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)

The effect of intermittent coronary sinus occlusion (ICSO) with a balloon-tipped catheter on coronary arterial flow and coronary sinus pressure (CSP) dynamics were studied in open-chest dogs. During coronary sinus occlusion (CSO), CSP gradually rose and finally reached a plateau, while left coronary arterial mean flow velocities decreased. After the release of CSO, CSP immediately returned to baseline values, and the flow velocities correspondingly increased over the baseline values (hyperemic response). The decrease in ratios of flow velocities during CSO were unrelated to the duration of CSO, whereas hyperemic responses were positively correlated with the CSO duration. In the repetitive application of CSO (ICSO), inadequately short duration of release period decreased the net volume of coronary arterial flow significantly. Moreover, hyperemic responses were abolished by maximal coronary vasodilation with intravenous adenosine, augmented by combination with coronary sinus retroperfusion and reduced by coronary arterial ischemia. These findings indicate the presence of a compensatory regulating mechanism in the coronary circulation during ICSO. We should attach much importance to this mechanism for the effectiveness of ICSO. To be accurate, the changes in coronary arterial flow as well as CSP dynamics should be considered when choosing adequate occlusion-release intervals of ICSO.
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PMID:The effect of intermittent coronary sinus occlusion on coronary sinus pressure dynamics and coronary arterial flow. 155 54

We studied brain retroperfusion in nine adult baboons. Experiments in four baboons determined techniques and the safety of retroperfusion, and experiments in three baboons determined the ability of retroperfusion to reverse cerebral ischemia. Two baboons died before retroperfusion. Arterial blood was continuously circulated by an external pumping system from one femoral artery into the intracranial sinuses through specially designed balloon-tipped catheters placed percutaneously into the sigmoid sinuses bilaterally. The balloons intermittently occluded the sinuses. Ischemia was produced by occluding the left middle cerebral artery. Standard and computed electroencephalography with topographic mapping monitored the onset and reversal of ischemia. Retroperfusion rate exceeded 50 ml/min with a mean intrasinus pressure increase of 27 (0-149) mm Hg in all seven experiments. Venograms demonstrated complete or partial filling of the superior sagittal sinus in each experiment. Four experiments without ischemia established maximal balloon occlusion cycles, retroperfusion rates, and sinus pressure changes. These four baboons were neurologically normal after retroperfusion; two had normal magnetic resonance imaging scans. Ischemic changes, detected by electroencephalography following middle cerebral artery occlusion, were reversed with retroperfusion in all three ischemia experiments. Autopsies in the seven baboons demonstrated no parenchymal hemorrhage or edema. Our results suggest that further investigation of retroperfusion, and possibly retroinfusion of agents for cerebral protection, is warranted.
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PMID:Ischemic brain rescue by transvenous perfusion in baboons with venous sinus occlusion. 230 Sep 96

The responses of eicosanoids to acute myocardial ischemia induced by either exercise stress testing (EX) or percutaneous transluminal coronary angioplasty (PTCA) were investigated in 23 patients with effort angina pectoris (EAP). EX was useful procedure to determine the therapeutic plan in each cases, and PTCA is the novel therapeutic operation for EAP. The relations between these metabolites and either hemodynamics or coronary circulation were then evaluated. The effect of the calcium entry blocker nisoldipine (oral administration of 5 mg) was also studied in 10 patients with EAP. The plasma levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6KPGF1 alpha) and leukotriene C4 (LTC4) were determined by radioimmunoassay. in arterial and coronary sinus blood samples before and immediately after acute myocardial ischemia. The changes in hemodynamics and coronary circulation during exercise stress testing were assessed by measuring direct brachial artery pressure, cardiac output by the dye dilution method and coronary sinus flow by the thermodilution method. The TXB2/6KPGF1 alpha ratio in coronary sinus blood significantly increased after ischemia in both EX and PTCA, but there was no significant change in LTC4 levels of coronary sinus blood immediately after acute ischemia. The 6KPGF1 alpha levels in both arterial and coronary venous blood were significantly correlated to coronary perfusion pressure and mean brachial artery pressure. Arterial LTC4 levels tended to correlate to mean brachial artery pressure and coronary sinus flow. Nisoldipine improved the ischemic electrocardiography response to EX. Nisoldipine also significantly increased arterial 6KPGF1 alpha at peak exercise. It significantly decreased brachial artery pressure, pressure rate product (PRP), mean coronary sinus pressure and coronary vascular resistance both at rest and peak exercise. The response of PRP significantly correlated with the response of arterial 6KPGF1 alpha. These results suggest: 1 The imbalance of the TXB2/6KPGF1 alpha ratio may be induced more rapidly than LTC4. 2 PGI2 and LTC4 may have some role in the regulation of hemodynamics and coronary circulation during acute myocardial ischemia. 3 Nisoldipine may ameliorate myocardial ischemia through improvement of systemic hemodynamics and prostaglandin metabolism apart from through direct action on the heart.
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PMID:[Responses of plasma eicosanoids and hemodynamics to myocardial ischemia and the salutary effect of calcium entry blocker]. 232 80

The purpose of this study was to evaluate the efficacy of time-controlled intermittent coronary sinus occlusion (ICSO) in preserving regional and global mechanical function during acute ischemia in an animal preparation without significant arterial collateral vessels. Seventeen (eight control, nine ICSO) swine heart preparations undergoing extracorporeal coronary perfusion in situ were subjected to ligation of the left anterior descending coronary artery (LAD) distal to the first major diagonal branch. Data were obtained before and immediately after coronary artery ligation in both animal groups. ICSO, 15 sec of occlusion alternating with 5 sec of release, was then begun in the treatment group. Additional data were obtained in both control and treatment groups at 15 min intervals for 1 hr starting immediately after coronary artery ligation. Global left ventricular function was assessed by shifts in left ventricular end-diastolic pressure and left ventricular dP/dt with left ventricular systolic pressure maintained at about 100 mm Hg. Regional mechanical function was evaluated with transmurally placed ultrasonic crystals. Pressure was also measured directly in the coronary sinus and LAD distal to the ligature. Regional myocardial blood flow was measured in the ischemic bed using 9 micron diameter radiolabeled microspheres injected before, immediately after, and 60 min after coronary artery ligation in both treated and control animals. LAD mean pressure measured distal to the ligation (less than 16 mm Hg) and ischemic bed myocardial blood flow (less than 0.01 ml/g/min) confirmed the absence of significant arterial-arterial collaterals in this preparation. Mean coronary sinus pressure increased significantly (p less than .001) in treated animals during ICSO (e.g., 11.2 +/- 1.6 to 66.2 +/- 10.0 mm Hg at 15 min after coronary ligation). Mean LAD pressure distal to the coronary ligature also increased during ICSO (14.2 +/- 1.2 to 26.8 +/- 1.6 mm Hg), with a similar but delayed rate of pressure rise. No significant differences in left ventricular end-diastolic pressure or left ventricular dP/dt were noted between control or treated animals after coronary ligation. Ischemic bed systolic wall thickening, present before coronary ligation, was not present after occlusion and was not improved during intermittent coronary sinus occlusion in the treatment group. We conclude that in an animal preparation without significant collateral circulation, intermittent coronary sinus occlusion is incapable of restoring regional or global left ventricular mechanical function during conditions of acute ischemia.
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PMID:The efficacy of intermittent coronary sinus occlusion in the absence of coronary artery collaterals. 362 26

The early concept of global retroperfusion and arterialisation of the coronary sinus was discarded because of unacceptable damage to the myocardium, although many authors provided evidence on the improvement of cardiac function during ischemia. Furthermore, the exact mechanism of coronary sinus retroperfusion remained poorly understood. The lack of a strong physiological basis for retroperfusion as well as the development of coronary bypass grafting lessened interest in this revascularisation technique. Renewed interest in myocardial protection via the coronary sinus emerged because of a more aggressive therapy of acute myocardial ischemia. We developed a simple retroperfusion system conceptualized as a periodical occlusion of the coronary sinus and as a redistribution of venous flow to compromised areas during acute myocardial ischemia, sweeping out toxic substances and edema during coronary venous drainage. To allow sufficient filling of the infarcted area as well as venous drainage, the occlusion versus release phase is controlled by the coronary sinus pressure. This pressure-controlled intermittent coronary sinus occlusion (P-ICSO) represents a closed loop system and therefore guarantees optimal physiologic function of the system. This report explains the proposed nature of action of enhanced washout of myocardial edema induced by P-ICSO. Moreover, beneficial effects of P-ICSO observed during canine studies are summarized. It is concluded that this new simple retroperfusion technique has the clinical potential to serve as interim support to protect deprived myocardium until definite reperfusion is available.
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PMID:The development and rationale of pressure-controlled intermittent coronary sinus occlusion--a new approach to protect ischemic myocardium. 660 32

Canine cerebral blood flow is supplied not only through carotid and vertebral arteries, but also through rich network of collaterals. Therefore, it is said that total body arrest is requested to assure the global brain ischemia. The global ischemic models, reported previously, were by the simultaneous occlusion of aorta and vena cava. In our model, however, the global cerebral ischemia was produced by clamping only the ascending aorta. Cardiovascular changes such as increases in left ventricular and pulmonary arterial pressure, and decrease in left ventricular dp/dt followed after ceasing of ascending aortic blood stream. The heart continued to beat during 60 minutes of the clamping. Despite of increased central venous pressure, sagittal sinus pressure and intracranial pressure remained unchanged during the aorta clamping. Ten-minutes of total cerebral ischemia was produced in 46 dogs and successful studies on cerebral and systemic variables were carried out in 68% of them. The method of clamping the aorta without occlusion of vena cava seems to be unsuitable for long term survival study because of severe loading of lung circulation. However, we conclude that this simple model is of great use for short term experiment on global brain ischemia.
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PMID:[Experimental model producing global brain ischemia by clamping the aorta in dogs]. 674 6

Partial coronary sinus obstruction (CSO) in the dog prevents or delays the predictable ventricular fibrillation (VF) of the early phase of acute ischemia, by normalizing regional electrophysiological disparities which presumably reflect inhomogeneous extracellular potassium ([K+]o) accumulation. To clarify whether CSO indeed affects [K+]o inhomogeneity, we determined in 12 chloralose anesthetized dogs the dynamic [K+]o changes occurring early during reversible coronary artery occlusion (CAO) involving the mid-left anterior descending branch. These changes were compared to those observed during CAO preceded by CSO sufficient to increase the coronary sinus pressure to 40 mmHg. [K+]o was determined using valinomycin coated electrodes implanted within the ischemic (IZ) and the normal (NZ) zones, as well as immediately inside (BZi) and outside (BZo) the visible border. [K+]o increased rapidly within the IZ and the BZi reaching plateau 5 min after CAO, at about three-fold control (11.89 +/- 1.12 mEq/l). Unexpectedly, [K+]o also increased initially outside the border (BZo) but declined after 3 min to a lower level (7.00 +/- 0.40 mEq/l), thus creating a steep gradient of up to 5.54 +/- 0.20 mEq/l, P < 0.001) across the visible border. In four trials, the gradient coincided with VF. With CSO preceding CAO, the development of this border zone gradient was entirely prevented. Moreover, [K+]o reached a significantly lower and similar level in the IZ, BZi and BZo (9.5 +/- 0.89 mEq/l, P < 0.001) and no VF was observed. Thus the beneficial electrophysiologic and antiarrhythmic effects of CSO in acute ischemia may be explained by [K+]o equalization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of extracellular K+ inhomogeneity across the ischemic border by coronary venous obstruction in the dog: salutary antiarrhythmic effects of enhanced myocardial hydration. 786 95

We examined whether partial coronary sinus obstruction affects the latency of the early ventricular fibrillation (VF) of acute ischemia. During baseline trials 15 of 19 open-chest dogs fibrillated repeatedly and predictably within 2 to 5 minutes (251.6 +/- 64 seconds) after reversible, double coronary artery occlusion without developing profound hemodynamic deterioration. The effect of partial coronary sinus obstruction sufficient to increase coronary sinus pressure to 40 mm Hg could be adequately tested in 11 dogs. Coronary sinus obstruction consistently prevented VF in five dogs, significantly prolonged the VF latency in three (p < 0.01 to p < 0.001), and had no clear effect in another three. The overall effect was significant at the p < 0.01 level. VF latency prolongation/prevention was also positively correlated to the residual coronary sinus pressure at the time of VF (r = 0.76; p < 0.008), as well as the baseline VF latency (r = 0.75; (p < 0.008). The protective effect of coronary venous hypertension most likely reflects preservation of adequate extracellular fluid in the ischemic region after the perfusion arrest. This extracellular fluid may constitute a key component in the prevention of early ischemic arrhythmias by preserving interstitial hydraulic continuity and tissue homogeneity through enhanced dilution and diffusion of solutes.
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PMID:Protective effect of coronary sinus obstruction from primary ischemia-induced ventricular fibrillation in the dog. 846 71

We present the first reported case of vision loss due to tension orbital emphysema associated with tension pneumocephalus resulting from blunt trauma. In the setting of trauma, intraorbital air indicates paranasal sinus-orbital communication. Tension orbital emphysema may cause vision loss through optic nerve compression, ischemia, or contusion; or central retinal artery occlusion. Vision impairment after craniofacial injury should prompt urgent computed tomography. Tension orbital emphysema with associated vision impairment requires treatment including direct decompression and, in some cases, high-dose steroids to preserve vision. Increases in sinus pressure from coughing, nose-blowing, or vomiting should be avoided until definitive treatment can be instituted.
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PMID:Tension pneumocephalus and tension orbital emphysema following blunt trauma. 883 34

Coronary venous hypertension induced by partial coronary sinus obstruction (CSO) in the dog, prevents or delays the predictable ventricular fibrillation (VF) of the early phase of acute ischemia. Also, CSO acting presumably through enhanced myocardial hydration, normalizes the inhomogenous extracellular potassium ([K+]o) accumulation, a major factor in producing the electrophysiological disparities, characteristic of arrhythmogenic substrate. To further clarify the mechanism of early ischemic VF prevention in dogs, radioactive microspheres were used to evaluate regional perfusion changes, resulting from CSO sufficient to raise the coronary sinus pressure to 40 mmHg, before and during ischemia induced by double coronary artery occlusion (CAO) (n=5). Also, global or regional unipolar electrogram mapping was used to assess changes of epicardial ventricular activation times (AT) and sequence and activation recovery intervals (ARI) during CSO, CAO and combined CSO and CAO, induced in random order (n=8). CSO did not affect regional perfusion nor improved collateral blood flow during ischemia. With CSO, AT shortened modestly over time (0.41+/-1.1 ms/min, r=0.85, P<0. 05) and ARI transiently decreased by up to 5.5%. With CAO, AT became variably delayed and isochrone map distortions were indicative of localized conduction delays or blocks, consistent with elevated [K+]o. In contrast, when CAO was preceded by CSO, AT delays were homogenous and normal activation sequence was preserved. Also, whereas with CAO, ARI shortened unequally over the ischemic region by as much as 43% at individual sites (average of 38.3+/-6.8 ms, P<0. 001), with combined CSO and CAO, ARI shortening was less pronounced and more homogenous (26.1+/-5.6 ms, P<0.05), not exceeding 29% at any site. Thus, in accordance with previous findings of enhanced [K+]o homogeneity, coronary venous hypertension reduces the disparities of activation and refractoriness of ischemia attributable, at least in part, to disparate [K+]o accumulation. Since no collateral blood flow improvement could be identified, the salutary electrophysiological effects of CSO may reflect a more homogenous extracellular environment, due to preservation of normal microvascular pressure (Pmv) and sustained filtration and lymph flow.
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PMID:Coronary venous hypertension prevents the formation of the electrophysiological arrhythmogenic substrate of acute ischemia in the dog: salutary effects of preserved myocardial hydration. 951 2


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