Effect of atropine on the bronchial response of asthmatic subjects to the inhalation of ultrasonically nebulized distilled water

To determine whether atropine provides protection against the bronchoconstriction that develops in asthmatic subjects after inhalation of ultrasonically nebulized distilled water, we exposed six asthmatic patients to this stimulus with and without pretreatment with atropine (0.04 mg/kg). The mean FEV1 decreased from 3.32 to 2.39 L (-28%) without and from 3.49 to 3.18 L (-9%) with atropine. This protective effect was statistically significant (p less than 0.05), suggesting that cholinergic pathways are involved in the obstructive response to the inhalation of ultrasonically nebulized distilled water.     

Mechanism of blood pressure elevation during angiotensin infusion

The mechanism of increased preload and its contribution to the rise in blood pressure during intravenous angiotensin infusion were studied in anesthetized dogs. In open-chest dogs angiotensin increased mean aortic blood pressure by 58±12 mmHg. Left ventricular end-diastolic dimension, measured as myocardial chord length (MCL) by ultrasonic technique, increased by 7±1 %. By inflating a balloon in the inferior vena cava, end-diastolic MCL was reduced to control value and the rise in mean aortic blood pressure was almost halved to 32±10 mmHg above control value. A similar preload effect was recorded in closed-chest dogs using end-diastolic left ventricular pressure as an estimate of left ventricular volume. During angiotensin infusion to the upper body only, end-diastolic MCL did not increase. When redistribution of the splanchnic blood volume was prevented, the effect of angiotensin on end-diastolic MCL was reduced to 1/3. Angiotensin reduced liver but not splenic dimension measured by ultrasonic technique. We conclude that about half of the rise in blood pressure during angiotensin infusion is due to increased end-diastolic volume caused by blood redistribution. About 2/3 of this increase in preload is due to redistribution from the splanchnic bed, mainly from the liver.     

Determinants of pulmonary blood volume. Effects of acute changes in pulmonary vascular pressures and flow

To examine the effects of pulmonary vascular pressures and flow on pulmonary blood volume (PBV), experiments were performed at constant heart rate and zone 3 conditions (mean left atrial pressure (LAP) above airway pressure) in six anesthetized, open-chest dogs. PBV was calculated as the product of electromagnetic aortic flow and pulmonary mean transit time for ascorbate, obtained without blood withdrawal by polarographic recording of aortic ascorbate changes. In three series of experiments LAP was raised similarly in three steps, from 4.5 to 14.8 mmHg: by mitral constriction which reduced pulmonary blood flow, by blood volume expansion which more than doubled pulmonary blood flow, or by a combination of the two procedures which kept pulmonary blood flow constant. In all three series, LAP and mean pulmonary arterial pressure (PAP) rose in proportion, but PBV was better correlated to PAP (r=0.87±0.02) than to LAP (r=0.66±0.09). These experiments suggest that PAP is the most important factor in determining PBV under zone 3 conditions, whether PAP is raised by increasing pulmonary blood flow or by mitral constriction.     

Hydration during exercise

Summary Five young unacclimatised subjects were exposed for 4 h at 34 C (10 C dew-point temperature and 0.6 m · s^–1 air velocity), while exercising on a bicycle ergometer: 25 min work — 5 min rest cycles for 2 hours followed by 20 min work — 10 min rest cycles for two further hours. 5 experimental sessions were carried out: one without rehydration (NO FLUID) resulting in 3.1% mean loss of body weight ( M_b), and four sessions with 20 C fluid ingestion of spring water (WATER), hypotonic (HYPO), isotonic (ISO) and hypertonic (HYPER) solutions to study the effects of fluid osmolarity on rehydration. Mean final rehydration (±SE) after fluid intake was 82.2% (±1.2). Heart rate was higher in NO FLUID while no difference among conditions was found in either M_b or hourly sweat rates. Sweating sensitivity was lowest in the dehydration condition, and highest in the WATER one. Modifications in plasma volume and osmolarity demonstrated that NO FLUID induced hyperosmotic hypovolemia, ISO rehydration rapidly led to plasma isoosmotic hypervolemia, while WATER led to slightly hypoosmotic normovolemia.It is concluded that adequate rehydration through ingestion of isotonic electrolyte-sucrose solution, although in quantities much smaller than evaporative heat loss, rapidly restored and expanded plasma volume. While osmolarity influenced sweating sensitivity, the plasma volume changes ( PV) within the range –6% PV+4% had little effect on temperature adjustments in our conditions.     

An Evaluation of Finger Pulse Volume as a Psychophysiological Measure of Anxiety

The present experiment explored the utility of finger pulse volume (FPV) as a measure of anxiety. Subjects were exposed to either a threatening or nonthreatening situation, and indices of physiological arousal (pulse rate (PR) and FPV) and self-report of anxiety (Affect Adjective Checklist (AACL)) were collected. Results indicated that FPV was responsive to changes in experimentally induced anxiety and significantly correlated with PR and AACL, although the strength of these relationships was not substantial. Relevance for psychophysiological theory and the clinical observation of anxiety is discussed.     

Changes of plasma volume and plasma composition in water-deprived rats

Summary Plasma volume, hematocrit, protein and electrolyte concentrations in plasma were measured in control and water-deprived rats every three days after starting the experiment until the 15th day. Plasma volume variations, as related to body weight, suggest that water loss from plasma was proportional to total body water at three days and after 9 days of water deprivation. Greater plasma water than body water loss was found during the period between 3 and 9 days. Plasma protein and electrolyte variations suggest that during water deprivation there is a loss of protein, sodium and potassium from plasma, which is proportionally less than that of plasma water. Potassium, calcium and inorganic phosphorus were lost proportionally to plasma water. The variations in plasma volume changes were partially explained as due to variations in plasma protein and electrolyte concentrations.     

Cardiac sympathetic denervation does not change the load dependence of the left ventricular end-systolic pressure/volume relationship in dogs

It has been shown that in the intact canine heart the left-ventricular end-systolic pressure/volume relation (ESPVR) depends on loading conditions: an increase in arterial vascular resistance causes a leftwards shift and a steeper slope of the ESPVR, suggesting an increased inotropic state. Our purpose was to investigate the possible contribution of the sympathetic nervous system to this load sensitivity of the ESPVR, using intact, but denervated, hearts with normal coronary perfusion and afterload. We used two types of loading intervention: venous volume infusion and gradual occlusion of the descending aorta. ESPVRs were obtained in six anaesthetized open-chest dogs, both before and after bilateral ablation of the stellate ganglia. To exclude the influence of heart rate changes, bilateral vagotomy was performed and the heart was paced. The absence of (unpaced) heart rate changes in response to pressure alterations was used to confirm total denervation. Left ventricular pressure was measured with a micromanometer and volume with a conductance catheter. ESPVRs were essentially linear and characterized by their slope (E _es) and volume intercept at 12 kPa (V ₁₂). We found that E _es (P<0.0001) and V₁₂ (P<0.05) were both significantly different during pressure and volume interventions (0.67±0.29 and 0.41±0.18 kPa/ml for E _es and 16.2±8.2 and 18.2±8.4ml for V₁₂ respectively). Denervation did not significantly affect the parameters of the ESPVR obtained by either volume infusion or aortic occlusion. Two-way analysis of variance revealed no significant interactive effect between denervation and intervention, indicating that the sympathetic nervous system does not influence the load dependency of the ESPVR. The dP/dt _max: EDV relationship behaved similarly. These results suggest that load dependency is an intrinsic property of the myocardium.     

三维超声测胎儿股容积估计胎重的价值

目的通过对57例妊娠分别使用二维、三维超声测量相关参数估计胎重，并作统计学比较，从而评价三维超声对于估测胎儿体重、诊断胎儿发育迟缓及巨大胎的优势和价值。方法对2005年10月至2006年3月间在我院分娩的57例妊娠，研究组用三维超声测胎儿股容积估计胎重，对照组用二维超声同步测量相关参数估计胎重。结果对两组估重结果与胎儿实际出生体重作相关统计学分析，研究组相关系数为0．983，对照组为0．906（P〈0．05），前者与实际体重关系更密切。结论三维超声测量胎儿股容积估测胎儿体重，较传统二维超声具有更大优势，对于发现胎儿发育迟缓（FGR）及巨大胎意义重大，有利于指导临床冶疗、选择分娩方式。     

Evidence for central reorganization of ventilatory chemoreflex pathways in the cat during regeneration of visceral afferents in the carotid sinus nerve

There are two sets of peripheral arterial chemoreceptors in the cat, the carotid bodies innervated by the carotid sinus nerve and the aortic bodies with afferents in the aortic depressor nerves. Reflex stimulation of ventilation in response to hypoxia is abolished acutely after interrupting the sensory pathway from the carotid body chemoreceptors in the cat even though the reflex pathway from the aortic body chemoreceptors is intact. However, in chronically maintained preparations, there is a restoration of the hypoxic response which is mediated by the aortic chemoreflex pathway. It was proposed that restoration was due to a ‘central reorganization’ of chemoreflex pathways which followed interruption of the sensory pathway from the carotid bodies and that the reorganization enhanced the efficacy of the aortic ventilation chemoreflex. This proposal was tested in the present experiments by measuring reflex ventilatory and cardiovascular responses to electrical stimulation of the sensory nerves containing aortic and carotid chemoreceptor afferents following bilateral interruption of carotid sinus nerves and carotid body resection. Responses measured acutely (1–6 h) after interruption were compared with those measured 60–80 and 110–140 days later. At 60–80 days, a chemoreflex response (increase in tidal volume of ventilation) to stimulation of the interrupted carotid sinus sensory pathway was markedly attenuated while the response to stimulation of the uninterrupted pathway in aortic depressor nerves was enhanced. At 110–140 days, the tidal volume response to carotid sinus nerve stimulation was greatly enhanced while the aortic depressor nerve response declined from the elevated level. There were significant but less pronounced changes in the response of other ventilatory and cardiovascular variables to aortic depressor nerve and carotid sinus nerve stimulation.The results support the idea that there is a ‘central reorganization’ of chemoreflex pathways which is reflected functionally by changes in the efficacy of reflexes evoked from aortic depressor nerve and carotid sinus nerve. The changes are analagous to those occurring in somatic reflexes during regeneration of sensory nerves. It is suggested that the changes in efficacy of carotid sinus nerve reflexes are due to a degenerative loss of synapses of the central projections of interrupted carotid sinus nerve sensory axons (degenerative atrophy) and subsequent regenerative like changes (regenerative proliferation) in the central projections. The changes in the efficacy of aortic depressor nerve reflexes may be attributed to formation of new synapses by converging central projections of this uninterrupted pathway (reactive synaptogenesis) and subsequent regression of the newly formed synapses.