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At least 19 recordsLinked to original sources
PubMed1979

The effects of hypothermia on myocardial oxygen consumption and transmural coronary blood flow in the potassium-arrested heart.

Hypothermia remains the primary adjunct employed to lower cellular metabolism during various cardiac procedures. In these experiments, left ventricular myocardial oxygen consumption (MVO2) and transmural blood flow (TBF) were measured during cardiopulmonary bypass with the range of temperatures used clinically. Determinations were made in empty beating normothermic hearts and after potassium cardioplegia at 37, 32, 28, 22, 18, and 15 degrees (K+ = 15--37 meq/L: Hct 25 volumes %). Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer (vs Van Slyke, R = 0.98). Transmural blood flow was measured at each temperature using microspheres (8 microns), and perfusion was maintained at 80 mmHg. Asystole (37 degrees) alone decreased MVO2 from 5.18 +/- 0.55 to 1.85 +/- 0.20 ml O2/min/100 g of left ventricle or approximately 65% (p less than 0.001). With progressive cooling to 15 degrees an additional 82% decrement in oxygen uptake occurred during asystole (p less than 0.001). During asystole at 37 degrees the decrease in MVO2 was reflected mainly by a large decrement (p less than 0.01) in TBF (1.27 +/- 0.19 to 0.74 +/- 0.17 ml/min/g of mean left ventricular flow). However, with cooling below 32 degrees, the arteriovenous oxygen difference narrowed progressively (p less than 0.001) while TBF paradoxically returned to control levels. Endocardial/epicardial flow ratios were not altered by cooling. These data not only confirm earlier reports describing a sequential drop in MVO2 with incremental myocardial cooling, but also establish MVO2 levels for perfused hearts arrested by potassium at lower temperatures (18--15 degrees). Moreover, as transmural blood flow becomes independent of metabolic necessity during hypothermia, coronary autoregulation appears to be impaired, possibly affecting detrimental tissue over perfusion.

Animals↗
PubMed1978

[Myocardial potassium and H-ion loss during normothermic, ischemic heart arrest].

Arterial and venous [K+] and [H+] concentrations were determined during normothermic ischemic arrest in cat hearts intermittently perfused without resuscitation. The slight loss in [K+] was taken as evidence of a stable membrane potential. The decrease in [H+] activity appearing in the perfusate correlated well with the previously described increase in coronary resistance. This was interpreted as a sign of restricted coronary perfusion and not as evidence for reduced anaerobic metabolic activity. Thus the functional impairment of the coronary system was confirmed to be a limiting factor when resuscitating ischemically arrested hearts.

Animals↗
PubMedDate not supplied

Metabolism and fine structure of the Mg++-procaine-arrested perfused heart.

Arrested rabbit hearts were perfused in normothermia for up to two hours by a cardioplegic erythrocyte-containing solution having an increased Mg++-, procaine-, and a reduced NaCl-content. After this time, hearts did not reveal any sign of anoxic or toxic damage in their metabolic pattern, in their ultrastructural picture, and in their functional capacity after reanimation. Despite a small loss in adenine nucleotide content, the ATP/ADP ratio and the PC content were raised. The contents of glycogen and glycolytic intermediates were normal or slightly reduced. After two hours of perfusion mitochondria showed no swelling, their membrane structure was unaltered. The myofibrils were well aggregated. The number of glycogen granules was increased. Hearts were reanimated after two hours of cardioplegia and could be loaded by pressure and volume.

Adenosine Diphosphate↗
PubMed1977

Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. I. The adequately perfused beating, fibrillating, and arrested heart.

The effects of hypothermia (32 degrees, 28 degrees, and 22 degrees C.) on left ventricular flow distribution (microspheres) and oxygen uptake in adequately perfused, beating, empty, fibrillating, and arrested hearts were studied. Minute left ventricular oxygen uptake fell progressively as myocardial temperature was reduced under all conditions. In beating hearts, however, left ventricular oxygen uptake per beat increased significantly due to the inotropic effect of hypothermia and diastolic compliance fell. Cold fibrillating hearts consumed slightly less oxygen per minute than beating hearts at comparable temperatures as fibrillation became less forceful with hypothermia. Myocardial wall tension, however, was always higher in fibrillating than beating hearts at each level of hypothermia. The lowest myocardial oxygen requirements were always found in arrested hearts (70 to 80 per cent less than either beating empty or fibrillating hearts) at any myocardial temperature. Left ventricular coronary flow remained distributed evenly across the beating heart at all myocardial temperatures and in fibrillating hearts at 28 degrees, and 22 degrees C. Left ventricular flow became redistributed toward the subendocardium in fibrillating hearts at 37 degreegs and 32 degrees C. and in arrested hearts at all myocardial temperatures.

Animals↗
PubMedDate not supplied

[Heart arrest and reanimation].

The author describes when stoppage of the heart muscle is really true and the most important causes of it. It is an emergency that must be prevented and to achieve this, the premonitory symtoms and their treatment are described.

Heart Arrest↗
PubMed1979

[Direct cardiac massage in refractory heart arrest. 2 cases sucessfully treated in the coronary care unit].

The open chest, or direct cardiac massage may be indicate in instances where closed chest techniques are ineffective. Direct cardiac massage was successfully applied by us in two patients who failed to resuscitate with closed chest massage. The patients, an 49 year old man with acute myocardial infarction and an 53 year old man who had a history of previous myocardial infarction with subsequent development of a ventricular aneurysm, had ventricular fibrillation who not responded to closed chest cardiac massage and to repeated electrical countershocks. When the pupils became dilated the decision was made to open the chest and apply direct massage. After several minutes of manual cardiac compression a single D.C. countershock returned the heart to a normal sinus rhythm in each of the patients. Although the thoracotomy was performed outside the operating room, none of the complications of the open chest resuscitation occurred, such as intrathoracic infection, rupture of the heart, and postresuscitative bleeding. The first patient recovered from the infarction, has been discharged from the hospital and is alive and well after 5 months. The second patient has been discharged from the U.C.C. and is alive and well after 15 days.

Electric Countershock↗
PubMed1975

[Metabolism and ultrastructure of magnesium aspartate-procaine arrested hearts of rabbit and man (author's transl)].

In normothermia, mild, and deep hypothermia the metabolism and the electron microscopic structure were investigated in human and rabbit heart muscle after magnesium aspartate-procaine cardioplegia. In comparison to plain ischaemic arrest splitting of adenine nucleotides and glycogen was significantly reduced in all experiments with the induced cardioplegic arrest. For 40 min at 32 degrees C almost no changes in ultrastructure were seen in heart muscle after induced arrest, while severe and/or irreversible damages were seen in the cell structure of the heart muscle due to plain ischaemic arrest.

Adenine Nucleotides↗
PubMed1977

Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. V. Profound topical hypothermia during ischemia in arrested hearts.

This study compares the effects of 60 minutes of ischemic arrest with profound topical hypothermia (10 dogs) on myocardial (1) blood flow and distribution (microspheres), (2) metabolism (oxygen and lactate), (3) water content (wet to dry weights), (4) compliance (intraventricular balloon), and (5) performance (isovolumetric function curves) with 180 minutes of cardiopulmonary bypass with the heart in the beating empty state (seven dogs). Studies performed before and 30 minutes after 1 hour of ischemic arrest with profound topical hypothermia showed: (1) total left ventricular blood flow increased 50 per cent but became redistributed away from the subendocardium (endocardial/epicardial flow ratio fell from 1.13 to 0.77,(2) left ventricular oxygen consumption fell 30 per cent while left ventricular oxygen extraction fell from 51 to 29 per cent; (3) lactate extraction fell from 15 to 4 per cent (two dogs produced lactate); (4) left ventricular endocardial (papillary muscle) water content rose 2.4 per cent; (5) left ventricular compliance decreased from 1.68 to 1.01 ml. H2O/mm. Hg (at 25 ml.); (6) left ventricular performance was depressed 49 per cent below control values. In contrast, 3 hours of cardiopulmonary bypass in the beating empty heart produced only minimal changes in these variables.

Animals↗
PubMed1975

[Restoration of the automatic contractile activity of K+-arrested heart muscle cells in culture by means of dibutyryl-3', 5'-adenosine monophosphate].

Cultured myocardial cells of new-born rats which were arrested by 17.6-37.6 mM KCl regained their ability to contract spontaneously after perfusion with 8-10(-4)-4-10(-3) M dibutyryl cyclic AMP. This adrenaline-like action of DbcAMP is compatible with the notion that cyclic AMP is involved as a second messenger in the action of cyclic AMP-raising adrenergic agents on cardiac activity.

Animals↗