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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured rat brain cortex PO2 (PtO2) with gold microelectrodes (tip diameter 5--10 micron) for up to 2 hours after 16 min of transient global brain ischemia with and without thiopental 90 mg/kg infused iv over 60 min beginning at 5 min postischemia. Seventeen rats were immobilized and mechanically ventilated on 1% halothane in oxygen with continuous monitoring of PtO2, ECG, end-expiratory CO2, rectal temperature, and arterial blood pressure. Global ischemia was induced by trimethaphan hypotension to an MAP of about 50 torr and a neck tourniquet inflated to 1500 torr. Postischemia, nine control rats (11 PtO2 measurements) were untreated and eight rats (8 PtO2 measurements) received thiopental 90 mg/kg. Preischemia, PtO2 values in both groups ranged from less than 5--70 torr with values of greatest frequency between 10 and 15 torr. Postischemia, PtO2 in control rats peaked at 45 +/- 8 (SEM) torr at 20 min. In thiopental treated rats, peak PtO2 was 24 +/- 6 torr at 10 min postischemia. Relative frequency histograms of PtO2 revealed that PtO2 in thiopental treated rats was lower (p less than 0.05) between 15 and 30 min postischemia. The magnitude of the decrease in PtO2 between 105 and 120 min postischemia appeared to correlate directly with the absolute preischemic value (i.e., the higher the preischemic PtO2, the greater the decrease in PtO2 postischemia). These results suggest that thiopental administered in large doses in early postischemia does not improve brain oxygenation secondary to a reduction in brain oxygen consumption. The relevance of the correlation between the magnitude of the fall in PtO2 postischemia and the magnitude of the preischemic value is discussed.
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PMID:Postischemic brain oxygenation with barbiturate therapy in rats. 3 43

In normothermic anesthetized cats complete cerebral circulatory arrest for one h was produced and followed by blood recirculation of the brain for 30 min to 4 h. Total and local blood flow of the brain, kidney, heart and liver were measured before and after ischemia using radioactive labelled microspheres. Before ischemia blood flow of the brain was 39.1 +/- 2.3 ml/100 g/min, of the kidney 307.2 +/- 28.3 ml/100 g/min, of the heart 241.1 +/- 32.5 ml/100 g/mmin and of the liver 87.8 +/- 25.6 ml/100 g/min (means +/- SEM). Regional flow rates within the brain varied between 35 and 51 ml/100 g/min. Reactive hyperemia was present in the brain 30 min after the beginning of recirculation following ischemia for 1 h. Local cerebral flow rates increased three to five times above the control flow, depending on the respective region. Mean cerebral blood flow returned to or slightly below normal, 2 to 4 h after ischemia, but there was considerable redistribution of flow rates within the brain. The filter capacity of the brain for microspheres of 15 mu and 50 mu diameter did not change after ischemia indicating that postischemic blood recirculation was not accompanied by an opening of arteriovenous shunts.
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PMID:Microsphere analysis of local cerebral and extracerebral blood flow after complete ischemia of the cat brain for one hour. 8 Dec 76

The amplitude and distribution of epicardial ST-segment elevation (ST) were examined for an 8-hour period after coronary occlusion in eight baboons and five pigs. ST was determined from unipolar epicardial electrograms obtained from a high-resolution matrix of fixed electrodes overlying a transmural region of ischemia. A relatively uniform degree of ST was observed overlying the ischemic region for 20 minutes after coronary occlusion. A gradient in ST from the periphery to the center of the ischemic region was documented after 20 minutes of ischemia. In 10 other pigs, change in the degree of ST was examined contingent on either an increase (five pigs) or decrease (five pigs) in the size of the ischemic region after 1 hour of preexisting ischemia. An abrupt increase in the number of electrodes that showed ST (NST) from 7.8 +/- 1.24 (SEM) to 14.8 +/- 1.35 (90%) was associated with an increase in mean ST of 58% from 4.28 +/- 0.61 mV to 6.78 +/- 0.84 (p less than 0.05). An abrupt decrease in NST from 25.2 +/- 2.63 to 14.6 +/- 2.22 (42%) was associated with a decrease in mean ST of 24%, from 8.2 +/- 0.36 mV to 6.3 +/- 0.30 mV (p less than 0.01). The results during early ischemia (less than 20 minutes of ischemia) are accurately represented by a model of ischemia in which injury current arises only at the ischemic boundary. The results during later ischemia (after 20 minutes of ischemia) may be represented by a model in which ST is considered dependent on injury currents generated throughout the ischemic region.
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PMID:Epicardial mapping and electrocardiographic models of myocardial ischemic injury. 11 30

First heart sound (S1) energy spectra in isovolumic systole, hemodynamics, and angiographic left ventricular wall motion (LVWM) at rest and with atrial pacing were compared in 27 patients who underwent diagnostic cardiac catheterization and angiography because of chest pain. Eighteen patients were found to have coronary artery disease (CAD) and nine patients, normal coronary arteries. Eleven of the 18 CAD patients (61%) had a mean reduction in the spectral energy of S1 of 6.5 +/- 1.4 (SEM) dB below control (-52%), during interruption of ischemic stress of rapid atrial pacing, compared to only one of nine patients without CAD (P less than 0.05). Only five CAD patients (28%) had an abnormal rise (greater than or equal to 5 mm) in left ventricular end-diastolic pressure (LVEDP) either during or upon interruption of pacing, and six (33%) had ischemic ST-segment depression greater than or equal to mv in the ECG. Similarly two patients free of CAD (22%) had an abnormal increase in LVEDP, and none had ECG evidence of ischemia. Seventeen CAD patients (94%) had segmental LVWM abnormalities at rest or with interruption of pacing, while three patients with normal coronary arteries (33%) had abnormal angiographic LVWM (P less than 0.01). Thus, reduction is S1 spectral energy is a common accompaniment of myocardial ischemia. In the present study, it was more frequently observed than abnormalities in either the ECG or LVEDP, but was not was consistently seen as segmental left ventricular wall motion abnormalities.
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PMID:Spectral energy of the first heart sound in acute myocardial ischemia. A correlation with electrocardiographic, hemodynamic, and wall motion abnormalities. 62 70

Ischemic brain damage can be partially ameliorated by barbiturate therapy applied postinsult. Catabolism-induced brain hyperosmolality during ischemia may contribute to the development of brain edema after restoration of circulation. To determine changes in brain osmolality during ischemia and the effect of barbiturate anesthetics in altering its course, we measured whole and regional (cerebral cortex, diencephalon-midbrain, and cerebellum) brain osmolality for up to 2 hours after decapitation ischemia in unanesthetized and pentobarbital anesthetized rats. Normal (nonischemic) brain osmolality in pentobarbital anesthetized rats was 319 +/- 2 mOsm/1 (mean +/- SEM) and higher than in unanesthetized rats (307 +/- 6 mOsm/1). The rate of increase in whole brain osmolality was 60% slower in pentobarbital anesthetized rats in the first 60 minutes of ischemia and regional brain osmolality increased by a maximum of 32 mOsm/1 compared to 45 mOsm/1 in unanesthetized rats. The potential for edema based on percent change in brain osmolality as well as the rapidity of the change was greater in unanesthetized rats. The significance of the increase in brain osmolality with barbiturate anesthesia and its attenuation of the rate and magnitude of increase during ischemia is discussed.
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PMID:Rat brain osmolality during barbiturate anesthesia and global brain ischemia. 64 23

Myocardial relaxation is an important energy-dependent process. Hypoxia, unlike ischemia, has not been shown to impair myocardial relaxation. This difference may be because (a) the traditional index to assess isometric muscle relaxation (half time to relaxation or RT((1/2))) reflects both changes in developed tension as well as relaxation and (b) the relaxation process is highly sensitive to temperature and previous papillary muscle studies have been conducted under hypothermic conditions. The present study examines the effect of hypoxia on the relaxation process of 31 isometrically contracting kitten papillary muscles at hypothermic (29 degrees C) and euthermic (38 degrees C) conditions using RT((1/2)), the peak rate of tension fall (-dT/dt) and -dT/dt normalized for tension ([peak -dT/dt]/T and max [-dT/dt per T]). Hypoxia at 29 degrees C resulted in a fall in RT((1/2)) from 278+/-11 (SEM) to 230+/-17 ms (P < 0.01) and no change in (peak -dT/dt)/T and max (-dT/dt per T). However, at 38 degrees C, hypoxia impaired relaxation as reflected in a prolongation of RT((1/2)) from 101+/-6 to 126+/-8 ms (P < 0.01) in spite of a substantial fall in peak tension. Moreover, (peak -dT/dt)/T decreased from -15.4+/-0.7 to -11.0+/-0.8/s (P < 0.01) and max (-dT/dt per T) decreased from -25.1+/-1.8 to -13.8+/-0.9/s (P < 0.01). In conclusion, the present study demonstrates that hypoxia impairs the relaxation process of cardiac muscle.
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PMID:Effect of hypoxia on myocardial relaxation in isometric cat papillary muscle. 65 89

Despite revascularization of the common femoral--profunda femoris system, many patients fail to obtain satisfactory relief from claudication or rest pain. Clinical observations were compared with objective physiological data in 54 technically successful aortoiliofemoral reconstructions for multilevel disease. Nine of 28 operations (32%) for claudication and five of 26 operations (19%) for ischemia at rest had poor results. While the average ankle pressure index (API = ankle blood pressure/arm blood pressure) rose from 0.52 +/- 0.03 (SEM) to 0.81 +/- 0.03 in limbs treated successfully for claudication, it changed insignificantly in those with an unsuccessful result (0.58 +/- 0.04 to 0.61 +/- 0.04). When ischemic symptoms were relieved, API rose from 0.23 +/- 0.04 to 0.55 +/- 0.03 but increased only from 0.22 +/- 0.09 to 0.40 +/- 0.02 in limbs with insufficient improvement. Preoperative thigh pressure index (TPI) in claudicating limbs with poor results (0.96 +/- 0.05) differed little from that in limbs with good results (0.92 +/- 0.05); nor was the TPI of ischemic limbs with poor results (0.83 +/- 0.13) significantly greater than that in limbs with good results (0.60 +/- 0.05). Neither the TPI nor the thigh to ankle pressure gradient was of value in predicting which extremities would respond poorly to aortoiliofemoral reconstruction.
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PMID:Aortoiliac reconstruction in patients with combined iliac and superficial femoral arterial occlusion. 68 26

This study examines the significance of epicardial Q waves as a marker of myocardial cell necrosis. Ischaemia was produced in dogs by two methods: coronary artery occlusion sustained for 24 h (Group 1) and occlusion for 1 h followed by reperfusion (Group 2). Q waves did not appear until after 3 h of sustained occlusion, but were present within 40 min of reperfusion. In both groups, Q waves were not transient but persisted for at least 24 h. CPK levels were determined at 24 h in specimens from each lead site. In Group 1, Q sites had 66.6 +/- 5.9% (mean +/- SEM) less CPK than R wave sites (P less than 0.005). In Group 2, Q sites had only 28.2 +/- 4.5% less CPK than R sites. These results suggest that the extent of necrosis was greater at Q sites with sustained occlusion than with reperfusion. A similar relationship existed for the levels of ATP and CP determined at Q and R sites at 24 h. Histological examination by light and electron microscopy confirmed that in both groups, Q sites corresponded to areas of necrosis, while R sites indicated normal myocardium. However, the type of necrosis depended on the pathogenesis. Our results demonstrated that epicardial Q waves were a reliable marker of cell death, but that the morphological picture and extent of cell death depended on the mechanism and manner of injury. These conclusions were tested in a final series (Group 3) in which propranolol was given before and with release of the occlusion (0.5 mg.kg-1 at each time). In 47 sites at risk, in five dogs only two Q waves appeared. In each of these two, cell death was confirmed by evidence of CPK depletion and morphological alteration. In the remaining sites, no CPK depletion occurred. Histological examination revealed only infrequent small islands of subendocardial necrosis. The results confirm the validity of the epicardial electrocardiographic findings and illustrate the role of propranolol in preventing reperfusion necrosis.
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PMID:Significance of epicardial Q waves as an acute marker of myocardial necrosis in dogs. 69 89

To evaluate the biological tolerance of the human liver to prolonged warm ischemia, two groups of extensive hepatic resection for tumor were compared. Group 1 (11 patients) performed with short hepatic inflow occlusion (7 [mean] +/- 2 [SEM] minutes), and group 2 (nine patients) operated with use of complete hepatic vascular exclusion and prolonged warm liver ischemia (38 [mean] +/- 5 [SEM] minutes). Comparison of biological values, such as transaminase, bilirubin, total protein, albumin, and fibrinogen levels, the platelet count, prothrombin complex, and proaccelerin level, did not show statistically significant differences between the two groups. Therefore, the hepatic warm ischemia period may be, if needed, safely extended beyond the classical 15 minutes. It lasted 65 minutes in one case without adverse effect. These clinical observations parallel recent experimental work and should destroy the myth of the high sensitivity of the liver to warm ischemia.
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PMID:Tolerance of the human liver to prolonged normothermic ischemia. A biological study of 20 patients submitted to extensive hepatectomy. 73 77

Renal phospholipid metabolism was studied after ischemia was induced by occlusion of the left renal artery in the rat. There was no change in the rate of cellular [14C]choline uptake after 25 or 60 minutes of ischemia. However, [14C]choline incorporation into phospholipid was two to three times greater in slices from the ischemic kidney than in slices from the contralateral control kidney. The increase occurred after 25 minutes of ischemia plus 15 minutes of reflow, and after 60 minutes of ischemia with or without reflow. When [14C]choline was injected into rats after a 60-minute period of renal ischemia, the rate of incorporation into phospholipid in the ischemic kidney was almost twice that of the control kidney. These results were similar to those of the in vitro experiments. Since virtually all of the cellular phospholipids of the kidney are present in cellular membranes, renal ischemia affects membrane metabolism. The mean distribution ratio of alpha-aminoisobutyric acid in slices of kidneys ischemic for 60 minutes was similar to that of control slices: 4.11 +/- 0.2 (SEM) vs. 4.30 +/- 0.30. The normal uptake of alpha-aminoisobutyric acid indicates that the increased incorporation of choline is associated with functional integrity of the membrane.
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PMID:Choline uptake into renal phospholipids following renal ischemia in rats. 75 33


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