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 development of metabolic acidosis during neonatal sepsis with group B streptococci (GBS) has been attributed to progressive tissue ischemia resulting from reduced oxygen delivery (QO2). Using an animal model of GBS disease, we attempted to test this hypothesis by comparing the development of metabolic acidosis in two groups of piglets with comparably diminished systemic QO2, one septic and one not. Eighteen anaesthetized piglets were instrumented to observe aortic pressure, cardiac output, arterial and mixed venous blood gases, oxygen content, and hemoglobin concentration. QO2, oxygen consumption, and oxygen extraction ratio were calculated. Six piglets (group 1) received continuous infusion of live GBS organisms; six piglets (group 2) received continuous infusion of phenylephrine (PE), beginning with 10-micrograms/kg/min and increasing as required to match the PE-induced reduction in QO2 to the fall observed in the group 1 (GBS) piglets at each 30-min interval. Group 3 piglets (n = 6) received 0.9% saline and served as controls. No differences in either cardiac output or QO2 were noted comparing GBS and PE piglets at any time interval from 0-180 minutes. At 120, 150, and 180 minutes, both QO2 and cardiac output were lower in GBS and PE piglets compared to controls. Despite equivalent reductions in cardiac output and QO2, only GBS piglets developed significant metabolic acidosis, while pH and base deficit for PE piglets did not differ from controls. Oxygen consumption did not differ significantly among the three experimental groups at any observation time. Oxygen extraction ratio did not differ comparing PE and GBS piglets at any observation time.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Oxygen delivery, oxygen consumption, and metabolic acidosis during group B streptococcal sepsis in piglets. 331 60

Superoxide dismutase (SOD) and catalase, natural scavengers of free oxygen radicals, or saline were administered as a continuous systemic infusion to 12 dogs, in a blind randomized fashion, starting 10 min prior to a 10-min episode of complete cerebral ischemia, and continued thereafter for 60 min. Reversible complete cerebral ischemia was achieved by simultaneously occluding the ascending aorta and venae cavae. There were no significant differences in physiological variables (arterial blood gases, hemoglobin, mean arterial blood pressure, heart rate, and temperature) between the two groups, either pre-ischemia or post-ischemia. There was no significant difference in neurologic outcome when evaluated at 48 h post-ischemia. It has previously been reported that the same dose of SOD and catalase as used in the current study could reduce infarct size by 50% when given systemically before reperfusion following coronary ischemia in dogs. The lack of a measurable effect on neurologic outcome in our cerebral ischemic model might be because of the failure of the free oxygen radical scavengers to reach the ischemic cells in sufficient amounts, or because free oxygen radicals do not contribute to brain injury following complete cerebral ischemia.
 ...
PMID:Superoxide dismutase and catalase failed to improve neurologic outcome after complete cerebral ischemia in the dog. 334 76

Blood flow and transcutaneous oxygen tension was measured by venous occlusion plethysmography and a transcutaneous oxygen electrode before and after 5 min of arterial occlusion in the forearm of young adult subjects with type I (insulin-dependent) diabetes without overt evidence of angiopathy. In control subjects (n = 21), the forearm blood flow increased by greater than or equal to 2.8-fold at 30 s after ischemia. Diabetic subjects with glycosylated hemoglobin (GHb) less than or equal to 9.5% (n = 15) exhibited a blood flow response that was not statistically different from normal control subjects. Diabetic subjects with GHb greater than or equal to 12.5% (n = 23) did not exhibit an increase in the postischemic blood flow. When blood flow patterns for the first 14 diabetic subjects were examined regardless of GHb value, four patterns of response were noted: 1) normal pattern (n = 3), 2) normal postischemic rise in blood flow with a prolonged elevation (n = 3), 3) no postischemic rise (n = 4), and 4) variable baseline blood flow with a decrease in blood flow postischemia (n = 4). This approach indicated that a comparison of means obscured potentially meaningful abnormal patterns. Abnormalities in the response of the transcutaneous oxygen tension to ischemia were observed in both groups of diabetic patients, but the difference between diabetic patients in good and poor control was less obvious. We have defined an abnormal response of blood flow and transcutaneous oxygen tension to ischemia that may correlate to glycemic control and have identified several patterns of blood flow after ischemia that may be important in defining the etiology and natural history of diabetic angiopathy.
 ...
PMID:Early detection of vascular dysfunction in type I diabetes. 337 62

Continuous (CW) and pulsed light were used for the noninvasive measurement of hemoglobin oxygenation in tissues. A dual wavelength method of continuous illumination spectroscopy used 760 nm (deoxyhemoglobin peak) and 800 nm (an oxyhemoglobin-deoxyhemoglobin isosbestic point) to measure the kinetics and extent of oxyhemoglobin deoxygenation in brains during mild ischemia/hypoxia. Absorption and scattering were modeled in an artificial milk/yeast blood system, which gave an exponential relationship between absorption and optical path length to a depth of 7 cm. Time-resolved spectroscopy (10-ps resolution) afforded a display of the times and distances of arrival of photons emitted by the cat brain in response to a 10-ps input pulse. The emitted photons rose to a peak in a fraction of a nanosecond and declined exponentially over a few nanoseconds. The half-time of exponential decay corresponds to photon migration over a distance of 4 cm. Exponential light emission continued for several more nanoseconds when the brain was encased by the skull, which plays a key role in prolonging light emission. The exponential decline of light intensity has a value [exp(-microL)], where L is the path length determined from the time/distance scale and mu is the characteristic of the migration of light in the brain. The factor mu is increased by increasing absorption, and mu' = epsilon C where epsilon and C are the Beer-Lambert parameters of extinction coefficient (epsilon) and concentration (C). Thus, deoxyhemoglobin can be quantified in brain tissues.
 ...
PMID:Comparison of time-resolved and -unresolved measurements of deoxyhemoglobin in brain. 339 26

The purpose of this study is to confirm previous evidence for reactive oxygen species (ROS) as critical mediators of postischemic renal injury by documenting lipid peroxidation after ischemic-hypoxic insults and by demonstrating that antioxidants confer protection. Renal malondialdehyde (MDA) concentrations, an index of lipid peroxidation, were measured using uncorrected and tissue-chromagen-corrected methods in 1) cortical (C), outer medullary stripe (OMS), inner medullary (IM) whole renal tissues, and C and OMS mitochondria obtained 15 min after in vivo renal artery occlusion (RAO; x 45 min); 2) C, OMS, and IM whole tissues obtained 15 min after completing 45 min of ischemia in an isolated perfused kidney; and 3) isolated proximal tubular cell (PTC) suspensions after 45 min of hypoxia with 15 min of reoxygenation. Despite significant oxygen deprivation-induced injury in each of these systems, no significant rise in MDA concentrations could be documented, with the sole exception of the in vivo IM region (by uncorrected MDA assay only). The latter rise could be attributed to medullary vascular congestion causing a hemoglobin-induced artifact in the MDA assay. Sixty-minute in vivo RAO plus reflow also did not raise MDA. To validate the MDA assay 4.2 mM H2O2 was added to PTC. An abrupt fourfold rise in MDA resulted. Pretreatment of 30- and 45-min RAO rats with two antioxidants (allopurinol or superoxide dismutase) failed to confer functional or morphological protection. We conclude that ROS may not be critical consistent mediators of in vivo postischemic acute renal failure.
 ...
PMID:Evidence against oxidant injury as a critical mediator of postischemic acute renal failure. 341 3

In ischemic acute renal failure oxygen free radicals may mediate injury. In addition, iron appears to play a critical role in hydroxyl radical formation and lipid peroxidation during reperfusion of ischemic kidneys. To determine whether iron may play a similar role in pigment (heme protein)-induced acute renal failure, we studied the effects of the iron chelator deferoxamine in two experimental models of pigment-induced acute renal failure, intramuscular glycerol injection and intravenous hemoglobin infusion without and with concurrent ischemia in the rat. Intramuscular injection of 50% glycerol (5 ml/kg) caused inulin clearance to fall to 0.13 +/- 0.03 (SE) ml/min (normal value, 1.0-1.2 ml/min). Continuous infusion of deferoxamine beginning at the time of glycerol injection significantly attenuated this renal dysfunction. Deferoxamine-treated animals had an inulin clearance of 0.37 +/- 0.06 ml/min (P less than 0.01). Glycerol injection was also associated with significant lipid peroxidation, measured as renal malondialdehyde content. Deferoxamine-treated glycerol-injected rats had renal malondialdehyde content not significantly different from control animals. In another model of heme pigment-induced renal injury, hemoglobin was infused to produce hemoglobinuria. Inulin clearance 1 h after hemoglobin infusion was significantly reduced to 0.84 +/- 0.5 ml/min (P less than 0.025). Infusion of deferoxamine after hemoglobin prevented the hemoglobin-induced decrease in inulin clearance. Thirty minutes of renal ischemia followed by infusion of hemoglobin resulted in more severe renal dysfunction with inulin clearance of 0.54 +/- 0.08 ml/min. Deferoxamine infused at the time of reperfusion attenuated the fall in glomerular filtration rate after ischemia and hemoglobin infusion:inulin clearance 1.04 +/- 0.07 (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hemoglobin- and myoglobin-induced acute renal failure in rats: role of iron in nephrotoxicity. 341 10

Twenty eight consecutive combined renal and pancreatic transplantations with enteric exocrine diversion were performed between June 1984 and May 1986. The one-year actuarial patient survival and renal and pancreatic graft survival were 90%, 67%, and 69%, respectively. Nineteen pancreatic grafts and eighteen renal grafts are currently functioning at 1-24 months. Of the pancreatic graft losses only 2 were attributable to nonimmunological complications. No pancreatic graft was lost due to pancreaticoenteric leakage or vascular thrombosis. This was achieved by reducing the cold ischemia time and by adopting an aggressive anticoagulant policy. In all patients with functioning grafts the fasting blood glucose, glycosylated hemoglobin level, and oral glucose tolerance test were normal. The intravenous glucose tolerance test was normal in most of the patients but subnormal in some.
 ...
PMID:Improved results in pancreatic transplantation by avoidance of nonimmunological graft failures. 355 60

Reflectance spectrophotometry in assessing gastroduodenal mucosal perfusion was evaluated. Ischemia without congestion, e.g., during hemorrhagic hypotension or celiac artery occlusion, was associated with a reduction in the indexes of mucosal hemoglobin concentration and of oxygen saturation. Ischemia with congestion, e.g., during portal vein occlusion, or in absolute ethanol or suction-induced mucosal lesions, was associated with an increase in the index of mucosal hemoglobin concentration but a reduction in the index of oxygen saturation. An increase in the index of mucosal hemoglobin concentration associated with a normal index of oxygen saturation was found in the postischemic hyperemia after release of celiac artery occlusion and during the sustained increase in corpus mucosal blood flow induced by vagus nerve stimulation. Thus reflectance spectrophotometric measurements reflected ischemia, without or with congestion, and hyperemia. Additionally, although regional differences in reflectance spectrophotometric measurements were demonstrated in the duodenal, antral, and corpus mucosa, such differences bore no consistent relationship to regional differences in blood flow demonstrated in previous studies.
 ...
PMID:Reflectance spectrophotometry for the assessment of gastroduodenal mucosal perfusion. 359 45

Cerebrovascular spasm in the cynomolgus monkey does not appear to be modified by nimodipine. It is possible that cerebral arteries from this species are unusually resistant to the action of calcium antagonists. To test this hypothesis, parallel studies on the in vitro response of cerebral arteries from monkey, dog, and man have been carried out. Rings of basilar or middle cerebral artery were tested with potassium chloride, noradrenaline, 5-hydroxytryptamine, prostaglandin F2 alpha, and hemoglobin. The responses were then reexamined in the presence of various concentrations of nimodipine. There is a significant variation among species in sensitivity to nimodipine, the vessels from the monkey being more resistant to nimodipine than those from other species. There is, as expected, a considerable difference in the ability of nimodipine to block the different agonists. Responses to potassium chloride are blocked by low concentrations of nimodipine in all species, whereas noradrenaline and 5-hydroxytryptamine are more resistant. It is noteworthy that, in all species tested, hemoglobin and prostaglandin F2 alpha were antagonized poorly even by higher concentrations of nimodipine. If these agonists play a major role in the development of vasospasm and subsequent delayed ischemia, it may be that the calcium antagonists exert a beneficial effect by some mechanism other than dilation of spastic arteries.
 ...
PMID:Effects of nimodipine on in vitro contractility of cerebral arteries of dog, monkey, and man. 373 87

Although the pathophysiologic manifestations of sickle cell disease have been assumed to result from microvascular occlusion consequent to in situ sickling of erythrocytes, actual blood vessel obstruction have been rarely demonstrated in vivo. Recent observations utilizing sophisticated biophysical techniques to study the intracellular hemoglobin S polymerization process has led to major revisions in this previously held pathophysiologic paradigm, but in vivo correlations are still lacking. With the development of new noninvasive imaging and para-imaging methods, it is now technically possible and feasible to characterize both regional organ perfusion and tissue biochemistry in quantitative terms. In addition, these modalities promise to clarify pathogenesis of the disease through definition of the events responsible for the progression from tissue ischemia and infarction through the resolution phase. Since these noninvasive techniques are amenable to sequential applications, they should facilitate objective evaluations of clinical trials of therapeutic agents designed to prevent or delay the vaso-occlusive manifestations of sickle cell disease.
 ...
PMID:Noninvasive techniques to evaluate the vaso-occlusive manifestations of sickle cell disease. 387 1


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