Klaus D. Torp
Mayo Clinic
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Featured researches published by Klaus D. Torp.
The Journal of Physiology | 2000
Ann S. Reed; Michael E. Tschakovsky; Christopher T. Minson; John R. Halliwill; Klaus D. Torp; Lee A. Nauss; Michael J. Joyner
1 Evidence for the existence of sympathetic vasodilator nerves in human skeletal muscle is controversial. Manoeuvres such as contralateral ischaemic handgripping to fatigue that cause vasoconstriction in the resting forearm evoke vasodilatation after local α‐adrenergic receptor blockade, raising the possibility that both constrictor and dilator fibres are present. The purpose of this study was to determine whether this dilatation is neurally mediated. 2 Ten subjects (3 women, 7 men) performed ischaemic handgripping to fatigue before and after acute local anaesthetic block of the sympathetic nerves (stellate ganglion) innervating the contralateral (resting) upper extremity. Forearm blood flow was measured with venous occlusion plethysmography in the resting forearm. 3 In control studies there was forearm vasoconstriction during contralateral handgripping to fatigue. During contralateral handgripping after stellate block, blood flow in the resting forearm increased from 6.1 ± 0.7 to 18.7 ± 2.2 ml dl−1 min−1 (P < 0.05). Mean arterial pressure measured concurrently increased from ≈90 to 130 mmHg and estimated vascular conductance rose from 6.5 ± 0.7 to 14.0 ± 1.5 units, indicating that most of the rise in forearm blood flow was due to vasodilatation. 4 Brachial artery administration of β‐blockers (propranolol) and the nitric oxide (NO) synthase inhibitor NG‐monomethyl‐L‐arginine (L‐NMMA) after stellate block virtually eliminated all of the vasodilatation to contralateral handgrip. 5 Since vasodilatation was seen after stellate block, our data suggest that sympathetic dilator nerves are not responsible for limb vasodilatation seen during sympathoexcitation evoked by contralateral ischaemic handgripping to fatigue. The results obtained with propranolol and L‐NMMA suggest that β‐adrenergic mechanisms and local NO release contribute to the dilatation.
Liver Transplantation | 2012
C. Burcin Taner; Darrin L. Willingham; Ilynn G. Bulatao; Timothy S. Shine; Prith Peiris; Klaus D. Torp; Juan M. Canabal; David J. Kramer
The continuation of hemodynamic, respiratory, and metabolic support for a variable period after liver transplantation (LT) in the intensive care unit (ICU) is considered routine by many transplant programs. However, some LT recipients may be liberated from mechanical ventilation shortly after the discontinuation of anesthesia. These patients might be appropriately discharged from the postanesthesia care unit (PACU) to the surgical ward and bypass the ICU entirely. In 2002, our program started a fast‐tracking program: select LT recipients are transferred from the operating room to the PACU for recovery and tracheal extubation with a subsequent transfer to the ward, and the ICU stay is completely eliminated. Between January 1, 2003 and December 31, 2007, 1045 patients underwent LT at our transplant program; 175 patients were excluded from the study. Five hundred twenty‐three of the remaining 870 patients (60.10%) were fast‐tracked to the surgical ward, and 347 (39.90%) were admitted to the ICU after LT. The failure rate after fast‐tracking to the surgical ward was 1.90%. The groups were significantly different with respect to the recipient age, the raw Model for End‐Stage Liver Disease (MELD) score at the time of LT, the recipient body mass index (BMI), the retransplantation status, the operative time, the warm ischemia time, and the intraoperative transfusion requirements. A multivariate logistic regression analysis revealed that the raw MELD score at the time of LT, the operative time, the intraoperative transfusion requirements, the recipient age, the recipient BMI, and the absence of hepatocellular cancer/cholangiocarcinoma were significant predictors of ICU admission. In conclusion, we are reporting the largest single‐center experience demonstrating the feasibility of bypassing an ICU stay after LT. Liver Transpl 18:361–369, 2012.
Anesthesia & Analgesia | 2000
Pierre Diemunsch; Klaus D. Torp; Thomas Van Dorsselaer; Didier Mutter; Anne M. Diemunsch; Roland Schaeffer; Gérard Teller; Alain Van Dorsselaer
UNLABELLED During prolonged laparoscopy, the diffusion of other gases in the carbon dioxide (CO(2)) pneumoperitoneum may lessen its safety. Nitrous oxide (N(2)O)/CO(2) gas mixtures may become hazardous with regard to gas embolization and fire risk. We therefore evaluated the kinetics of pneumoperitoneal intrusion of N(2)O. In five anesthetized domestic pigs, controlled ventilation, with an initial fraction of inspired oxygen = 1.0, was adjusted to keep ETCO(2) pressure between 35 and 45 mm Hg. The peritoneum was insufflated with CO(2) to a pressure of 12 mm Hg, which was maintained throughout the procedure. T0 was defined as the time when N(2)O was introduced in the breathing circuit (N(2)O end-tidal fraction = 66%). Gas samples (10 mL) from the pneumoperitoneum were analyzed every 10 min after T0. The N(2)O concentration was measured by using capillary gas chromatography coupled with mass spectrometry. Percentages of N(2)O in the CO(2) increased with time (t) according to the ideal equation: N(2)O((t)) = 66 (1 - exp(-0.005t)). In the peritoneal cavity, <2 h were required for the N(2)O to reach the concentration of 29%, which can support combustion. Eight hours to 10 h after T0, the intraperitoneal N(2)O fraction approaches the level of the N(2)O end-tidal fraction. Options to prevent accumulation of N(2)O are suggested. IMPLICATIONS Pig models were used to evaluate the time course of nitrous oxide (N(2)O) diffusion in the pneumoperitoneum during nitrous oxide/oxygen anesthesia. Although peritoneal N(2)O concentration approaches the end-expiratory value after 8-10 h, it reaches 29% within 2 h. At this level, N(2)O is known to support combustion. This N(2)O pollution should be prevented.
Transfusion | 2016
Abba C. Zubair; Klaus D. Torp; Quentin Eichbaum
T he liver is one of the most vascularized organs in the body. Liver transplant surgery may be associated with substantial blood loss necessitating “massive” blood transfusions in a patient population that frequently also has significant comorbidities. Managing inventories of blood products for large liver transplant programs can be challenging. This article outlines how the transfusion medicine services at Mayo Clinic Florida (MCF) and Vanderbilt University Medical Center (VUMC) support their liver transplant programs (Table 1). MCF and VUMC are among the largest liver transplant program centers in the United States. MCF and VUMC respectively performed 340 and 281 liver transplants between 2012 and 2014. The 10-year posttransplant patient survivals at MCF and VUMC were 93 and 94%, respectively, and our 1-year graft survivals were 90 and 91%. The median number of RBC units per case at MCF is 7 while at VUMC it is currently 6 RBC units per case. However, the range can be quite variable and this may add to the challenges of the blood bank. Common indications for liver transplant are outlined in Table 2. Multiorgan and retransplant surgeries are generally associated with increased blood product transfusion. The factors that influence blood utilization during surgery can be broadly classified into patient related and surgery related. The patient-related factors include patient demographics (age, sex, weight, disease), baseline hematocrit, platelets (PLTs), and coagulation profile. The surgery-related factors are primarily associated with surgical techniques but also include type of transplant and duration of surgery, volume expanders, and medications.
Revista Brasileira De Anestesiologia | 2018
Jimmy L. Moss; Benjamin W. Brown; Sher‐Lu L. Pai; Klaus D. Torp; Stephen Aniskevich
We describe an unusual case of hyperacute hepatic failure following general anesthesia in a patient receiving a simultaneous kidney-pancreas transplant. Despite an aggressive evaluation of structural, immunological, viral, and toxicological causes, a definitive cause could not be elucidated. The patient required a liver transplant and suffered a protracted hospital course. We discuss the potential causes of fulminant hepatic failure and the perioperative anesthesia management of her subsequent liver transplantation.
Anesthesia & Analgesia | 2007
Neil G. Feinglass; Steven R. Clendenen; Klaus D. Torp; R. Doris Wang; Ramon Castello; Roy A. Greengrass
Journal of Applied Physiology | 2001
Klaus D. Torp; Michael E. Tschakovsky; John R. Halliwill; Christopher T. Minson; Michael J. Joyner
Liver Transplantation | 2015
Prith Peiris; Sher Lu Pai; Stephen Aniskevich; Claudia C. Crawford; Klaus D. Torp; Beth L. Ladlie; Timothy S. Shine; C. Burcin Taner
SpringerPlus | 2015
Sher Lu Pai; Stephen Aniskevich; Neil G. Feinglass; Beth L. Ladlie; Claudia C. Crawford; Prith Peiris; Klaus D. Torp; Timothy S. Shine
Liver Transplantation | 2015
Prith Peiris; Sher Lu Pai; Stephen Aniskevich; Claudia C. Crawford; Klaus D. Torp; Beth L. Ladlie; Timothy S. Shine; C. Burcin Taner