 0.01, a plasma bicarbonate of 15.2 +/- 0.6 meq/l, and a plasma potassium of 3.28 +/- 0.06 meq/l. The vanadate-treated animals had a urine pH of 6.70 +/- 0.09, a value significantly higher than NH4Cl-treated animals with the same degree of acidemia (urine pH = 5.25 +/- 0.04). When cortical collecting tubules (CCT) from these animals were microdissected and H(+)-K(+)-ATPase was measured, it was decreased by approximately 75% (P less than 0.001); but H(+)-ATPase was no different from control. In medullary collecting tubule, H(+)-K(+)-ATPase was also decreased but less than in CCT. Muscle potassium concentration in the vanadate-treated animals was significantly lower than in controls. These results demonstrate that vanadate causes hypokalemic distal RTA in association with inhibition of collecting tubule H(+)-K(+)-ATPase activity.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"54 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1992-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124206546","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}
Pub Date : 1991-04-01DOI: 10.1016/0022-2828(91)91603-O
D. Rampe, A. E. Lacerda, R. C. Dage, A. Brown
{"title":"Parathyroid hormone: an endogenous modulator of cardiac calcium channels.","authors":"D. Rampe, A. E. Lacerda, R. C. Dage, A. Brown","doi":"10.1016/0022-2828(91)91603-O","DOIUrl":"https://doi.org/10.1016/0022-2828(91)91603-O","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"C-17 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126765788","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}
Pub Date : 1991-02-01DOI: 10.1016/0735-1097(91)91959-I
P. Chen
{"title":"Ventricular fibrillation is not an anodally induced phenomenon in open-chest dogs.","authors":"P. Chen","doi":"10.1016/0735-1097(91)91959-I","DOIUrl":"https://doi.org/10.1016/0735-1097(91)91959-I","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"24 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1991-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127384426","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}
Pub Date : 1991-02-01DOI: 10.1016/0735-1097(91)91937-A
L. Dell’Italia, G. Blackwell, B. Thorn, D. Pearce, S. Bishop, G. Pohost
{"title":"Time-varying wall stress: an index of ventricular vascular coupling.","authors":"L. Dell’Italia, G. Blackwell, B. Thorn, D. Pearce, S. Bishop, G. Pohost","doi":"10.1016/0735-1097(91)91937-A","DOIUrl":"https://doi.org/10.1016/0735-1097(91)91937-A","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"38 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1991-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115769772","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}
Pub Date : 1990-10-01DOI: 10.1016/0016-5085(90)90749-Q
C. Moummi, G. Gullikson, T. Gaginella
{"title":"Monochloramine induces contraction of guinea pig gallbladder via two different pathways.","authors":"C. Moummi, G. Gullikson, T. Gaginella","doi":"10.1016/0016-5085(90)90749-Q","DOIUrl":"https://doi.org/10.1016/0016-5085(90)90749-Q","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1990-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124262220","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}
Pub Date : 1990-07-01DOI: 10.1007/978-3-642-84628-1_14
S. Pelzer, Yaroslav Shuba, T. Asai, J. Codina, L. Birnbaumer, T. Mcdonald, D. Pelzer
{"title":"Membrane-delimited stimulation of heart cell calcium current by beta-adrenergic signal-transducing Gs protein.","authors":"S. Pelzer, Yaroslav Shuba, T. Asai, J. Codina, L. Birnbaumer, T. Mcdonald, D. Pelzer","doi":"10.1007/978-3-642-84628-1_14","DOIUrl":"https://doi.org/10.1007/978-3-642-84628-1_14","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"259 1 Pt 2 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129285722","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}
Pub Date : 1990-05-01DOI: 10.1016/0022-2828(90)91851-W
B. Siegmund, T. Klietz, P. Schwartz, H. Piper
{"title":"Temporary contractile blockade prevents hypercontracture in anoxic-reoxygenated cardiomyocytes.","authors":"B. Siegmund, T. Klietz, P. Schwartz, H. Piper","doi":"10.1016/0022-2828(90)91851-W","DOIUrl":"https://doi.org/10.1016/0022-2828(90)91851-W","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"20 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123680866","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}
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