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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four pigs were studied to assess the effect of potassium in a cardioplegic solution on the ability of the swine myocardium to maintain functional and metabolic integrity following induced ischemia. The pigs were evaluated on total and right heart bypass with measurement at normothermia and after a one-hour intervention of stroke volume (SV), coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and lactate extraction. Myocardial tissue gases (PmO2 and PmCO2) were continuously monitored and, at the conclusion of the procedure tissues were analyzed for adenosine triphosphate (ATP). There were five interventions: (1) hypothermic perfusion (28 degrees C) (Group 1); (2) hypothermic ischemia (28 degrees C) (Group 2); and hypothermic ischemia with a cardioplegic solution (nonlactated Ringer's solution, pH 7.4, 4 degrees C) using (3) normokalemia (4 mEq of potassium chloride/L, 300 mOsm/L (Group 3), (4) hyperkalemia (43 mEq of KCl/L, 390 mOsm/L) (Group 4), and (5) normokalemia with increased osmolarity (3.6 mEq of KCl/L, 400 mOsm/L) (Groups 5). A significant decrease in SV and elevation in peak PmCO2 were seen in all groups subjected to ischemia except those protected with hyperkalemic solution. We conclude that the presence of hyperkalemia in a cold root perfusion solution provides better myocardial protection than cold root perfusion alone. Furthermore, potassium arrest appears to be more protective than coronary perfusion at 28 degrees C.
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PMID:The importance of hyperkalemia in a cold perfusion solution: a correlative study examining myocardial function, metabolism, tissue gases, and substrates. 48 29

The effectiveness of the calcium antagonist nifedipine in preserving postischemic myocardial function and structural integrity was experimentally demonstrated in isolated rabbit hearts, in conscious dogs subjected to myocardial infarction, in open chest anesthetized dogs with normothermic regional ischemia induced for 1 to 2 hours and in dogs undergoing hypothermic global ischemia for 2 hours followed by 2 hours of reperfusion. Nifedipine had a beneficial effect on postischemic myocardial stiffness and mitochondrial calcium accumulation, which were correlated. Administration of nifedipine at the onset of myocardial infarction increased blood flow to ischemic zones of myocardial infarction and resulted in less loss of creatine kinase. It reduced by two- to three-fold the volume of the ischemia-reperfusion injury induced by left anterior descending coronary arterial occlusion and release and preserved indexes of hemodynamic function. Nifedipine was found effective in protecting myocardial performance and structure after 2 hours of global ischemia during hypothermic cardiopulmonary bypass. It is suggested that this agent may be useful as an adjunct to cold cardioplegia in man for enhanced myocardial protection during cardiac surgery.
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PMID:Nifedipine: a myocardial protective agent. 49 88

The effects of single forearm arterial injuries with and without associated neurological injuries were studied. Fifty subjects were evaluated: seven patients with isolated arterial lacerations, 15 patients with isolated nerve lacerations, 13 patients with combined nerve and arterial injuries, and 15 control subjects. A series of noninvasive peripheral vascular studies were correlated with the symptoms produced by a controlled cold-environment exposure. The hemodynamic alterations associated with symptoms of hand ischemia, and particularly with cold intolerance, were studied. Unrepaired single arterial injuries caused modest, consistent alterations in hand vascularity, but few signs of ischemia or symptoms of cold intolerance. The remaining intact artery demonstrated a consistent increase in flow velocity. Combined nerve and artery injuries caused the most significant alterations in hand vascularity, and median nerve and associated artery injuries caused the most disabling symptoms. Single arterial lacerations had no effect on the rate or completeness of recovery from associated nerve injuries.
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PMID:Forearm arterial injuries. 50 Oct 48

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.
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PMID:Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia. 50 72

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.
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PMID:Cold blood as the vehicle for potassium cardioplegia. 51 80

Acute mesenteric arterial occlusion is a curable disease, provided it is diagnosed and treated before irreversible changes occur in the ischemic bowel. Forty patients treated for proven mesenteric arterial occlusion were evaluated retrospectively in an effort to broaden the existing criteria for early diagnosis. Twenty-three patients suffered from mesenteric thrombosis and 17 sustained embolic occlusion of the superior mesenteric artery. The overall mortality rate was 77.5% (31 of 40 patients). Three patients survived without bowel resection. The appearance of acute abdominal pain accompanied by profuse cold sweating in a cardiac patient with apparently normal abdomen, hyperactive bowel sounds, and a history of embolic events should always raise the suspicion of acute mesenteric ischemia and should be verified immediately by mesenteric angiography. A high index of suspicion, aggressive measures for early diagnosis, and early operative treatment are presently the only possibilities to provide a better outcome.
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PMID:Acute superior mesenteric arterial occlusion: a plea for early diagnosis. 63 86

We studied the role of cardiopulmonary vagal afferents in the cardiovascular responses to coronary artery occlusion in conscious dogs with intact carotid sinuses and following functional denervation of the arterial baroreceptors. The contributions of vagal afferents were determined by cold blocking the vagi. In dogs with intact carotid sinuses, coronary artery occlusion produced small decreases in mean cardiac output and arterial pressure, whereas heart rate increased by 35 beats/min. In dogs with intact carotid sinuses, vagal cold block increased mean arterial pressure by 22 +/- 2 (mean +/- SE) mm Hg and heart rate by 90 +/- 6 beats/min. Mean cardiac output increased by 505 +/- 90 ml/min. With the exception of heart rate, responses to coronary occlusion during vagal cold block were similar to the occlusion response prior to vagal cold block. Furthermore, prior occlusion of the coronary artery did not significantly influence the responses to vagal cold block. After arterial baroreceptor denervation, coronary artery occlusion resulted in a substantially greater fall in systemic arterial pressure (-52 mm Hg as compared to -8 mm Hg, with intact carotid sinuses) and peripheral resistance decreased by -0.49 peripheral resistance units (PRU). Vagal cold block following denervation increased the arterial pressure by 49 +/- 10 mm Hg and peripheral resistance by 0.59 +/- 0.13 PRU. Both values were significantly greater than those observed during vagal cold block prior to denervation. In arterial baroreceptor-denervated dogs, vagal blockade significantly attenuated the response to coronary occlusion. Therefore, in conscious dogs, vagal afferents from cardiopulmonary receptors exert a significant inhibitory influence on the peripheral vascular tone. When the carotid sinuses are intact, this inhibitory influence appears to be marked during myocardial ischemia. In the absence of functional arterial baroreflexes, vagal afferent activity contributes to the depressor responses observed during ischemia.
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PMID:The circulatory influences of vagal afferents at rest and during coronary occlusion in conscious dogs. 70 45

Cold nonperfusional (flushing and ice storage) with Collins or Sacks solution and perfusional preservation with cryoprecipitated plasma or albumin were compared in dog kidneys. All these methods were effective in achieving excellent 48-hour preservation of fresh kidneys. After exposure to 20 minutes of ischemia at 37 C, neither of the flushing solutions yielded kidneys that permitted survival of recipients after 48 hours of preservation, and flushed kidneys functioned poorly after 24 hours of preservation. In contrast, both plasma- and albumin-perfused kidneys exposed to ischemia supported life satisfactorily and with normal function. Therefore, simple and inexpensive flushing and ice storage techniques are entirely satisfactorily for the preservation of ideally harvested cadaver kidneys, while the more complex and expensive perfusional techniques must be employed in preserving ischemia-damaged organs.
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PMID:Forty-eight-hour kidney preservation. A comparison of flushing and ice storage with perfusion. 76 32

The influence of the duration of warm and cold ischemia on initial graft function on patient survival, graft survival, and graft function one year after transplantation was assessed in 234 consecutive cadaveric renal transplants. The number of grafts with delayed function was found to increase with increasing duration of the warm and cold ischemia times. On the other hand, the duration of the ischemia times and consequently the initial function, whether immediate or delayed, did not influence the survival of graft and patient nor the function of the graft one year after transplantation.
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PMID:Influence of warm and cold ischemia time on initial function and one-year survival of renal allografts. 77 78

The measurement of lactate dehydrogenase (LDH) release into perfusates after hypothermic storage was found to be a reliable index of ischemic injury of rabbit kidneys. Kidneys were exposed to warm and cold ischemia for varying periods. Each kidney was perfused before and after storage at simple hypothermia with 25 ml of a modified Collins solution. The venous effuent was collected in 5 ml fractions. Total LDH activity was measured in the first fraction after storage and used as a measure of ischemic tissue damage. It was confirmed that increasing the period of cold ischemia result in significant increases in LDH activity. The release of LDH into perfusates was then used to compare kidney damage after preservation with various fluids. With this method, it was not possible to demonstrate any difference in the extent of tissue damage after preservation with sodium-rich vs. potassium-rich perfusion fluid. Addition of steroids, vitamins and essential amino acids did not prevent or reduce tissue damage, estimated in this way. The effects of adding cryoprotectants to the perfusion fluid varied; LDH release following addition of 5% DMSO was significantly greater, and after addition of 5% glycerol smaller than the release after perfusion with a modified Collins solution alone. Stepwise addition of DMSO up to 20% resulted in serious tissue damage with a large LDH release into the perfusate.
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PMID:LDH release into perfusates of preserved kidneys. 78 32


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