Aim of this study is to evaluate protective effect of AST in the lung injury caused by ischemia
reperfusion of the lower extremities.
When fibrinolytic therapy is indicated or chosen as the primary
reperfusion strategy, it should be administered within 30 minutes of hospital arrival.
Ischaemic preconditioning performed on the kidneys is claimed to repress the inflammatory response caused by
reperfusion. Direct ischaemic preconditioning (DIPC) for the kidney is performed by clamping and declamping the renal artery or pedicle, and the most well-accepted method is fourcycles of 4 minutes of clamping (ischaemia) and 11 minutes of
reperfusion (7, 8).
The rats were randomly divided into the groups as follows (n=5/group): IR group: following a stabilization period of 30 min, the rats were subjected to 10 min of ischemia followed by 10 min of
reperfusion (Figure 1).
Reperfusion is the only method to rescue salvageable myocardium, but
reperfusion itself may induce further myocardial injury, a phenomenon has been termed as myocardial ischemia-reperfusion injury (MIRI).[1] Since the discovery of the MIRI phenomenon in dogs by Jennings et al .[2] in 1960, numerous studies have been conducted to reveal the underlying mechanisms of MIRI and to explore the effective treatments for MIRI.[3] Experimental studies in this field have used in vivo , ex vivo , and in vitro models.
Although oxygen levels are restored upon
reperfusion, a surge in the generation of ROS occurs and pro-inflammatory neutrophils infiltrate ischemic tissues to exacerbate ischemic injury.
Morphine sulfate at doses of 3 [micro]mol and 30 [micro]mol, respectively, were administered to the experimental animals of the IRPC3 and IRPC30 groups over 20 min starting 5 min before
reperfusion by using the morphine sulfate venous route.
"Tenecteplase before thrombectomy was associated with a higher incidence of
reperfusion and better functional outcome than alteplase among patients with ischemic stroke treated within 4.5 hours after symptom onset," the authors write.
In the study, rats were randomly divided into five groups: sham control (Sham) group, ischemia and
reperfusion (IR) group, ischemia and
reperfusion plus XXMD (60g/kg/day, XXMD60) group, ischemia and
reperfusion plus cyclosporin A (10 mg/kg, CsA) group, and ischemia and
reperfusion plus dimethyl sulfoxide and ethanol (Vehicle) group.
Rats were subjected to 30 min of regional ischemia by ligating the artery, and then the ligature was loosened for 120 min as
reperfusion, while sham-operated group rats underwent the same progress except ligating the artery.
After
reperfusion, 3-5 ml of blood in the vena cava was collected by sterile syringes without anticoagulant and centrifuged to separate the serum.
My initial impression of the findings in the current case--a classic, early, and rapid increase of the myocardial-specific cardiac troponin I (cTnI) [2]--was that they represented a spontaneous
reperfusion of a type 1 non-ST segment elevation myocardial infarction, analogous to a rapid flushing out of a clogged drain (coronary artery) with chemicals.
