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

The clinical syndrome of "stroke" at first calls for a differentiation between the prognostic more unfavorable massive hemorrhage and the syndromes of cerebral hypoxia or ischemia. The ratio of hemorrhage to ischemia is about 1 to 5. Conclusions may already be drawn on the nature of the apoplectic insult from the clinical symptomatology. For example, the hemorrhagic insult in general begins with severe manifestations of neurological dysfunction such as hemiplegia and coma, while the symptoms of the ischemic insult frequently do not develop all of a sudden but in the course of hours, rarely from 1-2 days. Digitalisation in combination with dextran infusions is the method of choice in treating intermittent ischemias, particularly those provoked by hypertension. Rehabilitation, i.e. passive and active physical exercise, should be started as early as possible. In addition, particular importance must be attributed to prevention and especially to the early recognition of hypertension and of cardiac diseases as a socio-medical problem.
 ...
PMID:[Clinical picture and therapy of cerebral apoplexy]. 85 97

The role of arterial blood flow in hepatic metabolic functions was compared to that of portal flow in two groups of totally depancreatized dogs. Survival times and glucose and nitrogen excretion were significantly greater in dogs with ligation of the hepatic artery than in dogs with an Eck fistula. The dogs with ligated hepatic arteries also showed a significantly slower rise in plasma ketones. The course of diabetes was compared in three additional groups of partially depancreatized dogs consisting of a) dogs with ligated hepatic arteries, b) dogs with Eck fistulas, and c) controls. Hepatic arterial ischemia: 1) increased survival, without insulin treatment (a--650, b--167, c--124 days) 2) did not decrease tracer-determined rate of glucose production 3) led to a greater urinary excretion of glucose, ketone bodies and nitrogen than portal ischemia. Partially depancreatized dogs with either arterial or portal hepatic ischemia maintained a high rate of glucose disappearance on acute deprivation of endogenous insulin (clamping of vessels of their pancreatic remnant) due probably to decreased insulin degradation by the ischemic liver. The dogs died in coma after losing all fat depots. There was severe fatty change in the livers of dogs with hepatic artery ligation, slight in those with Eck fistulas and no fat in the livers of controls.
 ...
PMID:Effects of arterial or portal ischemia on survival and metabolism of partially and totally depancreatized dogs. 105 92

The 'chain-of-survival' concept has gained general acceptance in the care of cardiac arrest victims. Most standards and guidelines for cardiopulmonary resuscitation, however, focus on the initial links in the chain. We consider appropriate in-hospital care for the survivors a logical extension of the chain of survival. In recent years extensive research activity has probed the pathophysiology and pharmacology of postischemic reperfusion. The present review discusses the current understanding of mechanisms for cerebral damage following global ischemia. Promising pharmacological principles for protection or resuscitation from cerebral ischemia are reviewed. None of them are considered ready for clinical application. Clinical guidelines are proposed, based on the reviewed data and previously published clinical observations. Cornerstones of the proposed brain-oriented intensive care protocol are: (1) hemodynamic monitoring and meticulous treatment of circulatory disturbances, (2) controlled ventilation providing normoventilation and normoxia to all comatose patients, (3) avoiding hyperglycemia and hyperthermia in comatose patients, (4) adequate analgesia and sedation, tempered by the understanding that oversedation impedes neurological evaluation without promoting recovery. An accurate prognosis can usually be made 48-72 h after resuscitation. This permits reevaluation and assignment to an appropriate level of continued hospital care.
 ...
PMID:Brain-oriented intensive care after resuscitation from cardiac arrest. 829 Aug 16

Cerebral malaria is still a major cause of death in patients suffering from malaria. Much of the research work in the past two decades has been done to clarify the pathophysiology of cerebral malaria which hopes to improve the management of the disease and concomitantly reduce mortality. However, the pathogenesis of cerebral malaria is still not clear. The pathophysiology of coma is believed to be brain anoxia from ischemia due to sequestration of erythrocytes containing mature parasites in cerebral capillaries and venules. Three possible mechanisms of sequestration (cytoadherence, rosette formation and decreased deformability of the infected erythrocytes) are postulated. The management of cerebral malaria includes early diagnosis and early treatment with potent antimalarial drugs, early detection and treatment of complications, correction of fluid and electrolyte imbalance and proper nursing care. In spite of these efforts, a high mortality rate (ranging 10-40%) is still encountered.
 ...
PMID:Overview: pathophysiology and management of cerebral malaria. 136 63

A 46-year-old man underwent cosmetic facial surgery under general anesthesia. He was ventilated by mask with an oxygen-enriched gas mixture for 4 to 6 h and monitored by pulse oximetry. Despite adequate arterial saturation (SaO2 > 90 percent) throughout the procedure, he remained in a deep coma after termination of anesthesia. Initial arterial blood gas analysis revealed a pH of 6.60 and a PaCO2 of 375 mm Hg. The patient was intubated and placed on mechanical ventilation. As his respiratory acidosis resolved, he regained consciousness quickly and recovered without any neurologic deficits. This case of record extreme hypercapnia and review of the literature demonstrates that survival is possible in acute severe respiratory acidosis as long as tissue anoxia and ischemia are prevented. We discuss the tissue effects of acute hypercapnia and newer aspects of the nature of intracellular pH regulation in critical tissues that afford considerable tolerance to acidosis. The dependence of these mechanisms upon active ion transport underscores the importance of adequate tissue oxygenation and perfusion.
 ...
PMID:Resuscitation from severe acute hypercapnia. Determinants of tolerance and survival. 144 82

Numerous and extremely varied conditions (intense muscular activity, ischemia, metabolic and genetic disorders, infections, immunological diseases and toxic causes) may play a role in the genesis of non-traumatic rhabdomyolysis. Over the past years there has been an increased number of reports of forms due to drug or narcotic intoxication. Seven cases of rhabdomyolysis are reported in patients admitted to emergency wards in a state of coma due to heroin overdose (4 cases), cocaine overdose (1 case), carbamazepin (1 case), and tricyclic anti-depressives (1 case). In all cases it was possible to hypothesise a multifactorial pathogenesis of the disease in which other factors, such as acidosis, hypoxia, hypothermia and compression of the muscle mass during coma, were associated with the direct toxic damage caused by the drug. The most frequent complication was acute renal failure. One case of myocardial involvement with non-Q infarction characteristics was also observed.
 ...
PMID:[Rhabdomyolysis during acute poisoning with drugs and narcotics. Experience with 7 clinical cases]. 149 66

The role of cerebral ischemia in the pathophysiology of traumatic brain injury is unclear. Cerebral blood flow (CBF) measurements with 133Xe have thus far revealed ischemia in a substantial number of patients only when performed between 4 and 12 hours postinjury. But these studies cannot be performed sooner after injury, they cannot be done in patients with intracranial hematomas still in place, and they cannot detect focal ischemia. Therefore, the authors performed CBF measurements in 35 comatose head-injured patients using stable xenon-enhanced computerized tomography (CT), simultaneously with the initial CT scan (at a mean (+/- standard error of the mean) interval of 3.1 +/- 2.1 hours after injury). Seven patients with diffuse cerebral swelling had significantly lower flows in all brain regions measured as compared to patients without swelling or with focal contusions; in four of the seven, cerebral ischemia (CBF less than or equal to 18 ml/100 gm.min-1) was present. Acute intracranial hematomas were associated with decreased CBF and regional ischemia in the ipsilateral hemisphere, but did not disproportionately impair brain-stem blood flow. Overall, global or regional ischemia was found in 11 patients (31.4%). There was no correlation between the presence of hypoxia or hypertension before resuscitation and the occurrence of ischemia, neither could ischemia be attributed to low pCO2. Ischemia was significantly associated with early mortality (p less than 0.02), whereas normal or high CBF values were not predictive of favorable short-term outcome. These data support the hypothesis that ischemia is an important secondary injury mechanism after traumatic brain injury, and that trauma may share pathophysiological mechanisms with stroke in a large number of cases; this may have important implications for the use of hyperventilation and antihypertensive drugs in the acute management of severely head-injured patients, and may lead to testing of drugs that are effective or have shown promise in the treatment of ischemic stroke.
 ...
PMID:Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. 843 61

Clinical data on 10,451 high-dose (up to 0.84 mg/kg over 10 minutes) dipyridamole-echocardiography tests (DET) performed in 9,122 patients were prospectively collected from 33 echocardiographic laboratories, each contributing greater than 100 tests. All patients were studied for documented or suspected coronary artery disease (1,117 early [less than 18 days] after acute myocardial infarction and 293 had unstable angina). Significant side effects including major adverse reactions and minor but limiting side effects occurred in 113 patients (1.2%). Major adverse reactions occurred in 7 cases (0.07%). In 6 of these cases, adverse reactions were associated with echocardiographically assessed ischemia and included 1 prolonged cardiac asystole (complicated by acute myocardial infarction and coma, with death after 23 days), 1 short-lasting cardiac asystole, 2 myocardial infarctions, 1 pulmonary edema and 1 sustained ventricular tachycardia. In all 6 cases, the cardiologist-echocardiographer performing the study had a limited experience (less than 100 tests) with DET, and at off-line reading in 5 cases, the obvious echo-positivity preceded the onset of complications by 1 to 5 minutes. The only ischemia-independent major side effect was a short-lasting cardiac asystole that was reversed by aminophylline and atropine. Significant side effects associated with echocardiographically assessed ischemia occurred in 89 additional cases (21 with and 68 without concomitant echocardiographically assessed myocardial ischemia). The most frequent of these side effects was hypotension or bradycardia, or both, which occurred in 40 patients with negative and 6 with positive DET. In all cases, side effects promptly subsided after aminophylline. In 1,857 cases, the high dose was not given for echo-positivity before the eighth minute.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Safety of intravenous high-dose dipyridamole echocardiography. The Echo-Persantine International Cooperative Study Group. 162 16

Two benzodiazepine-receptor partial inverse agonists (Ro 15-4513, Ro 15-3505) and one benzodiazepine-receptor antagonist (flumazenil) were administered to rats with hepatic encephalopathy due to acute liver ischemia. Significant improvement (P less than 0.002) of both the clinical grade of hepatic encephalopathy and the electroencephalographic abnormalities was observed after administration of the benzodiazepine-receptor partial inverse agonists: comatose rats with no spontaneous righting reflex regained consciousness immediately after injection of the drug. Only slight improvement in clinical hepatic encephalopathy grade was seen after administration of 25 mg/kg of flumazenil. The present data strongly support a role of increased gamma-aminobutyric acid-ergic tone in the pathogenesis of acute hepatic encephalopathy and provide a rationale for trials of benzodiazepine-receptor partial inverse agonists to restore consciousness in hepatic encephalopathy in humans in the near future.
 ...
PMID:The effects of benzodiazepine-receptor antagonists and partial inverse agonists on acute hepatic encephalopathy in the rat. 165 Mar 20

Prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1 alpha were assayed in blood and cerebrospinal fluid samples from patients after subarachnoid hemorrhage (SAH) and from a control population. The levels found in samples obtained from patients after SAH were compared with those found in controls and were also correlated with a number of clinical and radiological variables, many of which are either significantly associated with or represent evidence of cerebral ischemia. The levels of prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1 alpha in blood samples from patients after SAH and from controls were below the level of sensitivity of the assays. Levels of prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1 alpha in cerebrospinal fluid from patients after SAH were significantly elevated when compared with those found in control samples. There was no significant correlation, however, between the level of each prostaglandin measured and the following variables: clinical grade on admission as assessed by the Glasgow Coma Score and the World Federation of Neurological Surgeons grading system; the amount of subarachnoid blood seen on computed tomographic scan; the occurrence of ischemic deterioration; the occurrence of low density change on computed tomographic scan; the presence of vasospasm on angiography; clinical outcome as assessed by the Glasgow Coma Score 3 months after the ictus; and the incidence of ischemia as a cause of death or disability as assessed 3 months after the ictus. A primary role for prostaglandins in the etiology of delayed cerebral ischemia after SAH is not therefore confirmed.
 ...
PMID:Role of prostaglandins in delayed cerebral ischemia after subarachnoid hemorrhage. 843 77


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>