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PubMed2003

Effects of inhibition of myocardial extracellular-responsive kinase and P38 mitogen-activated protein kinase on mechanical function of rat hearts after prolonged hypothermic ischemia.

BACKGROUND: Mitogen-activated protein kinases (MAPKs), including extracellular-responsive kinase (ERK) and p38 MAPK, are activated by stresses associated with hypothermia-rewarming and ischemia-reperfusion. Their activation in heart is associated with beneficial (preconditioning) and adverse effects (apoptosis and impaired contractility). This study determined whether ERK and p38 MAPK activities are altered by hypothermic ischemia and normothermic reperfusion and the consequences of their inhibition on recovery of myocardial function. METHODS: Left ventricular work (L x min(-1) x mm Hg) was assessed during normothermic perfusion (30 min) of isolated rat hearts that were either freshly excised or previously subjected to hypothermic storage (8 hr, 3 degrees C) and rewarming (10 min, 37 degrees C) before normothermic reperfusion (30 min). Phospho-specific immunoblot analysis of p38 MAPK was performed in hearts and various cultured cells. RESULTS: Compared with fresh hearts, hearts subjected to hypothermia and rewarming demonstrated impaired left ventricular work (1.96+/-0.53, n=12 vs. 8.37+/-0.46, n=4, <0.05) during reperfusion. The ERK inhibitor, PD98059 (20 microM), present during storage and rewarming, caused modest improvement (3.66+/-0.75, n=9, <0.05). The p38 MAPK inhibitor, SB202190 (10 microM), when present during reperfusion, improved recovery (to 6.12+/-0.75, n=6, <0.05); it was ineffective if present only during rewarming (1.52+/-0.88, n=4). In rat2 fibroblasts, hypothermia and rewarming activated p38 MAPK and its downstream kinase MAPK-activated protein kinase 2, but not c-Jun N-terminal kinase/stress-activated protein kinase. CONCLUSIONS: Myocardial p38 MAPK and MAPK-activated protein kinase 2 are stimulated by hypothermia, ischemia, and rewarming and are detrimental to recovery of mechanical function of hearts subjected to prolonged hypothermic storage. Inhibition of p38 MAPK may be useful in protocols to improve the recovery of mechanical function of cold-stored hearts.

Animals↗
PubMed1993

Inhibition of leukocyte adherence and aggregation for treatment of severe cold injury in rabbits.

We tested the hypothesis that blocking neutrophil adherence and/or aggregation reduces tissue injury that results when tissue is frozen and rewarmed. The left hindlimbs of three groups of New Zealand White rabbits were immersed in a -15 degrees C salt water bath for 30 min to freeze the foot. The foot was rewarmed in a 39 degrees C water bath. In two groups, adherence and aggregation were blocked with monoclonal antibody (MAb) 60.3, and the third group was treated with saline. Two of the groups were treated at the time of rewarming with either saline or MAb 60.3, and the third group received MAb 60.3 at the conclusion of rewarming. Tissue edema and tissue loss were significantly less in the two groups receiving MAb 60.3 than in the control group. Rabbits treated at the time of rewarming had less edema and tissue loss than those treated at the completion of rewarming. These studies indicate that a substantial component of severe cold injury is neutrophil mediated and occurs after rewarming.

Animals↗
PubMed1989

Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Ryanodine and voltage sensitivity.

We studied relaxation during rapid rewarming of rabbit ventricular muscles that had been activated by rapid cooling. Rewarming from 1 degree to 30 degrees C (in less than 0.5 second) activates mechanisms that contribute to the reduction of intracellular calcium concentration and thus relaxation (e.g., sarcoplasmic reticulum [SR] calcium pump and sarcolemmal Na-Ca exchange and calcium pump). Rapid rewarming in normal Tyrode's solution induces relaxation with a half-time (t1/2) of 217 +/- 14 msec (mean +/- SEM). During cold exposure, changing the superfusate to a sodium-free, calcium-free medium with 2 mM CoCl2 (to eliminate Na-Ca exchange) slightly slows relaxation upon rewarming in the same medium (t1/2 = 279 +/- 44 msec). Addition of 10 mM caffeine (which prevents SR calcium sequestration) to normal Tyrode's solution during cold superfusion slows relaxation somewhat more (t1/2 = 376 +/- 31 msec) than sodium-free, calcium-free solution. However, if both interventions are combined (sodium-free + caffeine) during the cold exposure and rewarming, the relaxation is greatly slowed (t1/2 = 2,580 +/- 810 msec). These results suggest that either the SR calcium pump or, to a lesser extent, sarcolemmal Na-Ca exchange can produce rapid relaxation, but if both systems are blocked, relaxation is very slow. If muscles are equilibrated with 500 nM ryanodine before cooling, relaxation upon rewarming is not greatly slowed (t1/2 = 266 +/- 37 msec) even if sodium-free, calcium-free solution is applied during the cold and rewarming phases (t1/2 = 305 +/- 66 msec). This result suggests that ryanodine does not prevent the SR from accumulating calcium to induce relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Regional cerebral oxygenation during cardiopulmonary bypass.

A significant number of patients suffer transient neuropsychological dysfunction after coronary artery bypass graft (CABG) surgery. Recent studies have implicated reduced levels of O2 supply/demand ratio during the rewarming phase of cardiopulmonary bypass (CPB). Using a near infrared spectroscopy (NIRS) system that permits continuous noninvasive monitoring of regional cerebral O2 saturation (rSO2), we investigated rSO2 during CPB. Following Institution Review Board approval and informed consent, 10 patients undergoing elective CABG were studied. Nonpulsatile CPB with a membrane oxygenator, haemodilution and alpha-state pH management was used. The NIRS system consisting of two low-power laser diode sources (780 nm and 810 nm) with a photodetector placed on the frontal cortex was used to measure continuously haemoglobin, oxyhaemoglobin and cerebral blood volume. Continuous rSO2 measurements were obtained before, during moderate hypothermia, and during the rewarming phase of CPB. A rSO2 < 50% was defined as abnormal. Onset of rSO2 < 50% was at 32 degrees C, and the highest incidence occurred during the late stages of rewarming (35-37 degrees C). On rewarming from hypothermic CPB, 70% of our patients sustained a rSO2 < 50% for an average total duration of 9.3 minutes, primarily at the end of the rewarming period. This suggests a transient global imbalance in cerebral O2 supply and demand in a large percentage of patients during the rewarming phase of CPB. However, it has not been determined how long a rSO2 < 50% can be permitted before neuropsychological dysfunction is induced. Additional studies correlating psychometric testing with rSO2 measurements should prove useful in detecting episodes of impaired cerebral oxygenation, and help define rewarming protocols.

Aged↗
PubMed1996

Moderate hypothermia in patients with severe head injury: cerebral and extracerebral effects.

Cerebral and extracerebral effects of moderate hypothermia (core temperature 32.5 degrees C-33.0 degrees C) were prospectively studied in 10 patients with severe closed head injury (Glasgow Coma Scale score < 7) in the intensive care unit of a university hospital. Hypothermia was induced by cooling the patient's body surface with water-circulating blankets. Before cooling, a conventional intracranial pressure (ICP) reduction therapy was applied, which remained unchanged throughout the study. Cerebral blood flow (CBF), cerebral metabolic rates for oxygen (CMRO2) and lactate (CMRL), and ICP were simultaneously measured prior to inducing hypothermia, after obtaining hypothermia, after 24 hours of hypothermia, and after rewarming. With respect to extracerebral effects, supplemental investigations were conducted 24 and 72 hours after rewarming. The median delay between injury and induction of hypothermia was 16 hours. Hypothermia reduced CMRO2 by 45% (p < 0.01), whereas CBF did not change significantly. Before cooling, six patients had elevated CMRL indicating cerebral ischemia. Cooling normalized CMRL in all patients (p < 0.01). The intracranial hypertension present prior to cooling declined markedly during hypothermia (p < 0.01) without significant rebound effects after rewarming. Cardiac index decreased by 18% after hypothermia was reached (p < 0.05), recovered at 24 hours of hypothermia, and surpassed baseline values after rewarming. Platelet counts dropped continuously up to 24 hours after rewarming (p < 0.01). Plasma coagulation tests did not show significant worsening. Creatinine clearance decreased during cooling (p < 0.01) and recovered by 24 hours after rewarming. Twenty-four hours after cooling had begun, eight patients had elevated serum lipase activity (p < 0.01) and four of them acquired pancreatitis. Rewarming normalized both pancreatic alterations. Seven patients made a good recovery; one survived severely disabled; and two patients died. Moderate hypothermia is effective in preventing secondary brain damage while reducing cerebral ischemia. However, there are potentially hazardous side effects that require additional monitoring.

Adolescent↗
PubMed1990

The effects of an iron chelator on cellular injury induced by vascular stasis caused by hypothermia.

Rewarming of a cooled rabbit leg was associated with the generation of oxygen-derived free radicals, shown to be instrumental for tissue injury occurring during rewarming. The present study used a compound that, by its ability to bind with free iron, can remove hydroxyl radical (OH.) from tissue. Deferoxamine reduced tissue injury during cooling and rewarming, as evidenced by its ability to decrease tissue release of lactic acid dehydrogenase and creatine kinase. Deferoxamine also reduced the formation of OH. and lipid peroxidation during the rewarming phase. This compound did not have any effect on the arterial blood flow pattern, which uniformly decreased during cooling and was restored during rewarming. The results of this study indicate the efficacy of deferoxamine in reducing cellular injury associated with cold and rewarming and further suggest a role for oxygen-derived free radicals in the pathophysiology of cold-rewarming injury.

Animals↗
PubMed1994

[Postoperative warming therapy in the recovery room. A comparison of radiative and convective warmers].

Hypothermia (Tcore < 36 degrees C) can be observed in 60%-80% of all admissions to the post-anaesthetic recovery unit. Effective warming devices may accelerate rewarming, improve patient comfort, and suppress shivering thermogenesis. This study was designed to compare the efficiency of warming devices in extubated postoperative patients and their effect on postoperative oxygen uptake (VO2). METHODS. Thirty-five ASA I and II patients after laparoscopic hernioplastic repair with core temperatures < 36 degrees C were randomly assigned to either postoperative nursing under a radiant heater (group R, n = 11, Aragona Thermal Ceilings CTC X, Aragona Medical AB, Täby, Sweden), a forced air system (group L, n = 12, Bair Hugger, Augustine Medical Inc., Eden Prairie, Minnesota, USA), or a normal cotton hospital blanket (group K, n = 12). Anaesthesia was conducted totally intravenously with propofol, alfentanil, and vecuronium. Mean body temperature and total body heat were calculated from urinary bladder temperature and four subcutaneous temperature measurements. The rate of thermogenesis was calculated from continuous measurement of VO2 (Datex Deltatrac Metabolic Monitor, Datex Instrumentarium Corp., Helsinki, Finland). Heat balance was derived from the increase in total body heat minus body heat production. Heart rate and noninvasive blood pressure were measured by the Cardiocap (Datex Instrumentarium Corp., Helsinki, Finland). All data were transferred to an IBM-compatible computer at 60-s intervals. Measurements were stopped when core temperature reached 37 degrees C. The rate of change was calculated for each variable for the period 15 min after the beginning of rewarming to attainment of 37 degrees C. Data are presented as median, minima, and maxima (min<==>max); the Mann-Whitney U test was used to test for significance of group differences. RESULTS. All groups were comparable for body weight, height, age, and amount of postoperative infusions. Temperatures at admission were 35.2 (33.4<==>35.9), 34.7 (34.3<==>35.8), and 35.4 (34.3<==>35.9) degrees C for groups R, B, and K, respectively. No significant differences in the rate of central rewarming could be found for these groups with 0.81 (0.41<==>1.32), 0.76 (0.40<==>1.07), and 0.70 (0.37<==>1.13) degrees C/h (Fig. 1). The mean VO2 of 3.41 (3.07<==>3.73), 3.55 (2.78<==>4.06), and 3.79 (2.51<==>7.00) ml/kg/min also did not differ significantly (Fig. 3). Significant differences between groups R and B [4.39 (3.74<==>6.19) and 4.30 (3.46<==>6.67) ml/kg/min] and K [5.92 (3.79<==>10.64) ml/kg/min] were found for VO2 maxima during the course of investigation (Fig. 4). The heat balance revealed significant differences among treatment and control groups with -88 (-226<==>+30), -41 (-212<==>+12), and -191 (-265<==>-86) kJ/h for groups R, B, and K. We additionally calculated the heat balance as a quotient, which showed 0.70 (0.22<==>1.07), 0.86 (0.44<==>1.04), and 0.49 (0.31<==>0.79) for groups R, B, and K (Fig. 4). The mean rate-pressure product of all groups did not differ significantly during the period of investigation. CONCLUSIONS. Neither external heat supply by radiant heat nor by a forced warm air system significantly reduced rewarming time in extubated, awake patients. As measured by heat balance, both active treatments saved about 20% more body heat production than in the control group. Continuing peripheral vasoconstriction may be the reason for the low efficiency of heat transfer. Thermal treatment did reduce the peak load (max. VO2) on the oxygen transport systems, though shivering was treated by pethidine if it occurred. External rewarming did not reduce the average load (mean VO2). Thus, concerning the goal of accelerating rewarming, it appears more rational to prevent intraoperative heat loss. For a comparison of efficiency of different warming devices, postoperative extubated patients do not appear to be an ideal model for study.

Adult↗
PubMed1998

Temporal relation of ATP-sensitive potassium-channel activation and contractility before cardioplegia.

BACKGROUND: Pharmacologic treatment using potassium-channel openers (PCOs) before cardioplegic arrest has been demonstrated to provide beneficial effects on left ventricular performance with subsequent reperfusion and rewarming. However, the PCO treatment interval necessary to provide protective effects during cardioplegic arrest remains to be defined. The present study was designed to determine the optimum period of PCO treatment that would impart beneficial effects on left ventricular myocyte contractility after simulated cardioplegic arrest. METHODS: Left ventricular porcine myocytes were assigned randomly to three groups: (1) normothermic control = 37 degrees C for 2 hours; (2) cardioplegia = K+ (24 mEq/L) at 4 degrees C for 2 hours followed by reperfusion and rewarming; and (3) PCO and cardioplegia = 1 to 15 minutes of treatment with the PCO aprikalim (100 micromol/L) at 37 degrees C followed by hypothermic (4 degrees C) cardioplegic arrest and subsequent rewarming. Myocyte contractility was measured after rewarming by videomicroscopy. A minimum of 50 myocytes were examined at each treatment and time point. RESULTS: Myocyte velocity of shortening was reduced after cardioplegic arrest and rewarming compared with normothermic controls (63+/-3 microm/s versus 32+/-2 microm/s, respectively; p < 0.05). With 3 minutes of PCO treatment, myocyte velocity of shortening was improved after cardioplegic arrest to values similar to those of normothermic controls (56+/-3 microm/s). Potassium channel opener treatment for less than 3 minutes did not impart a protective effect, and the protective effect was not improved further with more prolonged periods of PCO treatment. CONCLUSIONS: A brief interval of PCO treatment produced beneficial effects on left ventricular myocyte contractile function in a simulated model of cardioplegic arrest and rewarming. These results suggest that a brief period of PCO treatment may provide a strategy for myocardial protection during prolonged cardioplegic arrest in the setting of cardiac operation.

Adenosine Triphosphate↗
PubMed1996

Afterdrop after hypothermic cardiopulmonary bypass: the value of tympanic membrane temperature monitoring.

OBJECTIVES: After weaning from cardiopulmonary bypass (CPB), a decrease in nasopharyngeal temperature (NPT) occurs (afterdrop). The pathophysiology of the afterdrop remains unclear: It might be caused by either inadequate total body rewarming on CPB or to heterogenous distribution of heat during CPB, with subsequent redistribution of heat from the warmer core to the cooler shell tissues. The study objectives were (1) to determine whether post-CPB afterdrop is the result of a negative CPB thermal balance, and (2) to investigate which sites (if any) could best predict the afterdrop. DESIGN: Prospective evaluation using within-patient comparisons during CPB cooling, CPB rewarming, and 45 minutes post-CPB. SETTING: Adult patients gave informed consent before a cardiac surgical procedure in a university hospital. PARTICIPANTS: Eight patients undergoing CABG or valvular replacement with hypothermic CPB (NPT near 29 degrees C) and standardized general anesthesia. INTERVENTIONS: Each patient was studied with temperature monitors (Mon-a-therm 7000; Mallinckrodt-Medexel, Gemenos, France) attached to disposable thermocouple probes placed as follows: urinary bladder, rectum, deltoid, esophagus, nasopharynx, tympanic membrane, and four skin sites. In addition, the temperatures from the thermistors of the pulmonary artery catheter, and the arterial and venous lines of the CPB circuit were considered. Thirteen sites for monitoring temperature were studied. MEASUREMENTS AND MAIN RESULTS: Temperatures were recorded every 5 minutes, from the beginning of CPB to the 45th minute after CPB, and thermal exchanges were calculated: change in body heat (QBH), thermal exchanges between the patient and the pump (QCPB), metabolic heat production (Qm) (equal to calculated VO2 at the pump level), and heat loss to the environment (QS) (equal to QBH-QCPB-Qm). Thermal exchanges were obtained in six patients during the plateaus of cooling and rewarming, during the whole CPB phase, and after CPB. It was found that despite a change in QBH during rewarming (1,017 +/- 88 kJ) that was slightly greater than during cooling (-1,008 +/- 104 kJ) (mean +/- SEM), a significant decrease in post-CPB "core" temperature occurred (afterdrop: -1.4 degrees C). Magnitude of the afterdrop was directly related to the magnitude of tympanic membrane cooling and was negatively correlated to the temperature difference between the warmest site (tympanic membrane) and the coolest site (cutaneous thigh temperature) observed at the end of rewarming (r = -0.667; p < 0.05). CONCLUSIONS: It is suggested that besides post-CPB heat loss, redistribution of heat may be involved in the mechanism of the afterdrop and that measurements of tympanic membrane and cutaneous thigh temperatures are the best monitors of adequacy of rewarming during CPB.

Adult↗
PubMed2003

The neurologic sequelae of cardiopulmonary bypass-induced cerebral hyperthermia and cerebroprotective strategies.

Cerebral hyperthermia during the rewarming phase of cardiopulmonary bypass (CPB) is associated with adverse outcomes. Cerebral hyperthermia can exacerbate a preexisting injury prior to rewarming, and may be damaging in itself. Temperature and cerebral metabolic rate (CMRO2) play a vital role in cerebral autoregulation. Therefore, hyperthermia can have a strong impact on cerebral oxygen transfer, and neurologic outcome. Glutamate levels can increase during cerebral hyperthermia, leading to eventual cell death. Rapid rewarming decreases jugular venous hemoglobin saturation, creating a mismatch between cerebral oxygen consumption and delivery. With these ill effects in mind, cerebral protection during CPB is imperative. Special attention should be given during rewarming to prevent these harmful outcomes. Pharmacologic agents such as sodium nitroprusside can be used to assist the rewarming process. Temperature management is the key component during the rewarming phase of CPB in the prevention of cerebral hyperthermia.

Body Temperature Regulation↗
PubMed1993

Experimental studies on the treatment of frostbite in rats.

The effect of treatment by high dose of vitamin C, rapid rewarming by 37 degrees C water alone and with vitamin C, rapid rewarming by 37 degrees C decoction of Indian black tea alone and with vitamin C for experimentally produced frostbite was evaluated in 6 groups (25 each) of rats. Frostbite was produced experimentally in the hind limbs by exposing the animals at -15 degrees C for 1h using the harness technique. The degree of injury was assessed and classified on the basis of tissue necrosis at the end of 15 days. Administration of high dose of vitamin C for prolonged period and rapid rewarming at 37 degrees C water bath immediately after cold exposure apparently reduced the tissue damage. High dose of vitamin C therapy preceded by rapid rewarming in plain water showed additional benefit. Rapid rewarming in decoction of Indian tea resulted in identical beneficial effect. The degree of tissue preservation was highest with rapid rewarming in tea decoction followed by high dose of vitamin C.

Animals↗
PubMed1983

Raynaud's syndrome. Treatment with sublingual administration of nitroglycerin, swinging arm maneuver, and biofeedback training.

Sublingual (SL) administration of nitroglycerin, a swinging arm maneuver, and biofeedback were evaluated for their effectiveness in decreasing hand rewarming time after ice immersion in six patients with Raynaud's disease and four patients with Raynaud's phenomenon. After ice immersion of their hands, ten normal patients showed rewarming to baseline temperatures in less than six minutes, while in nine of ten patients with Raynaud's syndrome, rewarming took more than 40 minutes. Two of ten patients with Raynaud's syndrome showed rewarming in less than six minutes after SL administration of nitroglycerin, while eight of ten patients with Raynaud's syndrome showed rewarming in less than 20 minutes after biofeedback training sessions. Six of the ten still showed rewarming in 20 minutes or less eight weeks after the sessions were over. A swinging arm maneuver provided no objective improvement. Sublingual administration of nitroglycerin provides a new alternative therapy for certain individuals. Effective biofeedback training can be learned in a relatively short time but should be reserved for the well-motivated patient.

Adult↗
PubMed1998

[The effect of pump flow on cerebral oxygen metabolism during cardiopulmonary bypass].

We evaluated effects of pump flow on cerebral metabolism using transcranial Doppler (TCD) during cardiopulmonary bypass (CPB) in 22 adult patients undergoing coronary artery bypass grafting. All the patients were anesthetized with high dose fentanyl. The pump flow was controlled with non-pulsatile roller pump at 2.2-2.5 L/min/m2 in group L and 2.7-3.0 L/min/m2 in group H under alpha-stat acid-base regulation. Pharyngeal temperature was kept at 31 degrees C in steady CPB state. Mean velocity of middle cerebral artery (MCAV) was monitored with TCD fixed on the temple continuously. Cerebral oxygen consumption was estimated by relating the difference in oxygen content between arterial and venous (jugular bulb) blood (AVDO2) to flow velocity. In group L, blood oxygen saturation of jugular bulb (SjO2) was stable during hypothermic period, but decreased significantly during rewarming period. In group H, SjO2 was significantly increased with cooling, but went down to preoperative level during rewarming period. Significant difference of SjO2 between two groups was noticed in rewarming period (52.9 +/- 10.0% in group L and 65.6 +/- 11.8% in group H, p = 0.0133). MCAV tended to decrease with cooling and increase with rewarming, but which was not significant change respectively. Relative cerebral metabolic rate for oxygen (rCMRO2) was defined as the percent change of the product AVDO2 and MCAV. In each group, rCMRO2 was decreased with cooling and increased with rewarming significantly. Especially, rCMRO2 right after CPB discontinued was increased 1.7 times in L group and 2.0 times in group H as much as that of steady state of CPB. It is suggested that cerebral metabolism should be decreased during cooling to 31 degrees C of pharyngeal temperature, 2.2-2.5 l/min/m2 of pump flow was adequate to keep SjO2 stable. On the other hand, it is necessary to increase pump flow to 2.7-3.0 l/min/m2 during rewarming period as cerebral oxygen metabolic demand becomes greater.

Aged↗
PubMed2000

Dynamic thermography of the knee joints in rheumatoid arthritis (RA) in the course of the first therapy of the patient with methylprednisolone.

Thermography in rheumatology is most often used in a static manner: after having fulfilled the conditions of standardized preparation of the patient in a cold examination room one or more thermograms are taken in standard positions for the respective joints. In our hospital the thermograms are more or less supplementary. The main examination result is a rewarming curve of the skin over the knee joints. The rewarming is provoked by dry cooling of the skin for one minute. Calculation of the slope of the rewarming curve and plotting the slope on a logarithmic scale shows two different rewarming processes in the skin overlying inflamed joints. The faster one is the rewarming by the arterial blood flow in the skin and the slower one is an additional rewarming by a pathological venous skin blood flow originating from deeper tissues under the skin. One has to suppose that the occurrence of excessive nitric oxide production in inflamed tissues is responsible for this pathological venous skin blood flow. Until now only nine patients receiving for the first time methylprednisolone could be included in a therapy study. Therefore only slight indications can be seen in the results. Whereas the erythrocyte sedimentation rate (ESR [mm/h] becomes more homogeneous (lower confidence interval CI 95) over the course of the treatment with decreasing drug dose, the thermal signs of inflammatory activity as measured by dynamic thermography have greater CI 95 values at the end than at the beginning of the treatment under study. This indicates that not all patients had sufficient antiinflammatory medication with the final 6 mg/d of methylprednisolone as measured by dynamic thermography but not by ESR or CRP.

Arthritis, Rheumatoid↗
PubMed1995

3,5,3' Triiodo-L-thyronine pretreatment with cardioplegic arrest and chronic left ventricular dysfunction.

BACKGROUND: The active form of thyroid hormone, T3, may be an important determinant of left ventricular (LV) function after hypothermic cardioplegic arrest and rewarming, particularly in patients with preexisting LV dysfunction. Thus, the present project tested the hypothesis that T3 pretreatment will improve myocyte contractile performance after hypothermic cardioplegic arrest and rewarming in the setting of chronic LV dysfunction. METHODS: Control LV porcine myocytes (n = 160) and cardiomyopathic LV (rapid pacing for 3 weeks at 240 beats/min) myocytes (n = 100) were treated with or without 80 pmol/L T3. Myocytes then were maintained in normothermic conditions (2 hours at 37 degrees C in media) or exposed to hypothermic cardioplegic arrest ([K+], 24 mmol/L; 2 hours at 4 degrees C) with subsequent rewarming. RESULTS: After cardioplegic arrest and rewarming, T3 pretreatment increased myocyte velocity of shortening by 41% in control myocytes and by 35% in cardiomyopathic myocytes when compared to untreated myocytes. Furthermore, T3 pretreatment followed by beta-adrenergic receptor stimulation with isoproterenol (25 nmol/L) improved myocyte velocity of shortening by 24% in control myocytes and 90% in cardiomyopathic myocytes after hypothermic cardioplegic arrest and rewarming, as compared with untreated myocytes. CONCLUSIONS: In summary, this study provides evidence to suggest that preemptive treatment with T3 may improve LV pump function and beta-adrenergic responsiveness after hypothermic cardioplegic arrest and rewarming in patients with underlying LV dysfunction.

Animals↗
PubMed1987

Hypothermic cardiopulmonary bypass: a comparison between alpha and pH stat regulation in the dog.

The accepted normal pH of 7.40 may not be optimal at lower temperatures. This study evaluated the effect of maintaining pH in the accepted normal range at hypothermia (group 1, pH stat) or at normothermia (group 2, alpha stat) on organ blood flow and hemodynamics in dogs. The desired pH was achieved at all temperatures by adjusting pCO2. Hypothermia to 20 degrees C was induced by high flow bypass in both groups followed by 45 min of reduced flow before rewarming. In group 1 (n = 10), pH was 7.45 +/- 0.02 at 20 degrees C and in group 2 (n = 11) it was 7.64 +/- 0.01. A greater base excess developed by the end of the low flow period in pH stat animals (-9.4 +/- 1.1 vs -2.8 +/- 0.8, P less than .001) and resulted in continued acidosis after rewarming in the pH stat group compared to those in the alpha stat group (7.32 +/- 0.03 vs 7.38 +/- 0.01, P less than .02). Expressed as a percentage of baseline, regional blood flows after rewarming for group 1 were: brain 112 +/- 8%, renal cortex 48 +/- 8% (P less than 0.005, rewarm vs baseline), renal medulla 36 +/- 9% (P less than 0.005, rewarm vs baseline), epicardium 198 +/- 40% (P less than 0.05, rewarm vs baseline), endocardium 151 +/- 25%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Thermal and cardiovascular changes during three methods of resuscitation from mild hypothermia.

The interrelations among core temperatures (cardiac, esophageal, tympanic, rectal), skin temperature, and cardiovascular function (cardiac output, arterial pressure, heart rate, total peripheral resistance) were studied in a conscious subject during entry into mild hypothermia through cold water (10 degrees C) immersion, and during rewarming by three basic procedures: peripheral heat donation (bath); core heat donation (inhalation); and no exogenous heat (spontaneous). Swan-Ganz catheterization of the heart enabled measurement of cardiac temperature as well as cardiac output by the thermal dilution method. During cooling, all sites of core temperature measurement showed similar rates of entry into hypothermia. However, during the rewarming procedures, divergent patterns of temperature change among the four sites occurred. Rectal and tympanic temperatures were not representative of cardiac temperature, but esophageal temperature was, and is therefore most suitable as a criterion for experimental evaluation of the thermal benefit of various core rewarming techniques. During the first 30 min of rewarming, rates of increase in cardiac temperature for bath, inhalation, and spontaneous procedures varied according to the proportions 4:2:1, respectively. No afterdrop of cardiac temperature occurred with the inhalation or spontaneous procedures, but an afterdrop at this site did occur during the first 15 min of bath rewarming as soon as skin temperature was greater than 30 degrees C. This afterdrop coincided with cardiovascular changes including abrupt decreases in arterial pressure and total peripheral resistance, along with increases in heart rate and cardiac output. Such evidence of increased peripheral circulation was not observed with the inhalation and spontaneous methods. The findings relate to experimental evaluation of rewarming techniques and principles for resuscitation of hypothermia victims, especially in the first-aid situation.

Baths↗
PubMed1995

Cerebral blood flow velocity in pediatric patients is reduced after cardiopulmonary bypass with profound hypothermia.

Transcranial Doppler sonography of the middle cerebral artery was used to determine whether cerebral perfusion was detectable in low flow states during operations with cardiopulmonary bypass in pediatric patients. Quantitative and qualitative differences in cerebral blood flow velocity after rewarming in patients treated with continuous low-flow bypass or deep hypothermic circulatory arrest were assessed. To determine whether the alterations in cerebrovascular resistance pattern observed in our patients undergoing profound hypothermia was more a function of perfusion technique than of minimum temperature during operation, a third group of patients treated with moderate hypothermia was studied. The three patient groups were the arrest group (N = 16), comprised of patients undergoing circulatory arrest at 18 degrees to 20 degrees C; the low-flow group (N = 16), patients treated with continuous low-flow (cardiac index 0.5 L/min per square meter) bypass at 18 degrees to 20 degrees C; and the moderate group (N = 5), patients treated with moderate hypothermia at 24 degrees to 28 degrees C. Flow velocity was detectable in all patients in the low-flow group, with mean arterial pressures as low as 15 mm Hg. Mean flow velocity was reduced after bypass as compared with prebypass values in both the arrest and low-flow groups (p = 0.0001). Mean flow velocity increased after bypass in the moderate group (p = 0.0001). A Doppler waveform pattern consistent with high cerebrovascular resistance was found in 67% of patients in the arrest group and 44% of those in the low-flow group. None of the patients in the moderate group exhibited such a pattern. Patients treated with profound hypothermia who underwent a period of cold full-flow reperfusion before rewarming did not exhibit this high resistance pattern after rewarming. The present findings indicate that profound hypothermia may evoke changes in the cerebral vasculature that result in decreased mean cerebral blood flow velocity after cardiopulmonary bypass rewarming. A period of cold full-flow reperfusion before rewarming may prevent these alterations and improve cerebral perfusion during rewarming.

Blood Flow Velocity↗