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On the thermal capacity of a bird's egg warmed by a brood patch.

Eggs of intermittently incubating birds are periodically rewarmed by a transient pulse of heat from the parent's brood patch. Estimating the energy cost of rewarming such an egg requires knowledge of the egg's thermal capacity, typically assumed to be the product of the egg's mass and its specific heat, designated here as the gravimetric thermal capacity. When chicken eggs are transiently warmed by an artificial brood patch, the energetic costs of the rewarming indicate that they have thermal capacities about one-third the gravimetric thermal capacity. In this article, I show that birds' eggs warmed locally by a brood patch have effective thermal capacities that differ substantially from the eggs' gravimetric thermal capacities, both in absolute magnitude and in response to varying the temporal properties of the transient pulse of heat. An effective thermal capacity exists because heat from a brood patch flows unevenly through an egg and because of thermal impedance effects on the unsteady component of heat flow into the egg. If these conditions in any way characterize the rewarming of eggs by intermittently incubating birds in nature, intermittent incubation may be considerably less costly in time and energy than has heretofore been assumed.

Animals↗

The diagnostic value of finger systolic blood pressure and cold-provocation testing for the vascular component of hand-arm vibration syndrome in health surveillance.

BACKGROUND: Hand-arm vibration syndrome (HAVS) is a complex condition with vascular, sensorineural and musculoskeletal components. A number of quantitative tests have been used for assisting in the diagnosis of HAVS and grading disease severity. AIMS: To investigate and compare the diagnostic value of finger systolic blood pressure (FSBP) and rewarming of finger skin temperature (FST) following cold-provocation testing, in the assessment of vascular HAVS. METHODS: Twenty-four individuals with vascular HAVS (Stockholm Workshop stage 2 or 3V) and 22 control subjects underwent FSBP measurements at 30, 15 and 10 degrees C and monitoring of FST following immersion of the hands in water at 15 degrees C for 5 min. RESULTS: There was a significant reduction in median FSBP% in the vascular HAVS group in the change in FSBP from 30 to 15 degrees C adjusted for brachial blood pressure (FSBPC%). There was no difference in the median time for FST to rewarm by 4 degrees C between HAVS cases and controls. The sensitivity and specificity of FSBP to discriminate between the groups varied between 44 and 61% and 91 and 95%, respectively. The sensitivity and specificity for the time for FST to rewarm by 4 degrees C were 71 and 77%. CONCLUSIONS: There is little evidence that the described form of finger rewarming after cold-provocation testing is a useful diagnostic test for vascular HAVS, although it may have some moderate influence in ruling out vascular problems. Based on our data, the FSBP may also have limited use in confirming a positive diagnosis of vibration-induced vascular problems. The higher specificity of the FSBP test suggests it may have some value in ruling out the vascular component of HAVS. The data from this study do not confirm the diagnostic power of FSBP for the vascular component of HAVS reported by a few other investigators.

Adult↗

Jejunal mucosal perfusion is well maintained during mild hypothermic cardiopulmonary bypass in humans.

UNLABELLED: In the present study, the effects of mild hypothermic (34 degrees C) cardiopulmonary bypass (CPB) on jejunal mucosal perfusion (JMP), gastric tonometry, splanchnic lactate, and oxygen extraction were studied in low-risk cardiac surgical patients (n = 10), anesthetized and managed according to clinical routine. JMP was assessed by endoluminal laser Doppler flowmetry. Patients were studied during seven 10-min measurement periods before, during, and 1 h after the end of CPB. Splanchnic oxygen extraction increased during hypothermia and particularly during rewarming and warm CPB. JMP increased during hypothermia (26%), rewarming (31%), and warm CPB (38%) and was higher 1 h after CPB (42%), compared with pre-CPB control. The gastric-arterial PCO(2) difference was slightly increased (range 0.04-2.26 kPa) during rewarming and warm CPB as well as 1 h after CPB, indicating a mismatch between gastric mucosal oxygen delivery and demand. None of the patients produced lactate during CPB. We conclude that jejunal mucosal perfusion appears well preserved during CPB and moderate (34 degrees C) hypothermia; this finding is in contrast to previous studies showing gastric mucosal hypoperfusion during CPB. IMPLICATIONS: Jejunal mucosal perfusion increases during mild hypothermic cardiopulmonary bypass (CPB). Intestinal laser Doppler flowmetry, gastric tonometry, and measurements of splanchnic lactate extraction could not reveal a local or global splanchnic ischemia during or after CPB. A mismatch between splanchnic oxygen delivery and demand was seen, particularly during rewarming and warm CPB.

Aged↗

Differences between aortic and radial artery pressure associated with cardiopulmonary bypass.

Previous investigators have identified an aortic-to-radial artery pressure gradient thought to develop during rewarming and discontinuation of cardiopulmonary bypass. The authors measured mean aortic and radial artery pressures before, during, and after cardiopulmonary bypass in 30 patients, to determine when the pressure gradient develops. The pressure gradient was also measured before and after intravenous injections of sodium nitroprusside (1 microgram/kg) and phenylephrine (7 micrograms/kg) to determine the effect of changes in systemic vascular resistance. A significant (P less than 0.05) pressure gradient (mean +/- SEM = 4.9 +/- 0.7 mmHg) developed upon initiation of cardiopulmonary bypass. This gradient did not change significantly during the middle of bypass (4.2 +/- 0.5 mmHg), with rewarming (4.8 +/- 0.7 mmHg), immediately prior to discontinuation of bypass (4.6 +/- 0.7), or 5 and 10 min following bypass (4.9 +/- 0.9 and 4.8 +/- 0.7 mmHg). Sodium nitroprusside significantly decreased systemic vascular resistance, by 15 +/- 2%, during the middle of bypass but did not affect the pressure gradient. Likewise, phenylephrine increased the systemic vascular resistance by 52 +/- 6% and 34 +/- 4% during the middle of bypass and rewarming, respectively, without affecting the pressure gradient. Although the exact mechanisms responsible for the pressure gradient remain unknown, these results suggest its etiology is associated with events occurring during initiation of cardiopulmonary bypass rather than with rewarming or discontinuation of cardiopulmonary bypass.

Aorta↗

Effect of intraportal glucose infusion on hepatic glycogen content and degradation, and outcome of liver transplantation.

Recent animal studies suggest that nutritional repletion may improve function of liver allografts, and the authors have found that intraportal glucose infusion in pigs produces rapid and substantial hepatic glycogenation. A controlled prospective randomized study in 32 patients was done to determine glycogen content and degradation in human livers during transplantation, and the effect of intraportal glucose-insulin infusions during the donor operation on these variables and on outcome of transplantation. Peripheral blood glucose concentrations were "clamped" at 14 mmol/L during the glucose-insulin infusion. Liver biopsies were taken at various stages of the procedure. Liver glycogen decreased 2.0 +/- 1.2 g/100 g dry weight liver (mean +/- standard error of the mean) in controls, but increased 6.8 +/- 1.8 g/100 g dry weight in glucose-infused donors. In both groups there was glycogen degradation during periods of cold preservation, anoxic rewarming, and after reperfusion with portal blood. Degradation rates were greater in the glucose-infused group than in controls in all three periods (p less than 0.05). Despite wide variation in postoperative aspartate aminotransferase (AST) levels among recipients in both groups, the difference in peak postoperative AST levels approached significance (p = 0.06). In addition, peak AST levels were closely correlated to anoxic rewarming time in both groups, but the slope of the relationship was much lower (3834 versus 734, p less than 0.01) in the glucose-infused group. Thus at anoxic rewarming times over 90 minutes, glycogenation was protective of liver function. Peak postoperative AST was significantly correlated to glycogen degradation in the cold preservation and rewarming periods in the glucose-infused group only. Intraoperative glucose infusions in humans can reglycogenate the liver, increase glycogen degradation, and improve certain outcome measures in liver transplantation.

Adult↗

Reperfusion with adenosine and nitroprusside improves preservation of isolated guinea pig hearts after 22 hours of cold perfusion with 2,3 butanedione monoxime.

The function of isolated guinea pig hearts treated with 2,3 butanedione monoxime (BDM) before, during, and initially after 22 h of hypothermic perfusion was examined during 4 h of normothermic reperfusion. BDM is a vasodilatory and negative inotropic agent that reversibly decreases sensitivity of contractile proteins to Ca2+. Also examined were the effects of adenosine (ADE) and nitroprusside (NP) in improving coronary flow (CF) and contractile function when given with BDM during rewarming and during the initial period of normothermic reperfusion. Isovolumetric left ventricular pressure (LVP), CF, and percentage of O2 extraction (%O2E) were measured in Krebs-Ringer-perfused hearts divided into three groups of 11 hearts each: drug-free controls (0 BDM); 10 mM BDM alone; and 10 mM BDM + 10 microM ADE + 100 microM NP. BDM was given 20 min before hypothermia, during hypothermia (3.8 degrees +/- 0.1 degree C) for 22 h, and for 30 min after rewarming to 37 degrees +/- 0.1 degree C; ADE was given with NP for only 20 min before and during rewarming and for 30 min after rewarming. Hearts were perfused at low constant flow with oxygenated Krebs' solution during hypothermia. After 2.5-h normothermic reperfusion, LVP (initial controls 108 +/- 6 mm Hg) increased more with BDM + ADE + NP (80 +/- 4% of control) than with BDM alone (62 +/- 3%) or without BDM (28 +/- 5%). CF (controls 6.0 +/- 0.5 ml/g/min) decreased less with BDM + ADE + NP (77 +/- 4% of control) than with BDM alone (60 +/- 5%) or without BDM (53 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗

Effects of local cooling on microvascular hemodynamics and leukocyte adhesion in the striated muscle of hamsters.

OBJECTIVES: Cellular metabolism is dependent on the local temperature in tissues. Induced hypothermia has been shown to be protective in a number of conditions, especially traumatic, ischemic, burn, and neurological injury. However, the protective mechanisms of cold therapy remain controversial and the hemodynamic changes in the microcirculation of striated muscles in response to hypothermia have not been studied in detail previously. METHODS: In this study, we investigated the microvascular response of local cooling and rewarming in the striated muscle of hamsters by use of the dorsal skinfold preparation and in vivo fluorescence microscopy. RESULTS: We found that reduction of the surface temperature to 8 degrees C for 30 minutes caused arteriolar vasoconstriction with a decrease in diameters by 43+/-7% while the venular and capillary diameters remained unchanged. The cooling procedure also markedly reduced the functional capillary density and the blood flow velocity and diameters in all vessel types, i.e., arterioles, venules, and capillaries. Moreover, the percentage of capillaries with no flow increased from 0.4+/-0.5% to 44+/-14% after 10 minutes of cold therapy. However, these hemodynamic changes induced by local hypothermia were completely reversed to the precooling values after termination of cooling and 30 min of rewarming. Strikingly, we found no increase in the number of adherent leukocytes and vascular permeability after the cooling and rewarming period, while, in contrast, additional experiments with warm ischemia (30 minutes) and reperfusion (30 minutes), i.e., reduced microvascular perfusion and reperfusion at normothermia, caused a sustained decrease in local perfusion and a nine-fold increase in venular leukocyte adhesion. CONCLUSIONS: Taken together, our functional data demonstrate that hypothermia markedly reduces microvascular perfusion, which is completely restored upon rewarming. The reduced microvascular perfusion during hypothermia did not provoke an inflammatory response, whereas leukocyte recruitment was prominent after reduced perfusion at normothermia, indicating that transient hypothermia has no adverse effects on microvascular parameters in the striated muscle in vivo.

Animals↗

Chilling-Induced Lipid Degradation in Cucumber (Cucumis sativa L. cv Hybrid C) Fruit.

Chilling at 4 degrees C in the dark induced lipid degradation in cucumber (Cucumis sativa L.) fruit upon rewarming at 14 degrees C. Rates of ethane evolution by fruits rewarmed after 3 days of chilling were up to four-fold higher than those evolved by unchilled (14 degrees C) fruits (0.02-0.05 picomoles gram fresh weight(-1) hour(-1)). This potentiation of lipid peroxidation occurred prior to irreversible injury (requiring 3 to 7 days of chilling) as indicated by increases in ethylene evolution and visual observations. Decreases in unsaturation of peel tissue glycolipids were observed in fruits rewarmed after 3 days of chilling, indicating the plastids to be the site of the early phases of chilling-induced peroxidation. Losses in unsaturation of tissue phospholipids were first observed only after chilling for 7 days. Phospholipase D activity appeared to be potentiated in fruits rewarmed after 7 days of chilling as indicated by a decrease in phosphatidylcholine (and secondarily phosphatidylethanolamine) with a corresponding increase in phosphatidic acid. These results indicate that lipid peroxidation may have a role in conferring chilling injury.

Journal Article↗

Oesophageal thermal tube for intraoperative hypothermia in liver transplantation.

In order to prevent the occurrence of major hypothermia during liver transplantation, with its deleterious effects on intraoperative cardiovascular activity and on postoperative graft functioning, this study evaluated the benefit of an oesophageal rewarmer, used during surgery, in addition to the usual methods of warming (OR temperature at 22 degrees C, rewarming of fluids and blood, heating mattress, heat and moisture exchanger). We compared 10 patients with an oesophageal rewarmer (OeR group) to 10 patients without (Control group). The anaesthetic procedure was similar in all cases. Rectal (RT) and pulmonary artery (PT) temperatures were recorded during the three phases of surgery (pre-anhepatic, anhepatic, postanhepatic phase) and their time course was analysed with non-parametric tests. The two groups were comparable with regard to duration of surgery, blood and fluid requirements and veno-venous bypass flow rate. The RT decreased similarly in both groups, but was significantly higher in the OeR group at peritoneum closure (P < 0.01). The PT was higher in the OeR group after onset of venous shunting (P < 0.05) and during the third phase of surgery (P < 0.01). Three incidents (one leakage and two herniations of the latex tube) occurred, without detrimental effects on the patients. It is concluded that the oesophageal heat exchanger allows better rewarming after revascularization of the graft, but is unable to prevent cardiac hypothermia at unclamping.

Adult↗

Cardiovascular effects of neuromuscular blockade during induced hypothermia.

Young lambs were used to study the effects of progressive cooling and rewarming on cardiovascular function during neuromuscular blockade induced by gallamine. Initially, it was shown that gallamine exerted no immediate, direct haemodynamic effect in normothermic or hypothermic lambs (cooled by 10 degrees C). By comparison with hypothermic controls, neuromuscular blockade was associated with increases in left ventricular (LV) max dP/dt (153%; P less than 0.02) as cooling progressed, and even greater increases (232%; P less than 0.001) during rewarming. It was concluded that these changes seem likely to represent enhanced myocardial contractility since preload did not closely follow LV max dP/dt (heart rate and mean aortic pressure fell gradually during cooling but values were restored in the rewarming phase). LV max dP/dt in lambs given gallamine only after cooling also showed a similar response during rewarming. Results of this study may have clinical relevance relating to the mechanical recovery of the hypothermic heart in patients receiving neuromuscular blockade during cardiac surgery, and they argue against using gallamine as such an agent.

Animals↗

Intracellular Ca2+ transients during rapid cooling contractures in guinea-pig ventricular myocytes.

1. We measured intracellular Ca2+ transients during rapid cooling contractures (RCCs) in guinea-pig ventricular myocytes using the fluorescent Ca2+ indicator, Indo-1. 2. Rapid cooling of myocytes from 22 to 0-1 degrees C induced a rapid increase in [Ca2+]i which preceded the peak of the contraction and was sometimes large enough to saturate Indo-1. This indicates that [Ca2+]i may reach greater than 10 microM during an RCC. 3. The [Ca2+]i during the RCC slowly declined from its peak value and most of this decline in [Ca2+]i can be attributed to slow reaccumulation of Ca2+ by the sarcoplasmic reticulum (SR) in the cold. RCCs induced in the absence of Cao2+, were not different from control, supporting previous conclusions that RCCs depend exclusively on intracellular Ca2+ stores. 4. RCCs are depressed by long rest periods (rest decay) or by exposure to ryanodine or caffeine, which supports conclusions that RCCs are due to Ca2+ release from the SR. The rest decay of RCCs can be almost completely prevented by applying Nao(+)-free solution during the rest period. This implies that the loss of SR Ca2+ during rest depends on the sarcolemmal Na(+)-Ca2+ exchange (and not the sarcolemmal Ca2(+)-ATPase pump). 5. Rapid rewarming during an RCC normally leads to an additional transient contraction (or rewarming spike), without any increase in [Ca2+]i. Thus, the rewarming spike might be attributable to an increase in myofilament Ca2+ sensitivity induced by rewarming. 6. A second RCC is used to assess the fraction of Ca2+ which is re-sequestered by the SR during relaxation from the first RCC. In control solution progressive RCCs decline in amplitude, but in Na(+)-free, Ca2(+)-free solution they are of constant amplitude. We conclude that the SR Ca2+ pump and Na(+)-Ca2+ exchange are responsible for relaxation and that the latter may account for 20-50% of relaxation. 7. These results support the use of RCCs as a useful means of assessing SR Ca2+ content in intact cardiac muscle cells.

Animals↗

A morphometric study of endothelial cells of human corneas stored in MK media and warmed at 37 degrees C.

No study has yet been done to investigate the changes in endothelial cell size, perimeter, and density that may result from the warming of corneas in MK (McCarey-Kaufman) medium for specular microscopy. In the present investigation eye bank eyes were stored in MK medium at 4 degrees C and rewarmed daily for six days at 37 degrees C before specular photography of the endothelium was performed. These photographs were compared with wet mount preparations stained with trypan blue and alizarin red made from the same corneas and those stored without rewarming for six days. In addition all corneas were qualitatively analysed with the scanning electron microscope (SEM). The data from serial specular photography were insufficient to allow significant conclusions to be drawn about day to day changes in cell morphology. However, analysis of wet mount preparations revealed that cell density and perimeter varied significantly between those corneas rewarmed daily and those held in cold storage for six days. SEM studies showed an intact cell monolayer with cell loss along the folds of corneal endothelium. We therefore concluded that repeated rewarming at 37 degrees C of corneas stored in MK medium at 4 degrees has a deleterious effect on cell morphology and that folds induced by swelling of corneal tissue result in endothelial cell damage with some loss.

Cell Count↗

Temperature dependence of myofilament Ca sensitivity of rat, guinea pig, and frog ventricular muscle.

Cooling the superfusate of intact ventricular muscle, from 30 degrees C to below 4 degrees C in less than 2 s, leads to contractures thought to reflect the amount of Ca available for release from the sarcoplasmic reticulum (SR). On rewarming, tension transiently increases in guinea pig and rat ventricular muscle. It has been proposed that this rewarming tension spike reflects changes in myofilament Ca sensitivity and maximum Ca-activated force (Cmax) associated with rewarming. There are differences in intracellular Ca regulation among cardiac muscle preparations. Some characteristics of rapid-cooling contractures (e.g., the magnitude of the rewarming spike) also differ between species. Therefore, the Ca sensitivity of skinned ventricular muscle from the rat, guinea pig, and frog was determined at 29 (22 degrees C for frog ventricular preparations), 8, and 1 degrees C. The results show that cooling rat and guinea pig ventricular muscle from 29 to 1 degrees C shifts the pCa vs. tension relationship toward higher [Ca2+] by 0.65 and 0.55 pCa units, respectively. Cooling to 1 degrees C also reduced Cmax to 3.3 and 7.8% of that at 29 degrees C in rat and guinea pig ventricular muscle, respectively. Similar results were found for frog ventricular muscle, in which cooling from 22 to 1 degrees C reduced Ca sensitivity by 0.6 pCa units and Cmax to 45.7% of its value at 22 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Actin Cytoskeleton↗

Preservation of metabolic reserves and function after storage of myocytes in hypothermic UW solution.

Isolated rat myocytes cold stored anaerobically up to 24 h in University of Wisconsin solution lost 95% of their ATP and 100% of their glycogen. They underwent contracture when rewarmed in a Krebs-Henseleit (KH) medium that contained Ca unless Ca addition was delayed. In the latter case, cell function, measured by stimulation-induced cell shortening, was surprisingly well retained. Aerobically stored cells were resistant to Ca on rewarming, although 96% of glycogen was still lost, along with 46% of ATP. Cells that were incubated for 48 h aerobically with the substrates glucose and pyruvate at pH 6.2 retained 77% of their ATP and 59% of their glycogen, with good cell morphology. At pH 6.2, the demand for ATP was only 55% of that at pH 7.4. However, after rewarming, these cells functioned no better than anaerobically stored cells, although their inotropic response to isoproterenol was improved. We conclude that 1) aerobic conditions with substrates at low pH preserve myocyte metabolic reserves well for 48 h, partly by reducing the demand for ATP; 2) rewarming conditions are critical for anaerobically stored cells with metabolic stores that are severely depleted; and 3) unloaded cell function is surprisingly insensitive to a period of severe metabolic deprivation.

Adenosine↗

Sustained hypothermia accelerates microvascular thrombus formation in mice.

Cold is supposed to be associated with alterations in blood coagulation and a pronounced risk for thrombosis. We studied the effect of clinically encountered systemic hypothermia on microvascular thrombosis in vivo and in vitro. Ferric chloride-induced microvascular thrombus formation was analyzed in cremaster muscle preparations from hypothermic mice. Additionally, flow cytometry and Western blot analysis was used to evaluate the effect of hypothermia on platelet activation. To test whether preceding hypothermia predisposes for enhanced thrombosis, experiments were repeated after hypothermia and rewarming to 37 degrees C. Control animals revealed complete occlusion of arterioles and venules after 742 +/- 150 and 824 +/- 172 s, respectively. Systemic hypothermia of 34 degrees C accelerated thrombus formation in arterioles and venules (279 +/- 120 and 376 +/- 121 s; P < 0.05 vs. 37 degrees C). This was further pronounced after cooling to 31 degrees C (163 +/- 57 and 281 +/- 71 s; P < 0.05 vs. 37 degrees C). Magnitude of thrombin receptor activating peptide (TRAP)-induced platelet activation increased with decreasing temperatures, as shown by 1.8- and 3.0-fold increases in mean fluorescence after PAC-1 binding to glycoprotein (GP)IIb-IIIa and 1.6- and 2.9-fold increases of fibrinogen binding on incubation at 34 degrees C and 31 degrees C. Additionally, tyrosine-specific protein phosphorylation in platelets was increased at hypothermic temperatures. In rewarmed animals, kinetics of thrombus formation were comparable to those in normothermic controls. Concomitantly, spontaneous and TRAP-enhanced GPIIb-IIIa activation did not differ between rewarmed platelets and those maintained continuously at 37 degrees C. Moderate systemic hypothermia accelerates microvascular thrombosis, which might be mediated by increased GPIIb-IIIa activation on platelets but does not cause predisposition with increased risk for microvascular thrombus formation after rewarming.

Animals↗

Effect of cold preservation on pulmonary arterial smooth muscle cells.

The efficacy of preservation fluids on the cytoskeleton and contractile function of porcine pulmonary arterial smooth muscle (SM) cells during cooling and rewarming was evaluated, using EuroCollins solution (EC), University of Wisconsin solution (UW), Marshall's solution (MS), and tissue culture growth medium (GM). Functional studies included passive distensibility and contraction to prostaglandin F2a (PGF2a) in arterial rings and wrinkling of silicone membranes by cooled-rewarmed cultured SM cells. Immunofluorescence measurements were made of actin brightness in cooled arterial rings. Cultured SM monolayers were stained with antibodies to SM alpha-actin, SM myosin, and tubulin. In cooling, all solutions resulted in increased arterial distensibility, whereas EC and MS reduced cell wrinkling. With the use of all solutions, actin cables thinned, myosin filaments dissociated, and microtubules depolymerized. During rewarming, resistance to imposed tension increased in all arterial rings. After GM,ED, and MS preservation, contraction to PGF2a increased. Wrinkling increased and actin-myosin cables shortened after GM and EC; after UW, wrinkling decreased and actin-myosin cables thinned. No recovery occurred after MS. Thus the type of preservation solution influenced contractility during preservation and after rewarming. The absence of spontaneous contraction in cells cooled in UW may be advantageous.

Actins↗

Finger temperature after a finger-cooling test: influence of air temperature and smoking.

Skin temperature of one finger was measured before and after immersion of the gloved fingers of both hands in 16 degrees C water for 5 min [room temperature (Ta) 24 or 20 degrees C]. At Ta 24 degrees C, 23 of 25 normal nonsmokers (92%) had finger rewarming to above 24 degrees C in 12 min after cold immersion, at Ta 20 degrees C, only 1 of 12 (8%) had similar rewarming. Among 12 habitual smokers only 4 (33%) rewarmed above 24 degrees C (Ta 24 degrees C) following a 1-h abstinence from smoking, but 8 (67%) did so after a 24-h abstinence. Only 2 of these 8, however, did so in a retest 10 min after smoking a cigarette. The smokers were not tested at Ta 20 degrees C. We conclude that air temperature and cigarette smoking are important determinants of finger rewarming following a finger-cooling test.

Adult↗

Global and regional cerebral blood flow in neonatal piglets undergoing pulsatile cardiopulmonary bypass with continuous perfusion at 25 degrees C and circulatory arrest at 18 degrees C.

To investigate the influence of hypothermic cardiopulmonary bypass (HCPB) at 25 degrees C and circulatory arrest at 18 degrees C on the global and regional cerebral blood flow (CBF) during pulsatile perfusion, we performed the following studies in a neonatal piglet model. Using a pediatric physiologic pulsatile pump, we subjected six piglets to deep hypothermic circulatory arrest (DHCA) and six other piglets to HCPB. The DHCA group underwent hypothermia for 25 min, DHCA for 60min, cold reperfusion for 10 min, and rewarming for 40 min. The HCPB group underwent 15 min of cooling, followed by 60 min of HCPB, 10min of cold reperfusion, and 30 min of rewarming. The following variables remained constant in both groups: pump flow (150 ml/kg/min), pump rate (150 bpm), and stroke volume (1 ml/kg). During the 60-min aortic crossclamp period, the temperature was kept at 18 degrees C for DHCA and at 25 degrees C for HCPB. The global and regional CBF (ml/100g/min) was assessed with radiolabeled microspheres. The CBF was 48% lower during deep hypothermia at 18degrees C (before DHCA) than during hypothermia at 25 degrees C (55.2 +/- 14.3ml/100g/min vs 106.4 +/- 19.7 ml/100 g/min; p < 0.05). After rewarming, the global CBF was 45% lower in the DHCA group than in the HCPB group 48.3 +/- 18.1 ml/100g/min vs (87 +/- 35.9ml/100g/min; p < 0.05). Fifteen minutes after the termination of CPB, the global CBF was only 25% lower in the DHCA group than in the HCPB group (42.2 +/- 20.7 ml/100 g/min vs 56.4 +/- 25.8ml/100g/min; p = NS). In the right and left hemispheres, cerebellum, basal ganglia, and brain stem, blood flow resembled the global CBF. In conclusion, both HCPB and DHCA significantly decrease the regional and global CBF during CPB. Unlike HCPB, DHCA has a continued negative impact on the CBF after rewarming. However, 15 min after the end of CPB, there are no significant intergroup differences in the CBF.

Animals↗