Factors producing elevated core temperature in spontaneously hypertensive rats

Core temperature (Tco) of the spontaneously hypertensive rat (SHR) is consistently higher by approximately 1 degree C than that of normotensive controls. To analyze factors producing the elevated Tco, mean skin temperature (Tsk), metabolic heat production (M), respiratory evaporative heat loss (Eres), effective tissue thermal conductance (K), systolic blood pressure (BP), and Tco were determined in eight male SHR and nine male normotensive Wistar-Kyoto (WKY) rats habituated to rest quietly in neck stock restraint while exposed to ambient temperatures (Ta) of 12.5, 17, 23, 28.5, 32, 34, and 35 degrees C. At all temperatures steady-state BP, Tco, and M were higher for SHR's than for WKY's. SHR's could maintain thermal balance up to Ta 32 degrees C, and WKY's up to 34 degrees C. Eres from SHR's was greater than from WKY's at Ta of 12.5, 17, and 28.5 degrees C. K of SHR's was not different from or was higher than K of WKY's, and K for both groups was 2.6 times greater at Ta 32 degrees C than at 17 degrees C. These results indicate that the high Tco of SHR's is due to increased M uncompensated by increased K or Eres.     

Splanchnic sympathetic nerve activity and circulating catecholamines in the hyperthermic rat

The mechanisms responsible for the initial rise in splanchnic vascular resistance with environmental heating are controversial, and those responsible for the subsequent fall in splanchnic resistance in the severely hyperthermic animal are unknown. Thus we examined the effect of environmental heating on plasma catecholamine concentration, splanchnic sympathetic nerve activity (SNA), and select blood chemistries. In one study, 25 male Sprague-Dawley rats (270-300 g) were assigned to one of five groups on the basis of their core temperature (Tc, 37, 39, 41, 43, or 44 degrees C) at death. Heart rate (HR), mean arterial pressure (MAP), and Tc were monitored during heat stress under alpha-chloralose anesthesia (12.5 mg.ml-1.h-1). At each predetermined Tc, an aortic blood sample was drawn and analyzed for mean plasma concentration of norepinephrine (NE), epinephrine (E), Na+, K+, and lactate. From 41 to 43 degrees C, NE and E rose significantly, and the animals became hyperkalemic and lactacidemic. In a separate study, we quantitated SNA from the greater splanchnic nerve during heat exposure of artificially respired animals anesthetized with pentobarbital sodium (50 mg/kg). MAP, splanchnic SNA, and Tc were recorded. Tc was elevated from 37.0 +/- 0.12 to 41.3 +/- 0.18 degrees C in 70 min by increase of ambient temperature to 38 degrees C in an environmental chamber. Splanchnic SNA was 54 +/- 8 spikes/s at a Tc of 37 degrees C and increased significantly as Tc exceeded 39 degrees C (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Thermal adjustments to nonexertional heat stress in mature and senescent Fischer 344 rats

The purpose of this study was to test the hypothesis that the rise in colonic temperature (Tc) during nonexertional heat stress is exaggerated in senescent (SEN, 24 mo, n = 12) vs. mature (MAT, 12 mo, n = 15) conscious unrestrained Fischer 344 rats. On 2 separate days (48 h apart) each SEN and MAT animal was exposed to an ambient temperature (Ta) of 42 degrees C (relative humidity 20%) until a Tc of 41 degrees C was attained and then cooled at a Ta of 26 degrees C until Tc returned to the initial control level. Control Tc was similar in the two groups for both trials. The rate of Tc change during heating was 63% greater (0.070 +/- 0.005 vs. 0.043 +/- 0.004 degrees C/min, P less than 0.05) and the time to 41 degrees C reduced by 36% (54 +/- 6 vs. 85 +/- 10 min, P less than 0.05) in MAT vs. SEN animals during the first exposure, although the cooling rate was slower in the MAT (0.048 +/- 0.004 degrees C/min) vs. SEN (0.062 +/- 0.006 degrees C/min) animals (P less than 0.05). The heating rate was unchanged in MAT animals between trials 1 and 2. However, SEN animals had a 95% increase in heating rate in trial 2 compared with trial 1 (P less than 0.05), and the corresponding time to 41 degrees C was decreased by 44% (P less than 0.05). As a result, rate of heating and time to 41 degrees C were similar in the two groups during trial 2. The cooling rate was similar between trials within each group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heat acclimation: role of norepinephrine in the anterior hypothalamus

The hypothesis that anterior hypothalamic (AH) sensitivity to norepinephrine (NE) is altered by chronic exercise in the heat was tested in male Sprague-Dawley rats. Treadmill exercise 6 days/wk for 3 wk at 21 m/min was performed at 23 degrees C (control; C) or at 35 degrees C (heat acclimated; HA), progressing from 20 to 50 min/day in 2 wk. Time for core temperature (Tco) to rise from 39.5 to 40.5 degrees C during a heat-tolerance test after conditioning increased (P less than 0.05) in the HA group. To test for a change in AH sensitivity, the change in Tco to 2-, 5-, 10-, 20-, and 40-micrograms doses of NE injected bilaterally into the AH was determined after conditioning. Dose-response regression lines showed that exercise in the heat increased the slope and shifted the Tco-NE dose relation to the left. In a separate series of experiments on 6 sedentary(s), 10 C, and 10 HA animals, the amounts of NE, dopamine, and 3,4-dihydroxyphenylglycol (DOPEG) were determined by high-pressure liquid chromatography in the AH, median preoptic area (PO), cortex, and cerebellum after 9 wk of conditioning. Results showed that in the PO there was a significant increase in NE and DOPEG in the HA vs. C group and a trend of increasing NE from the S to C to HA groups. The data indicate that exercise in the heat increases NE-induced peripheral heat-dissipating capacity and increases catecholamine storage in the PO.     

右美托咪定对腹腔镜子宫切除术患者血流动力学及应激反应的影响

目的:探讨右美托咪定(Dex)对腹腔镜子宫切除术患者血流动力学及应激反应的影响。方法:选择2012年7月到2014年7月在我院行腹腔镜子宫切除术的36例患者,随机分为实验组和对照组各18例。实验组静脉注射Dex 1μg/kg直到手术结束,对照组同法给予生理盐水。于麻醉前15 min(T0)、插管后5 min(T1)、气腹后20 min(T2)、术后立刻(T3)和术后24 h(T4)四个时间点,分别监测其平均动脉压(MAP)、心率(HR),并测定血浆皮质醇(Cor)、去甲肾上腺素(NE)和白细胞介素6(IL-6)水平。结果:T0时两组患者的MAP和HR比较,无显著性差异(P0.05),对照组T1、T2、T3时明显升高(P0.05),实验组轻微升高,两组相比差异有显著性(P0.05)。T4时两组患者的MAP和HR均恢复至正常水平。T0时两组Cor、NE和IL-6比较,无显著性差异(P0.05),对照组T2、T3、T4时明显升高(P0.05),实验组轻微升高,两组相比差异有显著性(P0.05)。T4时除NE,其他指标均达到峰值。结论:Dex能维持围术期患者血流动力学稳定,降低术中的应激反应。     

Ontogeny of homeothermy in the immature rat: metabolic and thermal responses

Steady-state thermoregulatory responses were measured in the immature rat at 5, 7, 9, 11, 13, 15, 17, and 19 days of age. Tests were conducted at controlled ambient temperatures (Ta) ranging from 22.5 to 37.0 degrees C. Colonic (Tco) and skin (tail, interscapular, abdominal) temperatures were measured, as was O2 consumption from which metabolic rate (M) was calculated. Significant improvements in homeothermic ability occurred from 5 to 19 days of age. Although the resting level of M (RMR) increased by 6.9 W/m2 and the lower Ta limit for RMR (LCT) decreased by 2.5 degrees C as age advanced from 5 to 19 days, Tco at LCT was 36.8-37.1 degrees C at all ages studied. Below LCT the elevation of M to a given decrease in Tco was greater the older the animal. A comparable response to a change in skin temperature was not age dependent. Improvement in thermal insulation was the primary factor responsible for increases in homeothermic ability between 5 and 19 days of age.     

肌间沟臂丛神经阻滞复合静脉全麻对肩关节镜手术患者麻醉效果、MAP、HR以及血清Cor、NE的影响

目的:分析B超指引下实施肌间沟臂丛神经阻滞复合静脉全麻对肩关节镜手术患者麻醉效果、心率(HR)、平均动脉压(MAP)以及血清皮质醇(Cor)、去甲肾上腺素(NE)水平的影响。方法:选择本院2016年3月至2019年12月收治的80例肩关节镜手术患者,以随机数字表法作为分组原则(每组样本容量40例),对照组实施单纯全凭静脉麻醉,实验组实施B超指引下肌间沟臂丛神经阻滞复合静脉全麻,对比两组不同时点MAP、HR、血清Cor、NE水平以及瑞芬太尼、尼群地平(NIT)、丙泊酚使用剂量,并对比两组并发症发生情况。结果:实验组T1-4时点MAP、HR、血清Cor、NE水平均明显低于对照组(P0.05),瑞芬太尼、NIT以及丙泊酚使用剂量实验组均明显较对照组减少(P0.05);两组并发症发生率比较未见统计学差异(P0.05)。结论:B超指引下肌间沟臂丛神经阻滞复合静脉全麻应用于肩关节镜手术中可抑制患者体内应激物质释放,将MAP及HR维持在稳定范围内,极大地减少了麻醉药物、NIT使用剂量,麻醉效果理想、确切。     

Antihypertensive effects of I-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine on plasma renin activity and catecholamine responses in spontaneously hypertensive rats

Fourteen 23 week old male spontaneously hypertensive rats (SHR) were randomly divided into saline control or phospholipid (I-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine) treatment groups. Four weeks of baseline systolic blood pressure (SBP) and heart rate (HR) measurements were determined via tail plethysmography. On week 25 of the baseline period a 1.5 ml blood sample was taken by tail clip for analysis of norepinephrine (NE), epinephrine (E), and plasma renin activity (PRA). On the following week, a single injection of phospholipid (11 ug/kg, s.c.) was given to the experimental animals following baseline SBP and HR determinations. A similar procedure was employed for control subjects, except they received an injection of normal saline (0.5 ml, s.c.). Systolic BP and HR responses were monitored for 24 minutes following the injection. A 1.5 ml blood sample was taken at the end of the 4th minute for NE, E, and PRA assays. A significant drop in SBP (202 +/- 5 mmHg to 124 +/- 6 mmHg) and an increase in HR (431 +/- 17 bpm to 519 +/- 21 bpm) were observed for experimental animals, but not for control subjects. Plasma NE increased significantly (446 +/- 42 pg/ml to 1099 +/- 77 pg/ml), but E remained unchanged following treatment with the phospholipid. Plasma renin activity increased for both groups, but this change was only significant for the experimental group (18.1 +/- 5.7 ng Al/ml/hr to 34.3 +/- 3.6 ng Al/ml/hr). Thus, it appears that I-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine is a potent antihypertensive vasodilating agent which stimulates baroreceptor mediated sympathetic discharge to the heart and kidneys of the SHR.     

Thermoregulatory responses of guinea pigs with anteroventral third ventricle lesions

Guinea pigs with anteroventral third ventricle region (AV3V) lesions fail to develop fever and the associated rise in acute-phase plasma protein levels following systemic injections of lipopolysaccharide (LPS). Since endogenous pyrogen (EP) injected directly into the preoptic area of animals with AV3V lesions causes appropriate elevations in core temperature (Tco) and acute-phase plasma proteins levels, the blocked responses to LPS probably are not due to damage to the adjacent preoptic area. We proposed, therefore, that EP may pass from blood into brain in the AV3V, presumably through the organum vasculosum laminae terminalis. However, the possibility that a more generalized impairment due to damaged pathways within the AV3V could account for the observed effects was not examined. To investigate this possibility, guinea pigs were given AV3V lesions. Pending histological verification of the ablated sites, AV3V lesions were presumed to be placed correctly if the animals did not develop fever following LPS (Salmonella enteritidis, 2 micrograms/kg i.p., at ambient temperature (Ta) 22 degrees C); those failing to meet this criterion were designated as sham-operated. Two experiments were conducted. In the first, metabolic rates, Tco, and two skin temperatures (Tsk) were measured at Ta 12 degrees, 22 degrees, and 32 degrees C over an 8-month postlesion period during which failure to fever persisted; the data were collected during a 30-min period after thermal balance had been achieved at any given Ta. There were no differences in the variables measured between sham-operated and AV3V-lesioned animals at Ta 22 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thermoregulatory and nonthermoregulatory heat production in burned rat

Severely burned patients are hypermetabolic within their thermoneutral zone (TNZ), where there are no thermoregulatory demands on heat production. The rat has been used as a model of postburn hypermetabolism without clear evidence that it behaves in a similar way. Male rats (400-500 g; n = 34-39) were placed as a group in a respiration chamber and metabolic rates for the average rat were determined over 3-6 h at ambient temperatures between 9 and 36 degrees C. Colonic temperatures (Tco) and body weights were measured after each run. Animals were studied sequentially as normals (N), after clipping (C) and following 50% total body surface scald burns. Clipping increased the lower critical temperature (LCT) from 27.7 to 29.1 degrees C without affecting resting heat production (N = 42.6 +/- 0.5; C = 42.0 +/- 0.8 W/m2; mean +/- S.E.) or Tco (N = 36.6 +/- 0.1; C = 36.6 +/- 0.1 degrees C) in the TNZ. Injury increased LCT to 32.8 degrees C and the burned animals were hypermetabolic (47.2 +/- 0.6 W/m2; P less than 0.05 vs. N) and febrile (36.9 +/- 0.1 degrees C; P less than 0.05 vs. N) in the elevated TNZ. These metabolic and temperature responses of burned rats are limited in magnitude but are qualitatively similar to those of patients. The extra heat production in the TNZ reflects the basic metabolic cost of injury.     

右美托咪定联合氯胺酮与咪达唑仑麻醉诱导用于困难气道插管中的价值分析

目的:探讨右美托咪定联合氯胺酮与咪达唑仑麻醉诱导在困难气道插管中的应用价值。方法:选取2016年1月至2018年10月我院收治的80例困难气道患者进行回顾性研究,根据插管顺序将受试者分为对照组和研究组两组,每组40例。对照组患者给予氯胺酮与咪达唑仑进行麻醉诱导,研究组患者在对照组的基础上联合右美托咪定进行麻醉诱导。比较两组麻醉前(T1)、纤支镜经过会厌时(T2)、声门时(T3)、插管即刻(T4)、插管后60 s(T5)、插管后180 s(T6)、插管后300 s(T7)时的平均动脉压(mean arterial pressure,MAP)、心率(Heart rate,HR)、血氧饱和度(Blood oxygen saturation,SpO_2)及Ramsay评分变化,并监测T1、T4及T6时间点去甲肾上腺素(Norepinephrine,NE)、肾上腺素(epinephrine,E)及皮质醇(Cortisol,Cor)水平及不良反应的发生情况。结果:两组不同时间点Sp O_2比较无统计学差异(P0.05),但研究组患者在T3-T7时间点的MAP、HR显著低于对照组,Ramsay评分显著高于对照组(P0.05)。两组患者T1时的NE、E及Cor水平比较无统计学差异(P0.05),但研究组T4及T6时NE、E及Cor水平均显著低于对照组(P0.05)。研究组患者呛咳、恶心、躁动及呼吸抑制的发生率均显著低于对照组(P0.05)。结论:与氯胺酮联合咪达唑仑相比,右美托咪定联合氯胺酮与咪达唑仑对心血管系统影响小,安全性更高,患者应激反应较低,在困难气道插管麻醉诱导中具有较高的应用价值。     

Temperature regulation during acute heat loads in rats after short-term heat exposure.

Eleven rats were kept at an ambient temperature of 33.5 degrees C (HC) for 4-5 consecutive days, 9 additional rats were subjected to 33.5 degrees C for approximately 5 h daily (HI) for the same period, and 12 controls (Cn) were kept at 24 degrees C. After the exposure, the rats were placed in a direct calorimeter, where the wall temperature was set at 24 degrees C, and subjected to direct internal heating (6.2 W.kg-1, 30 min) through an intraperitoneal electric heater. After the first heat load and when thermal equilibrium had been attained again, the rats were subjected to indirect external warming by raising the jacket water temperature surrounding the calorimeter from 24.0 to 38.8 degrees C in 90 min. Hypothalamic (Thy) and colonic temperatures (Tco), evaporative and nonevaporative heat loss, and metabolic heat production (M) before the acute heat loads did not differ among the groups. During heat loads, the latent times for the onsets of the rises in tail skin temperature and evaporation were significantly longer, and Thy and Tco at the start of increases in heat losses tended to be higher, in the HC than in the Cn. M significantly decreased in all groups, but the magnitude and duration of reduction in M were significantly greater in the HC than in the Cn. There were no differences between the thermoregulatory responses to heat loads of the HI and Cn. These results suggest that in HC the threshold core temperature for heat loss response and the upper critical temperature have already shifted to a higher level and that HC respond to heat stress more strongly with the reduction of M than Cn. Short-term intermittent heat exposure had little effect on the thermoregulatory mechanisms in rats.     

Effects of inspiratory oxygen concentration and ventilation method on a model of hemorrhagic shock in rats.

The effect of inspiratory oxygen concentration and the ventilation method on hemorrhagic shock was investigated. Twenty-eight rats were divided into four groups: mechanical ventilation with pure oxygen (M100); mechanical ventilation with air (M21); spontaneous respiration with pure oxygen (S100); and spontaneous respiration with air (S21). Under intravenous pentobarbital anesthesia, hemorrhagic shock (HS) was induced by withdrawal of blood from the femoral artery. Mean arterial blood pressure (MAP) was maintained at 40-50 mmHg for 2 h. After HS, the blood remaining in the reservoir was reinfused. Then survival rate and MAP were monitored for 2 h. Blood samples were withdrawn and vascular reactivity to norepinephrine (NE; 3.0 micrograms/kg) was tested before and after HS. Results were shown by changes in MAP in response to NE. During HS, the survival rate of the S21 group was lower than that of the M100 and S100 groups (p < .05). Before HS, MAPs of M100 and S100 groups were significantly higher than those of M21 and S21 groups (p < .05). In the M100 and M21 groups, MAPs at 2 h after reinfusion were significantly lower than the baseline value (p < .05). Before HS, reactivity to NE of the M21 group was significantly higher than that of the other groups (p < .05). In the M21 group, reactivity to NE after HS was significantly lower than it was before HS (p < .05). Inspiratory oxygen concentration and the ventilation method affect the survival rate and vascular reactivity of the rat hemorrhagic shock model. Selection of the inspiratory oxygen concentration and the ventilation method should be made according to the purpose of the individual experiment.     

Effect of ambient temperatures ranging from cold to heat on thermoregulation in conscious MK801-treated rats

The glutamate NMDA receptor has been suggested to be involved in thermoregulation. To further analyse its role, the thermoregulatory responses of rats treated with 0.5 mg.kg-1 of dizocilpine (MK801) were compared with those of control rats treated only with the same volume of saline during a 180-min exposure at one of the six different ambient temperatures, ranging from cold to heat. Colonic temperature (Tco) and tail skin temperature (Ttail) were measured throughout using Cu-Ct thermocouples. In the cold (2.4 and 12.3 degrees C), Tco decreased either sharply (MK801) or progressively (saline), reaching the same final value (2.4 degrees C) or a lower value in the MK801-treated rats (12.3 degrees C). At the same time, Ttail decreased in both groups. In the cool environment (20.7 degrees C), Tco and Ttail decreased in both groups, with lower final values in MK801-treated rats. At thermoneutrality (28.8 degrees C), the MK801-induced hyperthermia remained steady, while Ttail increased in both groups. In the heat (34.6 and 36.2 degrees C), Tco and Ttail increased in both groups, with higher final values in MK801-treated rats. Moreover, at 36.2 degrees C, only MK801-treated rats exhibited heatstroke. It is thus suggested that MK801-induced inhibition of NMDA receptors impairs thermoregulation, especially in the heat.     

Nocturnal shifts in thermal and metabolic responses of the immature rat

Immature rats were tested at 2, 7, 11, and 15 days of age to determine steady-state thermoregulatory responses during light (L) and dark (D) phases of the daily cycle. Pups were housed with dams in a vivarium illuminated from 0700 to 1900 h. During each phase tests began approximately 1 h after the change in the light conditions of the vivarium. Duration of each test was approximately 7 h. Rats were tested individually in temperature-controlled cylinders at ambient temperatures (Ta) = 25.0, 30.0, 32.5, and 35.0 degrees C. Both colonic (Tco) and tail skin temperatures of each animal were measured continuously. O2 content of effluent air from each cylinder was determined to provide an estimate of metabolic rate (M). Immature rats, at 2 to 11 days of age, exhibited significant L:D differences in M and Tco. However, no significant L:D differences in these responses were noted at 15 days of age. In every case, nocturnal increases in Tco were associated with a rise in M. L:D differences in Tco response were not attributed to a significant change in total thermal conductance. These data support the conclusion that the immature rat exhibits daily variation in metabolic rate, which is the primary contributor to L:D shifts in Tco.     

Circulatory responses to heat after celiac ganglionectomy or adrenal demedullation

Chloraloseanesthetized rats were implanted with Doppler flow probes on the mesenteric, renal, and external caudal arteries and were exposed to an ambient temperature of 40 degrees C. Heart rate, core (Tc) and tail-skin temperatures, and mean arterial blood pressure (MAP) were also monitored. Before heating, the celiac ganglion was removed (ganglionectomy) from one group of animals (n = 11) and a bilateral adrenal demedullation was performed in a second group (n = 14). As Tc progressively increased from 37 degrees C to 43 degrees C, MAP rose to a plateau then fell precipitously as Tc exceeded 41 degrees C. Ganglionectomy eliminated the rise in mesenteric resistance (P less than 0.05) and attenuated the rise in MAP compared with an intact control group (n = 11). Ganglionectomy also increased the heating rate (P less than 0.05) and reduced heat tolerance time (P less than 0.05). Demedullation attenuated the rise in both mesenteric resistance and MAP (P less than 0.05) and increased the rate of heating (P less than 0.05) compared with controls (n = 10). Renal and caudal resistance changes were similar in all groups. These data show the importance of intact adrenal medullas and sympathetic innervation to the splanchnic region in contributing to thermal tolerance in the rat. However, neither factor alone can explain splanchnic vasoconstriction during severe heat stress.     

全凭静脉麻醉复合椎旁神经阻滞对胸腔镜下肺病损切除术患者应激反应、血流动力学及术后镇痛的影响

目的:研究全凭静脉麻醉复合胸椎旁神经阻滞(TPVB)对胸腔镜下肺病损切除术患者应激反应、血流动力学及术后镇痛的影响。方法:选择2016年6月至2017年12月在我院行胸腔镜下肺病损切除术的80例患者为研究对象。采用简单随机抽样方法,分为对照组(n=40)和观察组(n=40)。对照组行单纯全身麻醉,观察组在超声引导下行TPVB复合全身麻醉。比较两组麻醉前、术毕、术后24 h的血糖、肾上腺素(E)、去甲肾上腺素(NE)及多巴胺(DA)的浓度,以及两组在麻醉时、手术开始时、手术开始后0.5 h、手术开始后1 h、术毕时的平均动脉压(MAP)和心率(HR),同时比较两组术后2 h、6 h、12 h、24 h静息及活动时的视觉模拟评分(VAS)及相关并发症的发生率。结果:两组患者在麻醉前及术毕的各应激反应指标比较无差异(P0.05),而术后24 h比较,观察组低于对照组(P0.05);两组患者麻醉时的MAP、HR比较无差异(P0.05),除手术开始后1 h和术毕的HR外,观察组各时间的MAP、HR均显著低于对照组(P0.05);除静息时24 h外,观察组各时间静息时和活动时的VAS评分均低于对照组(P0.05);两组患者术后各并发症的发生率比较无统计学差异(P0.05)。结论:全凭静脉麻醉复合TPVB在胸腔镜下肺病损切除术中应激反应小,对血流动力学的波动影响小,术后镇痛效果良好,且安全有效。     

Endothermic heart rate response in broiler and White Leghorn chicks (Gallus gallus domesticus) during the first two days of post-hatch life

The embryonic modal value of heart rate (MHR) differs between broiler and White Leghorn chickens, but the initial development of cholinergic chronotropic control of embryonic heart rate (HR) does not. Thus, we hypothesized that hatchling MHR should also differ between broiler and White Leghorn strains, while the development of a physiological regulation, such as the endothermic HR response, should not be different between hatchlings of the two strains. To test this, we measured the response of HR and cloaca temperature (Tb) to alteration of ambient temperature (Ta); i.e., 35 degrees C-25 degrees C-35 degrees C, in four groups of hatchlings on Days 0 and 1 post-hatch. Fertile eggs of both strains with similar mass were incubated simultaneously in the same incubator. Eggs of broiler chickens hatched approximately 7 h earlier than White Leghorn chicken eggs. Chick mass at hatching was identical in both strains, but diverged during 2 days after hatching. Tb measured at the initial Ta of 35 degrees C was identical in both strains. MHR at the same Ta was approximately 30 bpm lower in broiler chicks than in White Leghorn chicks, but the difference was reversed to that observed in the embryos. The endothermic HR response was advanced by approximately 1 day in broiler chicks compared with White Leghorn chicks. As a result, eggs of similar mass in both strains produced chicks with similar mass and Tb at hatching, but during 2 days of post-hatch life their masses diverged and regulation of the endothermic HR response developed earlier in broiler than in White Leghorn hatchlings. This physiological heterochrony between strains is most likely due to genetic selection for fast growth in broiler chickens.     

Gender-dependent response in blood pressure changes following the inhibition of nitric oxide synthase

Many studies employed L-NAME (N(G)-nitro-L-arginine methyl ester), an L-arginine antagonist and nitric oxide (NO) synthase (NOS) inhibitor, to produce hypertension experimentally in male animals. It is not known whether females respond similarly. We thus examined the effect of long-term oral administration of L-NAME on body weight (BW), blood pressure (BP), and heart rate (HR) of both female and male rats. We found that L-NAME induced significant increase in mean BP (MAP) in both genders, however, L-NAME-treated females (F*) exhibited a significantly higher elevation than males (M*) did. This difference persisted for 5 wks and then diminished. L-NAME was thus withdrawn and a rapid decrease of MAP was observed. MAP of F* decreased less and thus remained higher than M* for 5 wks. MAP of control rats (F and M) remained unchanged during the period. Systolic BP (SBP) altered in a similar pattern. We also found that HR decreased immediately after L-NAME administration and that HR of F* was significantly less reduced. These findings indicate that L-NAME induced a more pronounced response in females than males, consistent with the view that females are more dependent on NOS activity for their regulation of BP.     

Peripheral vascular responses to hyperthermia in the rat

To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70-150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10-15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.