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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten clinically intact weaned piglets were experimentally intoxicated by intravenous injection of lipoproteide-free lipopolysaccharide endotoxin according to Westphal of E. coli O 127:B8. Severe endotoxin shock with all clinical manifestations of experimental coli-enterotoxaemia was induced in all animals and included circulatory disorder with tachycardia, intermittent pallor and/or cyanosis, symptoms of severe systemic intoxication, neurological symptoms, such as lack of coordination, hindleg staggering, spasm, paresis, paralysis, changes in respiration, such as rise in respiratory frequency and deepened breathing premortal deceleration of respiration and gasping for breath, temperature, variation, including hyperthermia and aggravating hypothermia, gastro-intestinal symptoms, such as temporary vomiting and persistent diarrhoea, leucopenia, eosinopenia, variation of haematocrit, edematisation, increased transudation, congestion, and gastro-intestinal shock lesions. Eight animals died. These experiments quite obviously have confirmed that endotoxin shock is the common pathogenetic principle behind all forms of coli-entertoxaemia (i.e, the forms of edematisation, cardiovascular failure, and gastro-intestinal processes.) Lipopolysaccharide endotoxin alone may be responsible for the development of both edemas and neurotoxic symptoms (edema disease) and diarrhoea (gastro-intestinal form of coli-enterotoxaemia). The pathogenetic relevance of additional toxins (neurotoxin and enterotoxin) is discussed under this aspect.
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PMID:[Experimental studies on the pathogenesis of Coli-enterotoxemia in swine. 4. Effect of lipopolysaccharide endotoxin on weaned piglets following parenteral administration]. 33 9

A 72-year-old male underwent radical operation for cancer of the tongue. Anesthesia was maintained with the combination of enflurane-N2O-vecuronium and cervical epidural block. Five minutes after the cessation of the longstanding operation, VT and circulatory collapse occurred. After administration of lidocaine and ephedrine, VPC and ST elevation were noted, followed by VT and Vf. Cardioversion successfully restored sinus rhythm with no ST change, suggesting an episode of coronary artery spasm. The possible inducing factors in this case were hypotension and acute imbalance in autonomic nervous systems caused by hypovolemia, hypothermia, insufficient anesthetic depth, loss of surgical stress, neostigmine and epidural block. The authors reviewed case reports on coronary spasm, especially looking for possible inducing factors of coronary artery spasm during anesthesia.
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PMID:[Coronary artery spasm immediately after the long-standing operation for cancer of the tongue]. 147 69

We report two cases of coronary artery spasm during coronary artery bypass surgery. As one of the complications during cardiac surgeries, coronary vasoconstriction occurs mainly after coming off cardiopulmonary bypass. The factors responsible for the spasm include high endogenous catecholamine levels due to inadequate anesthesia and hypothermia, exogenous catecholamines for circulatory support, various chemical mediators and combination of these factors. Coronary artery spasm was suspected strongly because of sudden ischemic change in electrocardiography and simultaneous aggravation of circulatory parameters, which improved immediately after direct injection of coronary vasodilators into vein graft. This method, popular in coronary angiography and catheterization, is effective for release of coronary-artery spasm observed particularly after cardiopulmonary bypass. Then mechanical circulatory assist is readily available to treat possible systemic side effect of the vasodilators.
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PMID:[Coronary artery spasm during coronary artery bypass surgery]. 149 92

Hypothermia may contribute to vascular spasm during bypass surgery. The effect of cooling on the reactivity of the human coronary artery (CA), saphenous vein (SV) and internal mammary artery (IMA) was studied in vitro. In CA and IMA cooling diminished the resting tension and the contraction to potassium, noradrenaline and 5-hydroxytryptamine. In contrast, in SV the contraction to noradrenaline and 5-hydroxytryptamine was augmented by cooling. The effect of cold was reversible. These results demonstrate different effects of hypothermia in CA and the graft vessels. Thus, hypothermia augments the receptor-mediated contraction in SV but depresses it in IMA which thereby resembles CA. The difference is most marked in the contractile response to 5-hydroxytryptamine, which may accumulate during surgery. This may contribute to spasm in the saphenous vein grafts and may be involved in the mechanisms responsible for the inferior patency of SV compared to IMA as a graft vessel.
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PMID:Differential effect of hypothermia on the vascular tone and reactivity of the human coronary artery and graft vessels. 205 21

Morphine slows hepatobiliary elimination of sulfobromophthalein in rodents, raising dye levels in plasma and liver. Earlier studies showed these effects to be independent of other opiate effects such as bile duct spasm, hypothermia or blood gas changes resulting from respiratory depression. Because opiate receptors are distributed throughout the body, within the central nervous system and at peripheral sites including the gastrointestinal tract, experiments were performed to ascertain whether central or peripheral sites mediate the hepatobiliary effects of morphine. Sulfobromophthalein was administered intravenously to mice and its levels were measured in plasma and liver. Tail-flick latency indicated centrally mediated analgesia. Inhibited intestinal transit of India ink reflected an opiate effect with a significant peripheral component. When injected into a cerebral ventricle morphine was much more potent in producing analgesia and raising sulfobromophthalein levels than when administered intravenously or intraperitoneally. An intravenous dose of naloxone that reversed morphine analgesia also prevented sulfobromophthalein elevation but did not prevent gut slowing. Naltrexone injected in a cerebral ventricle also reversed analgesia and sulfobromophthalein elevation but not intestinal slowing. The polar opiate agonist N-methylmorphine did not cause analgesia or raise sulfobromophthalein levels at peripheral intraperitoneal doses to 100 mg/kg. When given in a central ventricle at 4 x 10(-3) mg/kg, this agent produced analgesia and raised sulfobromophthalein but did not slow intestinal transit. After spinal cord transection, intravenous morphine did not retard the tail-flick response or affect sulfobromophthalein disposition, but peripherally mediated intestinal transit was slowed as it was in intact mice. These experiments demonstrate parallel opiate effects on analgesia and on BSP disposition but not on intestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatobiliary effects of morphine are mediated in the brain. 217 93

The effect of hypothermia on traumatically induced vasospasm was studied in an in vivo model of the rabbit ear artery. Spasm was induced by standardized compression of a 3.2 mm segment of the artery for 3 s. The internal diameter was continuously measured with the aid of an operating microscope during transillumination of the artery. Measurements were begun before spasm induction and continued until the spasm was completely resolved. Spasm was first induced at normothermia and then after reduction of the body temperature by 1.0 degrees C and 1.75 degrees C. The spasm was evaluated in terms of its duration, intensity (% reduction of initial diameter) and severity (area under the curve where diameter was plotted against time). The results were compared with those in a control group which was kept normothermic. Reduction of the body temperature caused a significant increase in the duration of the spasm and increased its severity, but did not influence its intensity.
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PMID:The influence of body temperature on traumatic vasospasm. 221 62

Perioperative myocardial infarction (PMI) is a well-known complication of coronary artery surgery, but rarely encountered in valvular surgery. We have experienced 6 cases of valve replacement with PMI, using blood cardioplegia since 1979. Those patients (5 men, one woman; mean age 47 +/- 8 years) had no previous angina, and preoperative CAG revealed no significant stenosis. Three patients were reoperative cases. A diagnosis of PMI was established by the following criteria; an abnormal increase in maxCPK-MB (greater than 150 IU/l), new Q waves at ECG, positive 99mTc-PYP scan (grade 3-4). The area of PMI was inferior in 4 patients, posterior in one, and anterior infarction was seen in only one case. Three cases required IABP, but all 6 cases showed good exercise capacity by Treadmill exercise test in late stage. Several factors are thought to be the cause of PMI at valvular surgery; such as coronary air embolism, perioperative coronary spasm, inappropriate topical hypothermia, etc. Prognosis is not necessarily poor, however much attention should be paid to prevent PMI in valve replacement.
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PMID:[Clinical evaluation of perioperative myocardial infarction as a complication of valve replacement]. 259

Calcium plays an essential role in ischemic events observed during cardiac surgery. Many experiments have studied the effects of calcium channel blockers on intracellular calcium overload during the periods of cardiac ischemia and reperfusion. Calcium channel blockers are no longer used before and during cardiac surgery because hypothermia inhibits their pharmacological action. However, during the post-operative period, calcium channel blockers are the drugs of choice to control coronary spasm, and arterial hypertension which is secondary to peripheral vasoconstriction.
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PMID:[Role of calcium blockers in protecting the myocardium in cardiac surgery]. 267 78

The effect of cold cardioplegic solution and hypothermia on the response to acetylcholine, a major postganglionic neurotransmitter of the parasympathetic nervous system, was studied using perfused epicardial coronary arteries of pigs. Cold crystalloid cardioplegic solution (5 degrees C) and hypothermia including topical cooling with slushed ice significantly augmented the coronary flow reduction by acetylcholine at one and two hours after rewarming. Cold Krebs-Henseleit solution (5 degrees C) with hypothermia showed similar effects. However, cardioplegic solution at 37 degrees C did not affect the responsiveness. The coronary flow reduction induced by potassium chloride (60 mmol/L) did not change even after the administration of cold cardioplegic solution (5 degrees C) or cold Krebs-Henseleit solution (5 degrees C), indicating that cooling did not necessarily augment the coronary contractile response generally. It is concluded that cooling and subsequent rewarming can potentiate the contractile response of the coronary artery of the pig to acetylcholine. This suggests that cold cardioplegic solution with hypothermia can promote intraoperative coronary spasm upon activation of the parasympathetic nervous system.
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PMID:Effect of cold cardioplegic solution and hypothermia on response to acetylcholine in perfused epicardial coronary artery of pig. 291 15

Calcium channel blockers have an important role in the pharmacotherapy of cardiovascular disorders. These agents act by inhibiting the slow inward current into excitable cells, exert direct negative inotropic, chronotropic, and dromotropic activity, and are potent vasodilators. These direct effects are modified by reflex autonomic stimulation and by pathologic states. Serious adverse effects of the calcium channel blockers are most frequently observed in patients with ventricular dysfunction, conduction system disease, or concomitant beta blockade. Calcium channel blockers are indicated in the treatment of angina pectoris, supraventricular arrhythmias, and hypertension. The use of these agents in patients with hypertrophic cardiomyopathy, congestive heart failure, and pulmonary hypertension is investigational. The calcium channel blockers are gaining increased importance in the management of patients undergoing cardiac surgery. Verapamil is indicated for the treatment of post-cardiac-surgical atrial flutter and fibrillation; however, the calcium antagonists are not effective as prophylaxis against postoperative supraventricular arrhythmias. Laboratory studies have shown that drug interactions exist between calcium channel blockers and inhalational anesthetics and nondepolarizing neuromuscular blocking agents; clinical studies have demonstrated that these interactions are rarely significant. Perioperative coronary spasm can be effectively treated with the calcium channel blockers. The timing of calcium antagonist withdrawal prior to surgery is controversial, but continuation of therapy until surgery is usually safe. The clinical significance of platelet function inhibition by the calcium antagonists is unknown. Protection of ischemic myocardium by calcium channel blockers has been demonstrated. Important interactions between the calcium antagonists, hypothermia, and the ionic constituents of cardioplegia require further study before the role of these agents as adjuncts to clinical cardioplegia is defined. Expanded indications and the introduction of new calcium channel blockers will result in increased use of these agents in the future.
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PMID:Calcium channel blockers and cardiac surgery. 297 80


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