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  • 1
    ISSN: 1435-1803
    Keywords: acute myocardial ischemia ; collateral blood flow ; border zone ; nifedipine ; dog
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In open-chest dogs (n=5) the effects of nifedipine (25 ⧎g/kg infused over a period of 15 min) on the collateral blood flow after left anterior descending coronary artery (LAD) ligation were separated from those on heterogeneous blood supply, i.e. flow of collateral origin plus flow in nonischemic myocardium projecting into the ischemic area. This separation was possible using a technique based on microspheres, allowing analysis of perfusion via the left anterior descending coronary artery (LAD). Secondary effects on the ischemic heart induced by the hypotensive effect of nifedipine per se were minimized by counterbalancing the blood pressure change with an intra-aortic balloon. Nifedipine increased non-ischemic myocardial blood flow in the subendocardium from 1.11±0.10 to 2.71±0.17 (p〈0.001) and in the subepicardium from 1.12±0.08 to 3.95±0.49 (p〈0.001) (ml/min/g, mean ±SE). Collateral blood flow in the centre of the ischemic area was not affected by nifedipine. In the subendocardium, it was 0.12±0.05 before and 0.09±0.09 after nifedipine, and in the subepicardium, the corresponding values were 0.21±0.10 and 0.29±0.04, respectively. At the lateral ischemic border, the nifedipine-induced increase in myocardial blood flow was only directed to the admixed normal tissue. When the blood flow was corrected for this overlapping non-ischemic tissue, no significant effect of nifedipine was measurable in the subendocardial blood flow, which was 0.12±0.03 before and 0.18±0.04 ml/min/g after drug administration. However, in the subepicardium, the collateral blood flow was significantly reduced from 0.33±0.09 to 0.15±0.05 (p〈0.05). It is concluded that nifedipine was able to decrease collateral blood flow at the lateral border, while leaving the blood flow unaffected in the centre of the ischemic are.
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  • 2
    ISSN: 1435-1803
    Keywords: acute ischemia ; collateral blood flow ; border zone ; pig ; dog
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Residual blood flow in pigs (n=8) and dogs (n=11) was measured by tracer microspheres (58Sr) 1 hour after occlusion of the left anterior descending coronary artery (LAD). Collateral blood flow was distinguished from overlap flow, defined as the blood flow of non-ischemic myocardium interdigitating into the ischemic area, by direct LAD injection of isotope-labelled microspheres (125I) prior to ligation. In the center of the acutely ischemic pig myocardium the residual blood flow, i.e., the myocardial perfusion remaining after LAD occlusion, was 0.01±0.01 ml/min/g subendocardially and 0.02±0.01 ml/min/g subepicardially, as estimated with85Sr-labelled microspheres. These values were significantly lower than the corresponding values for the dog, 0.13±0.05 ml/min/kg (p〈0.05) subendocardially and 0.28±0.08 ml/min/g (p〈0.01) subepicardially. In the lateral aspects of the ischemic area, calculations of overlap flow were made with the aid of the distribution of the microspheres injected into the LAD. Values of the residual blood flow were normalized and nonischemic myocardial perfusion was set to 100 units. In subepicardial layers of the myocardium with calculated overlap flows corresponding to 20, 50 or 80 units, respectively, the residual blood flow (overlap flow + collateral flow) actually measured in the pig was 31±4 55±4 and 75±7 units and in the dog 65±6, 79±5 and 91±2 units. The values for the dog were significantly different from the respective value for the pig (p〈0.01). In the subendocardial layers the difference between the two species regarding residual blood flow was similar, although the difference was statistically significant only for myocardium with a calculated overlap flow of 80 units. When the calculated overlap flow was subtracted from the measured residual blood flow, the collateral blood flow was found to be extensive in the dog and virtually absent in the pig. When, in the dog, the collateral blood flow across the lateral border of the ischemic area was related to the amount of myocardium it supplies, it was found to be homogeneously distributed. Thus neither subendocardially nor subepicardially could a gradient of collateral blood flow be detected. It is concluded that in the pig the collateral blood flow is almost nil throughout the acutely ischemic myocardium, both in subendocardial and subepicardial layers. In contrast, the dog has an extensive collateral flow. No lateral gradient of this collateral blood flow could, however, be detected.
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  • 3
    ISSN: 1435-1803
    Keywords: Ischemiareperfusion ; superoxidedismutase ; catalase (SOD) ; contractilefunction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Earlier studies have demonstrated an improvement in the recovery of the regional myocardial function after reversible myocardial ischemia when dogs were treated with superoxide dismutase (SOD) + catalase (CAT). In all these studies, drug administration was started prior to the ischemic period. The aim of this study was to investigate the effects of SOD and CAT on the recovery of the regional contractile function in anesthetized beagle dogs when the drugs were administered at the time of reperfusion. The animals were subjected to 20 min of left coronary artery occlusion followed by 3 h reperfusion. The regional myocardial contractile function, measured as subendocardial segment shortening (SS, sonomicrometry) decreased to below zero and the regional blood flow in the ischemic subendocardium was reduced to about 5 % of pre-ischemic values during the coronary artery occlusion period. The size of the occluded bed was similar in the two groups. Saline (n = 8) or SOD (10 mg/kg) + CAT (3.4 mg/kg) (n = 8) were infused into the left atrium from 2.5 min prior to until 20 min after the start of reperfusion. The peak plasma level of SOD was 102 ± 15 mg/1 at 20 min reperfusion. There were no significant differences in the arterial blood pressure, cardiac contractile function and regional blood flow between the two groups at any time during the experiment. During reperfusion in the dogs given vehicle, SS recovered to 48 ± 7 % (mean ± SEM) after the first hour of reperfusion, and to 51 ± 6 % of pre-ischemic values after 3 h of reperfusion. The corresponding values in SOD + CAT treated dogs were 50 ± 5 % (1 h) and 53 ± 8 % (3 h), respectively. It is concluded that SOD + CAT, when given at the time of reperfusion, did not improve the regional contractile function after reversible ischemia in the anesthetized beagle dog.
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  • 4
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Hyperthermia ; Heat stress ; Brain edema ; Nitric oxide synthase ; Heme oxygenase ; Oxidative stress ; H-290/51 ; Cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Influence of a new anti-oxidant compound H-290/51 on expression of nitric oxide synthase (NOS) and heme oxygenase (HO) enzymes responsible for nitric oxide (NO) and carbon monoxide (CO) production, respectively was examined in the CNS following heat stress in relation to cell injury. Exposure of rats to 4 h heat stress at 38°C in a biological oxygen demand (BOD) incubator (relative humidity 50–55%, wind velocity 20–25 cm/sec) resulted in profound edema and cell injury in many parts of the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus and brain stem. Immunostaining of constitutive isoforms of neuronal NOS (nNOS) and HO-2 revealed marked upregulation in damaged and distorted neurons located within the edematous brain regions. Pretreatment with H-290/51 (50 mg/kg, p.o., 30 min before heat stress) significantly reduced the edematous swelling and cell injury and resulted in a marked attenuation of nNOS and HO-2 expression. These observations suggest that upregulation of NOS and HO is associated with cell injury, and the antioxidant compound H-290/51 is neuroprotective in heat stress.
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  • 5
    ISSN: 1438-2199
    Keywords: Heat stress ; Nitric oxide ; Cell injury ; Antioxidant ; H-290/51Blood-brain barrier ; Brain edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that nitric oxide (NO) is involved in the pathophysiology of brain injury caused by heat stress (HS) was examined using neuronal nitric oxide synthase (NOS) immunohistochemistry in a rat model. In addition, to find out a role of oxidative stress in NOS upregulation and cell injury, the effect of a new antioxidant compound H-290/51 (Astra Hässle, Mälndal, Sweden) was examined in this model. Subjection of conscious young rats to 4 h HS in a biological oxygen demand (BOD) incubator at 38°C resulted in a marked upregulation of NOS in many brain regions compared to control rats kept at room temperature (21 ± 1°C. This NOS immunoreactivity was found mainly in distorted neurons located in the edematous regions not normally showing NOS activity. Breakdown of the blood-brain barrier (BBB) permeability, increase in brain water content and marked neuronal, glial and myelin reaction were common findings in several brain regions exhibiting upregulation of NOS activity. Pretreatment with H-290/51 significantly attenuated the upregulation of NOS in rats subjected to HS. In these animals breakdown of the BBB permeability, edema and cell changes were considerably reduced. Our results suggest that hyperthermic brain injury is associated with a marked upregulation of NOS activity in the CNS and this upregulation of NOS and concomitant cell injury can be reduced by prior treatment with an antioxidant compound H 290/51. These observations indicate that oxidative stress seems to be an important endogenous signals for NOS upregulation and cell reaction in hyperthermic brain injury.
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  • 6
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The regional distribution of flow was studied at different times after the onset of reperfusion in isolated rat heart preparations. The hearts were submitted to 30 min of global ischaemia followed by 60 min of reperfusion. Microspheres labelled with various nuclides were added to the perfusate before ischaemia and 1, 5, 20, and 60 min after the onset of reperfusion.2. One minute after the start of reperfusion, the flow to the left ventricular inner layer was restricted to 0.5 ± 0.2 mL/min per g (2–3% of the pre-ischaemic flow). In this segment, the perfusion remained at the same low level during the entire reperfusion period studied. At the onset of reperfusion the flow to the outer layer of the left ventricle was 4.8 ± 1.7 mL/min per g (37% of the pre-ischaemic flow), and 3.0 ± 1.3 mL/min per g (27% of the pre-ischaemic value) to the free wall of the right ventricle. The flow was progressively reduced in the outer layer of the left ventricle in the course of reperfusion. After 60 min of reperfusion the flow to the left ventricular outer layer was 2.5 ± 0.9 mL/min per g (19% of pre-ischaemic flow when compared with the onset of reperfusion [P 〈 0.05]).3. It is concluded that a ‘no-reflow’ condition develops very early during reperfusion and becomes more marked during this period.
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