Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study determined if hyperglycemia: (1) augments ischemic cerebral cortical lactate accumulation during complete cerebral ischemia; and (2) exacerbates subsequent neurologic morbidity and mortality. Dextrose (D5W, n = 8) or normal saline (n = 6) was administered i.v. prior to 10 min of global cerebral ischemia induced by normothermic cardiac arrest in dogs. Before arrest plasma glucose was significantly higher in the D5W-treated group than saline-infused (407 +/- 31 vs. 11 9 +/- 20 mg/dl, P less than 0.05). By 6 h post-arrest, seven of eight D5W-infused dogs died, compared to one of six saline-infused dogs (P = 0.002). D5W-infused dogs showed significantly greater neurologic deficit at 2, 6, and 12 h post-arrest. In a complementary protocol, dogs were pretreated in the same manner, however, six cerebral cortical brain biopsies were taken before, during, and immediately after cardiac arrest. Plasma glucose was 320 +/- 17 mg/dl in the D5W-infused dogs and lower (P less than 0.001), 140 +/- 5 mg/dl, in the saline-infused group. Cerebral cortical lactate accumulation was slightly but significantly greater during ischemia and early reperfusion in animals receiving dextrose. Neither plasma nor cerebrospinal fluid (CSF) creatine kinase isoenzymes nor plasma or CSF lactate concentrations, measured during and for 25 min after cardiac arrest, served as a good prognostic indicator of 24 h neurologic morbidity or mortality. Therefore, induction of complete cerebral ischemia in the presence of moderate hyperglycemia is associated with profound neurologic dysfunction and striking mortality. A qualitative but not quantitative increase in brain lactate accumulation is consistent with the hypothesis that lactate may contribute to the increased severity of neurologic dysfunction with hyperglycemia.
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PMID:Elevated brain lactate accumulation and increased neurologic deficit are associated with modest hyperglycemia in global brain ischemia. 216 49

For no organ is the need more acute than for the lung or heart-lung block. The new improved "freezing" technique with simultaneous use of intravenous prostaglandin E1 will result in reliable and adequate heart-lung block preservation. The lungs are flushed with high-volume (60 ml/kg), low-pressure (less than 20 mmHg), low-flow (15 ml/kg/min), using modified Euro-Collins solution (added 12 Meq/L of MgSO4 and 65 ml/L of 50% Dextrose). Additional topical cooling has been achieved by cold Physiosol and the excised graft is then placed in a plastic bag filled with Physiosol. This static hypothermia has been successfully used with extended ischemia times of more than six hours in primates and almost four hours in man. Forty heart-lung transplantations have been done from March 1981 to September 1986 and nine of them have been performed using this "freezing" technique with prostaglandin E1. Distant graft procurement has been used twice for heart-lung transplantation. All nine most recent patients who have received the graft harvested with this new "freezing" technique are doing well.
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PMID:Intravenous prostaglandin E1, cold crystalloid flush and topical hypothermia for cardiopulmonary graft preservation. 329 33

Atrial natriuretic factor (ANF) has been demonstrated to be effective in the treatment of acute renal failure (ARF) in both rat and humans. The biological effects of ANF are presumed to be mediated by the generation of intracellular 3',5'-cyclic guanosine monophosphate (cGMP). Therefore, the current investigation examined whether zaprinast (M&B 22948), a guanosine 3',5'-cyclic monophosphate (cGMP)-specific phosphodiesterase inhibitor, would be effective in the treatment of established acute renal failure in the rat. Acute renal failure was induced by 60 minutes of bilateral renal artery clamping. Twenty-four hours after the ischemic insult, rats received either vehicle (5% Dextrose), zaprinast (0.03 or 0.3 mg/kg/min) or ANF24 (0.2 micrograms/kg/min) intravenously for four hours. Renal function, as measured by daily serum creatinine (days 1 to 7) and day 2 inulin clearances, was dramatically improved by zaprinast but not ANF treatment. Forty-eight hours post-renal ischemia, glomerular filtration rate (GFR) was 0.14 +/- 0.04 (ml/min/100 g body wt) in the vehicle and 0.94 +/- 0.29 in the zaprinast treated animals. To evaluate the mechanism by which zaprinast accelerated renal recovery, we measured regional blood flow in the postischemic rat kidneys during drug treatment with a laser doppler flowmeter. Both high and low dose zaprinast significantly increased cortical (17%) and outer medullary blood flow (40% and 60%), an effect not seen with ANF. In summary, zaprinast is effective in the treatment of established ischemic ARF. The mechanism by which zaprinast accelerates renal recovery is due to its unique ability to stimulate regional renal blood flow and increase intracellular cGMP in the setting of tissue ischemia.
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PMID:Zaprinast accelerates recovery from established acute renal failure in the rat. 764 25

Since the 1985 Emergency Cardiac Care Conference, numerous controversies about the pharmacology of CPR have arisen (eg, questions about the pharmacokinetics and pharmacodynamics of drugs during CPR, the optimal vehicle for delivery of medications, and the dose of atropine in brady-asystolic cardiac arrest). This article has three objectives: 1) to critically explore these controversies, 2) to provide recommendations for clinical practice, and 3) to identify areas for future study. The ideal route is one which combines rapid access with quick delivery of drug to the central circulation. Because of hemodynamic changes during CPR, administration of drugs into the central circulation is preferable when compared with peripheral venous injection. Whenever drugs are administered from a peripheral i.v. site, the extremity should be elevated, and a 20-mL bolus of i.v. fluid should be given to facilitate access of the agent to the central circulation. If there is a delay in obtaining venous access, epinephrine, lidocaine, and atropine may be administered through the endotracheal tube at 2.5 times the i.v. dose. When administering these drugs through the endotracheal tube, dilute the drug in 10 mL of saline or water and inject it through a long catheter beyond the tip of the endotracheal tube. Dextrose 5% water is the primary vehicle for drug delivery during CPR. However, the administration of glucose during CPR is controversial because of the potentially detrimental effects of hyperglycemia on neuronal function during periods of ischemia. Data are inconclusive regarding the effects of glucose levels on neurologic outcome following resuscitation. Hyperglycemia may be a marker for prolonged resuscitation with subsequent impairment in insulin release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacologic controversies in CPR. 843 31