Kazmaier, Stephan

[["dc.bibliographiccitation.firstpage","1470"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow & Metabolism"],["dc.bibliographiccitation.lastpage","1477"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Grune, Frank F. G."],["dc.contributor.author","Kazmaier, Stephan"],["dc.contributor.author","Stolker, Robert Jan"],["dc.contributor.author","Visser, Gerhard H."],["dc.contributor.author","Weyland, Andreas"],["dc.date.accessioned","2018-11-07T09:52:39Z"],["dc.date.available","2018-11-07T09:52:39Z"],["dc.date.issued","2015"],["dc.description.abstract","In addition to cerebrovascular resistance (CVR) zero flow pressure (ZFP), effective cerebral perfusion pressure (CPPe) and the resistance area product (RAP) are supplemental determinants of cerebral blood flow (CBF). Until now, the interrelationship of PaCO2-induced changes in CBF, CVR, CPPe, ZFP, and RAP is not fully understood. In a controlled crossover trial, we investigated 10 anesthetized patients aiming at PaCO2 levels of 30, 37, 43, and 50 mm Hg. Cerebral blood flow was measured with a modified Kety-Schmidt-technique. Zero flow pressure and RAP was estimated by linear regression analysis of pressure-flow velocity relationships of the middle cerebral artery. Effective cerebral perfusion pressure was calculated as the difference between mean arterial pressure and ZFP, CVR as the ratio CPPe/CBF. Statistical analysis was performed by one-way RM-ANOVA. When comparing hypocapnia with hypercapnia, CBF showed a significant exponential reduction by 55% and mean V-MCA by 41%. Effective cerebral perfusion pressure linearly decreased by 17% while ZFP increased from 14 to 29 mm Hg. Cerebrovascular resistance increased by 96% and RAP by 39%; despite these concordant changes in mean CVR and Doppler-derived RAP correlation between these variables was weak (r = 0.43). In conclusion, under general anesthesia hypocapnia-induced reduction in CBF is caused by both an increase in CVR and a decrease in CPPe, as a consequence of an increase in ZFP."],["dc.identifier.doi","10.1038/jcbfm.2015.63"],["dc.identifier.isi","000360689500014"],["dc.identifier.pmid","25873428"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36175"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1559-7016"],["dc.relation.issn","0271-678X"],["dc.title","Carbon dioxide induced changes in cerebral blood flow and flow velocity: role of cerebrovascular resistance and effective cerebral perfusion pressure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","538"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie"],["dc.bibliographiccitation.lastpage","544"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Grune, Frank F. G."],["dc.contributor.author","Buhre, W."],["dc.contributor.author","Kazmaier, Stefan"],["dc.contributor.author","Weyland, Wolfgang"],["dc.contributor.author","Rieke, H."],["dc.contributor.author","Weyland, A."],["dc.date.accessioned","2018-11-07T08:39:46Z"],["dc.date.available","2018-11-07T08:39:46Z"],["dc.date.issued","2001"],["dc.description.abstract","Objective: This controlled study was designed to investigate 1.) the effects of 0,8% halothane and 2.) the effects of a variation in PaCO2 on the relationship between global cerebral blood flow (CBF) and middle cerebral artery flow velocity (CBFVMCA). Method: With ethical committee approval and informed patient consent we investigated 10 patients undergoing coronary artery bypass surgery. Measurements were performed under fentanyl/midazolam anaesthesia prior to the start of surgery. First, during a baseline period, ventilation was changed in a random sequence to achieve two different levels of arterial PCO2. (30 and 50 mmHg, respectively). Consequently, measurements were repeated during application of 0.8% halothane at identical PaCO2 levels. Measurements of global CBF were performed by the Kety-Schmidt-technique with argon as an indicator. Simultaneously, CBFVMCA was recorded by use of a 2-MHz transcranial Doppler system. Results: Application of 0.8% halothane caused a significant decrease in cerebrovascular resistance (CVR) both at hypocapnia and hypercapnia by 36 and 23%, respectively. Because of a concomitant reduction in cerebral perfusion pressure (CPP), however, CBF remained unchanged during application of halothane. The relationship between CBF and CBFVMCA was not altered when compared to the baseline period. Similarly, CO2 reactivity of CBF and CBFVMCA remained unchanged. CO2 reactivity of CBF significantly exceeded CO2 reactivity of CBFVMCA. Conclusion: The results of this clinical study demonstrate that Doppler-sonographic estimation of relative changes in CBF is not altered by application of 1 MAC halothane indicating that the decrease in CVR is not associated with a vasodilation of the proximal segments of basal cerebral arteries. The difference between CO2 reactivity of CBF and CBFVMCA, however, suggests that CO2-induced changes in CBF are slightly underestimated by TCD monitoring of CBFVMCA."],["dc.identifier.doi","10.1055/s-2001-17259"],["dc.identifier.isi","000171381700003"],["dc.identifier.pmid","11577352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19075"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0939-2661"],["dc.title","The relationship between cerebral blood flow (CBF) and the cerebral blood flow velocity (CBFV): Influence of halothane and cerebral CO2 reactivity."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","335"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Anesthesiology"],["dc.bibliographiccitation.lastpage","342"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Grune, Frank F. G."],["dc.contributor.author","Kazmaier, Stephan"],["dc.contributor.author","Sonntag, Hans"],["dc.contributor.author","Stolker, Robert Jan"],["dc.contributor.author","Weyland, Andreas"],["dc.date.accessioned","2018-11-07T09:44:11Z"],["dc.date.available","2018-11-07T09:44:11Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Hyperventilation is known to decrease cerebral blood flow (CBF) and to impair cerebral metabolism, but the threshold in patients undergoing intravenous anesthesia is unknown. The authors hypothesized that reduced CBF associated with moderate hyperventilation might impair cerebral aerobic metabolism in patients undergoing intravenous anesthesia. Methods: Thirty male patients scheduled for coronary surgery were included in a prospective, controlled crossover trial. Measurements were performed under fentanyl-midazolam anesthesia in a randomized sequence aiming at partial pressures of carbon dioxide of 30 and 50 mmHg. Endpoints were CBF, blood flow velocity in the middle cerebral artery, and cerebral metabolic rates for oxygen, glucose, and lactate. Global CBF was measured using a modified Kety-Schmidt technique with argon as inert gas tracer. CBF velocity of the middle cerebral artery was recorded by transcranial Doppler sonography. Data were presented as mean (SD). Two-sided paired t tests and one-way ANOVA for repeated measures were used for statistical analysis. Results: Moderate hyperventilation significantly decreased CBF by 60%, blood flow velocity by 41%, cerebral oxygen delivery by 58%, and partial pressure of oxygen of the jugular venous bulb by 45%. Cerebral metabolic rates for oxygen and glucose remained unchanged; however, net cerebral lactate efflux significantly increased from -0.38 (2.18) to -2.41(2.43) mu mol min(-1) 100 g(-1). Conclusions: Moderate hyperventilation, when compared with moderate hypoventilation, in patients with cardiovascular disease undergoing intravenous anesthesia increased net cerebral lactate efflux and markedly reduced CBF and partial pressure of oxygen of the jugular venous bulb, suggesting partial impairment of cerebral aerobic metabolism at clinically relevant levels of hypocapnia."],["dc.identifier.doi","10.1097/ALN.0b013e3182a8eb09"],["dc.identifier.isi","000331559900012"],["dc.identifier.pmid","24008921"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34337"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1528-1175"],["dc.relation.issn","0003-3022"],["dc.title","Moderate Hyperventilation during Intravenous Anesthesia Increases Net Cerebral Lactate Efflux"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]