Reperfusion of ischaemic tissues is often associated with microvascular dysfunction that is manifested as impaired endothelium-dependent dilation in arterioles, enhanced fluid filtration and leukocyte plugging in capillaries, and the trafficking of leukocytes and plasma protein extravasation in postcapillary venules Activated endothelial cells in all segments of the microcirculation produce more oxygen radicals, but less nitric oxide, in the initial period following reperfusion The resulting imbalance between superoxide and nitric oxide in endothelial cells leads to the production and release of inflammatory mediators (eg platelet-activating factor, tumour necrosis factor) and enhances the biosynthesis of adhesion molecules that mediate leukocyte-endothelial cell adhesion Some of the known risk factors for cardiovascular disease (hypercholesterolaemia, hypertension, and diabetes) appear to exaggerate many of the microvascular alterations elicited by ischaemia and reperfusion (I/R) The inflammatory mediators released as a consequence of reperfusion also appear to activate endothelial cells in remote organs that are not exposed to the initial ischaemic insult This distant response to I/R can result in leukocyte-dependent microvascular injury that is characteristic of the multiple organ dysfunction syndrome Adaptational responses to I/R injury have been demonstrated that allow for protection of briefly ischaemic tissues against the harmful effects of subsequent, prolonged ischaemia, a phenomenon called ischaemic preconditioning There are two temporally and mechanistically distinct types of protection afforded by this adaptational response, ie acute and delayed preconditioning The factors (eg protein kinase C activation) that initiate the acute and delayed preconditioning responses appear to be similar; however the protective effects of acute preconditioning are protein synthesis-independent, while the effects of delayed preconditioning require protein synthesis The published literature in this field of investigation suggests that there are several potential targets for therapeutic intervention against I/R-induced microvascular injury

https://onlinelibrary.wiley.com/doi/pdf/10.1002/%28SICI%291096-9896%28200002%29190%3A3%3C255%3A%3AAID-PATH526%3E3.0.CO%3B2-6

Pathophysiology of ischaemia-reperfusion injury

Rupture or laceration of the aorta is a more common result of nonpenetrating traumatic injury than is generally appreciated. Approximately 15 per cent of individuals with traumatic rupture survive temporarily. If the lesion is promptly diagnosed appropriate surgical treatment may be life-saving. Diagnosis may be difficult and at times the rupture may remain clinically silent for variable periods. The natural course from aortic rupture to false aneurysm formation with secondary rupture of the aneurysm may be brief or extend over many years. Surgical treatment of a false aneurysm that has remained stable for a prolonged period has been successful, but in some instances conservative management may be the treatment of choice.

Nonpenetrating Traumatic Injury of the Aorta

Clinical application of transvenous mitral commissurotomy by a new balloon catheter

Method and apparatus for utilizing the vascular system as a conduit to reach other vascular and extravascular locations within the body. Included are methods for revascularization wherein the extravascular passageways are formed to permit blood flow between vascular locations. Also included are methods for performing transvascular interstitial surgery (TVIS) wherein extravascular passageways are formed from a blood vessel to another vascular or non-vascular intracorporeal location. Also disclosed are devices usable for forming extravascular passageways in accordance with the invention, or for modifying, valving, maintaining or closing such passageways.

Device, system and method for interstitial transvascular intervention

The "2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care" increased the focus on methods to ensure that high-quality cardiopulmonary resus...

Cardiopulmonary resuscitation quality: Improving cardiac resuscitation outcomes both inside and outside the hospital: A consensus statement from the American heart association

Ventricular fibrillation occurs as the terminal arrhythmia in approximately 50 per cent of patients 1 If ventricular fibrillation develops in hearts that are relatively normal, especially during operations, defibrillation may be life saving During the period before regular rhythm is restored the heart must be exposed and rhythmically massaged in the interval This method of cardiac resuscitation has been developed in the laboratory by Hooker, 2 Wiggers, 3 and Beck, 4 and applied to patients by the latter The method consists of the injection of 5 cc of 2 per cent procaine hydrochloride into the right side of the heart followed by a brief period of cardiac massage to distribute the drug throughout the myocardial bed The heart is then placed between two large electrodes and ordinary 110 volt alternating current with 15 amperes is momentarily impressed through the heart between the electrodes Usually a series of such shocks is

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Ventricular fibrillation of long duration abolished by electric shock.

The development of a new blood supply to the heart by operation

Nonpenetrating wounds of the heart

Lesions of the pericardium are generally difficult problems in diagnosis. Auenbrugger, Corvisart and Laennec early recognized these difficulties. Osler not infrequently lamented his failure to recognize a lesion of the pericardium and it would seem that these problems in diagnosis still exist. The chief reason for failure in the diagnosis of pericardial lesions is the fact that the physiologic concept of acute and chronic compression of the heart has not found the place in applied medicine that it deserves. Clinically, almost all of the intrapericardial lesions express themselves, if they express themselves at all, by producing either acute or chronic compression of the heart. Some lesions of the pericardium are entirely silent; they produce no clinical signs whatever and clinical recognition of these silent lesions is not to be expected. 1 However, the important group of lesions—important because treatment is effective—produces either acute or chronic compression of the heart. In

Two cardiac compression triads

The first experiments to improve the arterial circulation to the heart were carried out by one of us (Claude S. Beck) in 1932. At that time the idea of improving coronary circulation by operative methods was a radical departure from established medical thought. A serious study of this subject was undertaken and several thousand operations were done on dogs during the next ten years. The results of these studies cannot be given here, but a general statement can be made to the effect that the circulation to the heart was improved by operative methods. 1 The degree of benefit produced by operation was measured by mortality after ligation of a major coronary artery in an operative group as compared to that in a normal control group. The size of the infarct following ligation of a coronary artery was also an index of benefit. That the heart was protected by operative methods

Claude S. Beck

Papers

Ventricular fibrillation of long duration abolished by electric shock.

The development of a new blood supply to the heart by operation

Nonpenetrating wounds of the heart

Two cardiac compression triads

Revascularization of heart by graft of systemic artery into coronary sinus.