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)

Small mesenteric arteries supplying partially isolated jejunal segments were totally occluded for 5 minutes and then released. With video microscopy, blood flow was calculated from measurements of submucosal arteriolar diameter and red blood cell velocity. For the first 30 minutes of reperfusion, the serosa was superfused with a Ringer's vehicle containing either adenosine (ADO; 10(-4) M), acetylcholine (ACh; 10(-5) M), or prostacyclin (PGI2; 3 x 10(-7) M). Thereafter, the substances were removed from the suffusate, and superfusion continued with vehicle alone for an additional 10-30 minutes. These concentrations were equieffective for causing vasodilation. During the first minute of reperfusion, blood flow increased more than 300% of baseline in all groups. Within the subsequent 30 minutes, blood flow fell to 45 +/- 3% of baseline with vehicle alone, which demonstrates the no-reflow phenomenon. While either ADO, ACh, or PGI2 was in the suffusate, vasodilation was persistent. After washout of these substances, the postocclusion blood flows were significantly higher with each treatment than with vehicle alone, which shows that each substance had a positive action. However, with ADO, blood flow was 121 +/- 7% of baseline after washout, whereas with ACh or PGI2, it was 64 +/- 10% or 69 +/- 5% of baseline after washout. This property of ADO was observed if the mucosa was superfused with a Ringer's solution or with a bile salt solution, which suggests that ADO might have similar properties in situ. After 60 minutes of reperfusion, the intestinal villi were short, thick, and edematous with epithelial necrosis and crypt degeneration. ADO attenuated most of these histological changes to a greater extent than either PGI2 or ACh. Furthermore, ADO reduced a biochemical index of neutrophil infiltration; tissue myeloperoxidase concentration was increased to 169 +/- 14% of baseline with vehicle but was increased to 120 +/- 8% with ADO. Overall, these observations suggest that ADO protects the intestine from ischemia-reperfusion injury by causing vasodilation and by inhibiting neutrophil function. The vasodilatory effect probably is a minor component because other vasodilators (ACh and PGI2) had minimal protective effects in these conditions.
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PMID:Attenuation of no-reflow phenomenon, neutrophil activation, and reperfusion injury in intestinal microcirculation by topical adenosine. 266 71

To compare the effects of hypoxia and ischemia on left ventricular (LV) diastolic function, we studied 17 isolated, isovolumic dog hearts by measuring LV diastolic chamber distensibility (LV end diastolic pressure at constant volume), wall thickness, and myocardial pH in response to hypoxia at constant coronary flow or pressure versus global ischemia (zero coronary blood flow). Hypoxic perfusates consisted of methemoglobin-containing red blood cells suspended in lactated Ringer's solution. Brief cross-clamping of the coronary perfusion line was used to assess the contribution of coronary turgor to chamber distensibility and wall thickness. With hypoxia, left ventricles showed a significant early (5 minutes) decrease in diastolic distensibility and an increase in wall thickness, at either constant coronary perfusion pressure or flow. The increase in wall thickness was independent of hypoxia-induced changes in coronary turgor. In contrast, global ischemia produced an early increase in LV diastolic chamber distensibility and a decrease in wall thickness. When global ischemia was continued beyond 60 minutes, a decrease in LV chamber distensibility developed. This diastolic contracture was not associated with an increase in LV wall thickness. Myocardial pH decreased slightly during 15 minutes of hypoxia and markedly with 15 minutes of global ischemia. Thus, LV diastolic chamber distensibility decreased during 15 minutes of hypoxia, while an increase in distensibility was seen during global ischemia of similar duration. During hypoxia, these changes were associated with increased LV wall thickness, at either constant coronary perfusion pressure or constant coronary flow. Prolonged ischemia led to diastolic contracture without an increase in wall thickness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative effects of hypoxia and ischemia in the isolated, blood-perfused dog heart: evaluation of left ventricular diastolic chamber distensibility and wall thickness. 290 95

The influence of dextrose administration on neurologic outcome after temporary spinal cord ischemia was examined in New Zealand white rabbits. Spinal cord ischemia was produced by infrarenal balloon occlusion of the aorta in unanesthetized animals. Animals were observed for 3 days for neurologic evaluation. Fasted animals received intravenous dextrose, 0.5 g.kg-1, or placebo before a period spinal cord ischemia. The dextrose was administered as either a bolus of a 50% solution (D50) 15 min before ischemia or as an infusion of a 5% solution (D5W) over 90 min before ischemia. With either mode of administration, preocclusion plasma glucose level was moderately increased as compared with that in animals that received lactated Ringer's solution in equivalent volume, i.e., for the D50 bolus: 291 +/- 82 (SD) versus 166 +/- 67 mg.dl-1 (P less than 0.005); and for D5W infusion: 177 +/- 38 versus 137 +/- 13 mg.dl-1 (P less than 0.01). With either mode of administration, neurologic outcome was poorer (P less than 0.025) at 72 h in the animals that had received dextrose. For example, of the 10 animals that received D5W by infusion, nine were paraplegic (unable to walk) 72 h after ischemia, whereas only three of 10 control animals were paraplegic. The adverse effect of an increased blood glucose level has been demonstrated previously for cerebral ischemia. The present results are the first demonstration that increased plasma glucose may result in a worsened neurologic outcome after spinal cord ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of dextrose administration on neurologic outcome after temporary spinal cord ischemia in the rabbit. 291 17

Perfusion of the coronary artery distal to an occluding angioplasty balloon was performed in 34 patients undergoing coronary angioplasty (PTCA). A randomized crossover study was employed using two exogenous substances as perfusates: lactated Ringer's solution (LR) and a fluorocarbon emulsion (FL), Fluosol-DA 20%. Both substances are electrolyte solutions, but the FL will dissolve more oxygen than the LR. During two attempted coronary artery occlusions of 90 seconds each, we perfused through the central lumen (guidewire channel) of the PTCA catheter at 60 ml/min. With FL perfusion the mean time to onset of angina after occlusion was delayed (41 +/- 21 vs 33 +/- 16 seconds, mean +/- SD; p less than 0.05), the mean duration of angina was shortened (77 +/- 58 vs 92 +/- 70 seconds, p less than 0.05), and the rise in the ST segment of the ECG was reduced (0.15 +/- 0.24 vs 0.2 +/- 0.23 mV, p less than 0.001) when compared to LR perfusion. Balloon occlusion time was able to be extended with FL perfusion (71 +/- 22 vs 59 +/- 22 seconds p less than 0.001). These results indicate that perfusion of the distal coronary artery is possible during PTCA and can reduce ischemia during a prolonged balloon occlusion time.
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PMID:Distal coronary artery perfusion during percutaneous transluminal coronary angioplasty. 293 68

In distant heart procurement, optimal storage conditions remain to be defined, especially with respect to the electrolytic concentrations of storage solutions. Between December 1986 and April 1987, heart transplants were carried out in 18 patients. After cardioplegic arrest (St. Thomas), the hearts were randomly stored in either Euro-Collins' solution (ECS; n = 9) or Ringer's solution (RS; n = 9) at 4 degrees C. For the first 24 h postsurgery, atrial pressures (LAP, RAP), systemic (MAP) and pulmonary pressures (PAP), and cardiac output (CO) were monitored. In addition, catecholamine and nitroglycerin requirements as well as the type of cardiac rhythm were documented. There was no significant difference between the groups in terms of the period of graft ischemia (ECS, 162 +/- 28 min; RS, 141 +/- 47 min); the MAP, RAP, LAP, and CO were also similar in both groups. The total amount of epinephrine needed to maintain the MAP between 60 and 80 mm Hg was 10.5 mg/24 h +/- 4.1 mg in ECS compared with 19.9 mg/24 h +/- 12 mg in RS (P less than 0.05). Despite less inotropic support, the left cardiac work index was considerably higher in the ECS group (P less than 0.05). In the first few postoperative hours, 8/9 RS patients needed either atrial (n = 4) or ventricular pacing (n = 4) for a heart rate of 90-100 beats/min (bpm), whereas only three ECS patients required atrial pacing (P less than 0.05). All other ECS hearts showed a spontaneous sinus rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distant heart procurement. Impacts of storage solution composition on cardiac performance following transplantation. 307 73

Intracellular pH (pHi) was measured with proton-sensitive liquid sensor microelectrodes in isolated Necturus antral mucosa, paying special attention to arranging experimental conditions to simulate conditions frequently associated with in vivo "stress ulceration." Intracellular pH in mucosas perfused under standard conditions (Ringer's solution containing HCO3-/CO2) was 7.22 + 0.02 (n = 27). Removal of Na+ and HCO3- or addition of amiloride or 4-acetamido-4-isothiocyanostillbene-2,2-disulfonic acid (blockers of Na+/H+ and Cl-/HCO3-exchangers) had no influence on steady-state pHi, suggesting that these ion exchangers do not significantly contribute to the maintenance of pHi in the presence of normal external pH. Acidification of mucosal (luminal) perfusate to pH 3 (mimicking the presence of gastric acid) had no influence on pHi, but mucosal pH 2 (10 mM HCl) acidified pHi to 6.93 +/- 0.07. Acidification of serosal (nutrient) perfusate to pH 6 (mimicking intramucosal acidosis caused by back-diffusion of luminal H+) acidified pHi to 6.72 +/- 0.10. Removal of Na+ from and addition of amiloride to the serosal perfusate during exposure to serosal pH 6.0 induced further acidification of pHi, suggesting that in this acidotic situation (with very low ambient HCO3- concentration) a Na+/H+ exchanger does contribute to the maintenance of steady-state pHi. Increased PCO2 (10% vol/vol in the gas) in a slightly acidic milieu (mimicking mucosal ischemia) likewise acidified pHi to 6.73 +/- 0.05. A combination of mucosal acid (pH 3), high PCO2 (10% CO2), and low serosal pH (pH 6) (mimicking conditions that prevail, for example, during hemorrhagic shock) acidified pHi and ultimately resulted in cell death. These derangements of intracellular acid-base balance may have pathogenetic importance also in in vivo stress ulceration.
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PMID:Intracellular pH in isolated Necturus antral mucosa in simulated ulcerogenic conditions. 316 88

To determine if moderate hyperglycemia produced by dextrose administration was detrimental in normothermic renal ischemia, 15 halothane-anesthetized mongrel dogs underwent right nephrectomy and 60 minutes of left renal artery and vein occlusion. Six dogs received 1 L of lactated Ringer's solution (LR) and six others received 1 L of 5% dextrose in lactated Ringer's solution (D5LR). Three sham-operated dogs received 1 L of D5LR and underwent right nephrectomy but no occlusions. All dogs received 500 mL of fluid before occlusion and 500 mL after occlusion. The blood glucose concentration for the LR group was 7.6 mmol/L (137 mg/dL) after 500 mL and 7.2 mmol/L (130 mg/dL) after 1000 mL. In the D5LR group, the blood glucose concentration was 21.5 mmol/L (387 mg/dL) after 500 mL and 20.2 mmol/L (363 mg/dL) after 1000 mL. In the sham-operated group, the blood glucose concentration was 22.8 mmol/L (410 mg/dL) after 500 mL and 20.7 mmol/L (373 mg/dL) after 1000 mL. At 30 hours, the plasma creatinine concentration rose from 70 to 300 mumol/L (0.8 to 3.4 mg/dL) in the LR group and from 90 to 500 mumol/L (1.0 to 5.8 mg/dL) in the D5LR group; the increase for the D5LR group was significantly greater than that for the LR group. In the sham-operated group, the plasma creatinine concentration was stable throughout the 30-hour period. This study demonstrates a significant detrimental effect of dextrose administration on renal function during normothermic ischemia.
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PMID:Dextrose administration exacerbates acute renal ischemic damage in anesthetized dogs. 359 69

This study examined the hypothesis that ethanol-induced alterations in cardiac function and regional blood flow impair recovery from shock after resuscitation. Blood ethanol levels 45 minutes after ethanol (3 gm/kg) was administered intrajejunally were 276 +/- 30 mg/100 ml (N = 14 dogs). Twelve dogs received saline solution and served as control animals. Elevated blood ethanol levels increased the rate of left ventricular pressure rise (+763 +/- 80 mm Hg X sec) and coronary blood flow (+0.77 +/- 0.18 ml X min X gm), decreased respiration, and caused a significant metabolic acidosis (arterial pH, 7.25 +/- 0.02; arterial lactate, 1.5 +/- 0.07 mmol/L). Two hours of hemorrhagic shock impaired cardiovascular function and regional blood flow to a similar extent in all dogs. Volume replacement (shed blood and lactated Ringer's solution, 50 ml/kg) transiently improved cardiac performance in the ethanol group. Two hours after volume replacement, a lower cardiac output, stroke volume, stroke work, myocardial oxygen efficiency, and persistent acidosis occurred in the intoxicated dogs (p less than 0.05) despite adequate coronary perfusion. Myocardial sensitivity to acidosis after shock may account for the reduced cardiac function in the ethanol group. However, it is possible that shock aggravated ethanol-induced pancreatic ischemia and contributed to impaired cardiocirculatory function in postinfusion shock.
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PMID:Ethanol impairs cardiocirculatory function in treated canine hemorrhagic shock. 373 72

Microcirculatory derangements in the pancreas associated with acute pancreatitis may contribute to a low-flow state and lead to pancreatic necrosis. This study investigated the effects of glucagon, a selective mesenteric arterial dilator, on pancreatic ischemia in canine bile-trypsin-induced pancreatitis (BTP). Measurements of cardiac Index (CI), total pancreatic blood flow (QP), pancreatic oxygen consumption (O2CP), and pancreatic arteriovenous shunt flow (QAVS) were obtained prior to and after inducing BTP. Bile-trypsin-induced pancreatitis was induced in 18 dogs. Nine received lactated Ringer's solution alone (LRPAN) at 6.5 mL/kg/hr, nine received lactated Ringer's solution plus continuous Intravenous (IV) glucagon hydrochloride (GLUPAN) at 1.0 micrograms/kg/min, and nine undergoing periportal dissection without BTP received IV glucagon (GLUCON). Following BTP, CI, QP, and O2CP decreased significantly and QAVS remained unchanged in crystalloid-treated animals (LRPAN). Glucagon administration (GLUPAN) transiently increased CI and QP but failed to improve O2CP and did not change QAVS. The decrease in O2CP observed after BTP in association with a constant QAVS suggests a metabolic block to oxygen uptake at the cellular level. Glucagon in pharmacologic doses does not reverse abnormalities in O2CP and is therefore of questionable physiologic benefit in the treatment of acute pancreatitis.
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PMID:Efficacy of pharmacologic glucagon in acute experimental pancreatitis. 397 Jun 71

Rats were implanted with 0.3-mm-diameter dialysis tubing through the hippocampus and subsequently perfused with Ringer's solution at a flow rate of 2 microliter/min. Samples of the perfusate representing the extracellular fluid were collected over 5-min periods and subsequently analyzed for contents of the amino acids glutamate, aspartate, glutamine, taurine, alanine, and serine. Samples were collected before, during, and after a 10-min period of transient complete cerebral ischemia. The extracellular contents of glutamate and aspartate were increased, respectively, eight- and threefold during the ischemic period; the taurine concentration also was increased 2.6-fold. During the same period the extracellular content of glutamine was significantly decreased (to 68% of the control value), whereas the concentrations of alanine and serine did not change significantly during the ischemic period. The concentrations of gamma-aminobutyric acid (GABA) were too low to be measured reliably. It is suggested that the large increase in the content of extracellular glutamate and aspartate in the hippocampus induced by the ischemia may be one of the causal factors in the damage to certain neurons observed after ischemia.
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PMID:Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis. 614 59


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