CLINICAL TRIALS PROFILE FOR ADRENALIN
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All Clinical Trials for Adrenalin
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00202358 ↗ | Perioperative Effect of Atenolol on Cytokine Profiles | Unknown status | Medtronic - MITG | Phase 4 | 2002-11-01 | Studies have shown that beta-blockers such as atenolol when given in the perioperative period reduce morbidity and mortality. One study showed that atenolol given just during the surgery period, seemed to improve outcomes up to 2 years later. This is hard to explain since beta-blockers act on the body by blocking the effects of adrenalin and thereby lowering heart rate and blood pressure. This study is designed to find out if perioperative atenolol might exert its long term effects through an anti-inflammatory mechanism rather than by lowering heart rate and blood pressure. It is known that inflammation increases after surgery as part of the healing process. However, it is also becoming clear that low-grade chronic inflammation can also lead to long term adverse effects. |
| NCT00202358 ↗ | Perioperative Effect of Atenolol on Cytokine Profiles | Unknown status | Saini Foundation | Phase 4 | 2002-11-01 | Studies have shown that beta-blockers such as atenolol when given in the perioperative period reduce morbidity and mortality. One study showed that atenolol given just during the surgery period, seemed to improve outcomes up to 2 years later. This is hard to explain since beta-blockers act on the body by blocking the effects of adrenalin and thereby lowering heart rate and blood pressure. This study is designed to find out if perioperative atenolol might exert its long term effects through an anti-inflammatory mechanism rather than by lowering heart rate and blood pressure. It is known that inflammation increases after surgery as part of the healing process. However, it is also becoming clear that low-grade chronic inflammation can also lead to long term adverse effects. |
| NCT00562627 ↗ | Efficacy of Multimodal Peri- and Intraarticular Drug Injections in Total Knee Arthroplasty | Completed | Asker & Baerum Hospital | Phase 4 | 2007-11-01 | Total knee arthroplasty (TKA) is associated with moderate to severe postoperative pain, causing patient discomfort, mobilisation and hospital discharge. The aim of this study is to: 1. Compare analgetic efficacy of to types of local infiltration analgesia in total knee arthroplasty. 2. Compare analgetic efficacy of local infiltration analgesia with continuous epidural analgesia. |
| NCT00622817 ↗ | The Influence of Inhaled Adrenalin Versus Decongestant as a Local Nasal Treatment in Bronchiolitis | Completed | Schneider Children's Medical Center, Israel | N/A | 2004-10-01 | This was a randomized, double blinded, controlled trial. The aim of the study was to compare xylometazoline HCL nasal drops to inhalation of epinephrine as a treatment for bronchiolitis. The study hypothesis is:xylometazoline HCL nasal drops treatment is good as epinephrine inhalation for treatment of bronchiolitis. Signed informed consent was obtained from a parent of each child. And the human ethics committee of our hospital approved the study according to the principles of the Declaration of Helsinki.(Approved - 2002) Patients: 65 infants who were admitted to Pediatric A- a general pediatric ward, in Schneider Children's Medical Center because of bronchiolitis during winter in two consecutive years 2004-2005. The inclusion criteria were: Full term previously healthy Infants, ages 1-12 months, after informed consent was signed with clinical presentation of mild to moderate bronchiolitis according to a clinical score .Exclusion criteria were as follows: prematurity, congenital lung or cardiac disease, infants who had past hospitalization due to respiratory illness and severe bronchiolitis (score>7 with a range scale 0-10). |
| NCT00678145 ↗ | Mechanisms of Hypoglycemia Associated Autonomic Failure | Active, not recruiting | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) | Phase 2 | 2008-03-01 | Intensive glucose control in type 1 diabetes mellitus (T1DM) is associated with clear health benefits (1). However, despite development of insulin analogs, pump/multi-dose treatment and continuous glucose monitoring, maintaining near-normal glycemia remains an elusive goal for most patients, in large part owing to the risk of hypoglycemia. T1DM patients are susceptible to hypoglycemia due to defective counterregulatory responses (CR) characterized by: 1) deficient glucagon release during impending/early hypoglycemia; 2) additional hypoglycemia-associated autonomic failure (HAAF) and exercise-associated autonomic failure (EAAF) that blunt the sympathoadrenal responses to hypoglycemia following repeated episodes of hypoglycemia or exercise as well as degrading other CR; and 3) hypoglycemia unawareness (HU), lowering the threshold for symptoms that trigger behavioral responses (e.g. eating). Thus, the risk of hypoglycemia in T1DM impedes ideal insulin treatment and leads to defaulting to suboptimal glycemic control (2). There are two approaches that could resolve this important clinical problem: 1) perfection of glucose sensing and insulin and glucagon delivery approaches (bioengineered or cell-based) that mimic normal islet function and precisely regulate glucose continuously, or 2) a drug to enhance or normalize the pattern of CR to hypoglycemia. Despite much research and important advances in the field, neither islet transplantation nor biosensor devices have emerged as viable long-term solutions for the majority of patients (3, 4). Over the past several years, our lab has explored the approach of enhancing CR by examining mechanisms responsible for HAAF/EAAF and searching for potential pharmacological methods to modulate the CR to hypoglycemia (5-11). Our work has led to a paradigm shift in the field of hypoglycemia, exemplified by the novel hypothesis and published experimental data supporting a role for opioid signaling that resulted in the initiation of exploratory clinical trials by other research groups. |
| NCT00678145 ↗ | Mechanisms of Hypoglycemia Associated Autonomic Failure | Active, not recruiting | National Institutes of Health (NIH) | Phase 2 | 2008-03-01 | Intensive glucose control in type 1 diabetes mellitus (T1DM) is associated with clear health benefits (1). However, despite development of insulin analogs, pump/multi-dose treatment and continuous glucose monitoring, maintaining near-normal glycemia remains an elusive goal for most patients, in large part owing to the risk of hypoglycemia. T1DM patients are susceptible to hypoglycemia due to defective counterregulatory responses (CR) characterized by: 1) deficient glucagon release during impending/early hypoglycemia; 2) additional hypoglycemia-associated autonomic failure (HAAF) and exercise-associated autonomic failure (EAAF) that blunt the sympathoadrenal responses to hypoglycemia following repeated episodes of hypoglycemia or exercise as well as degrading other CR; and 3) hypoglycemia unawareness (HU), lowering the threshold for symptoms that trigger behavioral responses (e.g. eating). Thus, the risk of hypoglycemia in T1DM impedes ideal insulin treatment and leads to defaulting to suboptimal glycemic control (2). There are two approaches that could resolve this important clinical problem: 1) perfection of glucose sensing and insulin and glucagon delivery approaches (bioengineered or cell-based) that mimic normal islet function and precisely regulate glucose continuously, or 2) a drug to enhance or normalize the pattern of CR to hypoglycemia. Despite much research and important advances in the field, neither islet transplantation nor biosensor devices have emerged as viable long-term solutions for the majority of patients (3, 4). Over the past several years, our lab has explored the approach of enhancing CR by examining mechanisms responsible for HAAF/EAAF and searching for potential pharmacological methods to modulate the CR to hypoglycemia (5-11). Our work has led to a paradigm shift in the field of hypoglycemia, exemplified by the novel hypothesis and published experimental data supporting a role for opioid signaling that resulted in the initiation of exploratory clinical trials by other research groups. |
| NCT00678145 ↗ | Mechanisms of Hypoglycemia Associated Autonomic Failure | Active, not recruiting | Albert Einstein College of Medicine | Phase 2 | 2008-03-01 | Intensive glucose control in type 1 diabetes mellitus (T1DM) is associated with clear health benefits (1). However, despite development of insulin analogs, pump/multi-dose treatment and continuous glucose monitoring, maintaining near-normal glycemia remains an elusive goal for most patients, in large part owing to the risk of hypoglycemia. T1DM patients are susceptible to hypoglycemia due to defective counterregulatory responses (CR) characterized by: 1) deficient glucagon release during impending/early hypoglycemia; 2) additional hypoglycemia-associated autonomic failure (HAAF) and exercise-associated autonomic failure (EAAF) that blunt the sympathoadrenal responses to hypoglycemia following repeated episodes of hypoglycemia or exercise as well as degrading other CR; and 3) hypoglycemia unawareness (HU), lowering the threshold for symptoms that trigger behavioral responses (e.g. eating). Thus, the risk of hypoglycemia in T1DM impedes ideal insulin treatment and leads to defaulting to suboptimal glycemic control (2). There are two approaches that could resolve this important clinical problem: 1) perfection of glucose sensing and insulin and glucagon delivery approaches (bioengineered or cell-based) that mimic normal islet function and precisely regulate glucose continuously, or 2) a drug to enhance or normalize the pattern of CR to hypoglycemia. Despite much research and important advances in the field, neither islet transplantation nor biosensor devices have emerged as viable long-term solutions for the majority of patients (3, 4). Over the past several years, our lab has explored the approach of enhancing CR by examining mechanisms responsible for HAAF/EAAF and searching for potential pharmacological methods to modulate the CR to hypoglycemia (5-11). Our work has led to a paradigm shift in the field of hypoglycemia, exemplified by the novel hypothesis and published experimental data supporting a role for opioid signaling that resulted in the initiation of exploratory clinical trials by other research groups. |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
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