Blood flow distribution in dogs during hypothermia and posthypothermia

Blood flow distribution in tissues of mongrel dogs during hypothermia was studied with radionuclide-tagged microspheres. The animals were cooled at 21 degrees C and rewarmed under thiamylal sodiuni anesthesia. During hypothermia, cardiac output fell to 20% of the control; the highest rate of blood flow relative to normothermic values was observed in the subendocardium of the left ventricle, and the lowest in the hypophysis. Each tissue showed specific reactions to hypothermia. During hypothermia the myocardial and brain-stem blood flows were about 40% of the control; almost all of the digestive tract, striated muscle, adrenal gland, and hypophysis blood flows were maintained at 20% or less of the control. After rewarming, cardiac output recovered to values significantly lower than control. The myocardium, brain, renal cortex, and striated and smooth muscle recovered to control levels; however, blood flow to the digestive organs, bronchial artery flow to the lung, and flow to the endocrine organs did not completely recover by 2 after rewarming.     

L-vasopressin inhibits oxytocin-induced increases of plasma levels of insulin conscious dogs

Oxytocin is known to increase plasma levels of insulin, glucagon and glucose in dogs. Plasma levels of vasopressin rise during stressful conditions. Since vasopressin counteracts several oxytocin-induced effects, it was decided to study how vasopressin influences the oxytocin-induced elevation of plasma levels of insulin, glucagon and glucose. Therefore oxytocin at 0.11 (which gives rise to physiological plasma concentrations) was infused i.v. for 10 min into fasted, conscious dogs either alone or in combination with 0.033 or 0.17 nmol kg-1 h-1 of L-vasopressin. Accordingly, 1.1 nmol kg-1 h-1 of oxytocin was infused alone or in combination with 0.67 or 1.7 nmol kg-1 h-1 of L-vasopressin. Repeated blood samples were drawn during and after the infusions and insulin and glucagon levels were determined by radioimmunoassay. Plasma levels of insulin increased three- and six-fold in response to 0.11 and 1.1 nmol kg-1 h-1 of oxytocin, respectively, and the elevations were inhibited by L-vasopressin. Slight (1.5-fold) increases in plasma levels of glucagon were observed following 0.11 and 1.1 nmol kg-1 h-1 of oxytocin, although the effect was significant only after the latter dose. Concomitant infusion with L-vasopressin did not markedly influence the effect caused by oxytocin. Small, insignificant increases in blood glucose levels were induced by both doses of oxytocin. These effects were not affected by concomitant infusions of L-vasopressin. The insulin levels rose before glucose levels suggesting that oxytocin stimulates the release of insulin without a previous rise in glucose levels. In conclusion, it has been shown that vasopressin, in amounts which give rise to physiological plasma concentrations, inhibits oxytocin-induced effects on insulin levels, and that oxytocin stimulates the release of insulin via a mechanism which is independent of elevations in blood glucose levels.     

Estimation of plasma volume from hematocrit and plasma oncotic pressure during volume expansion in dogs

Changes in hematocrit and plasma oncotic pressure were measured continuously during and after isotonic volume expansion in splenectomized dogs in order to test the potential of these types of measurements to predict changes in plasma volume. A volume of Ringer's solution amounting to 15% of the initial blood volume was infused over 10 min. At the end of the infusion, 54% of infused fluid remained within the intravascular space and 9% of the infused volume was retained within the intravascular space at 50 min after the end of the infusion. Hematocrit and plasma oncotic pressure decreased by 2.4% and 2.4 mmHg, respectively, at the end of infusion and then variables returned to their control levels gradually. Changes in plasma volume were estimated indirectly from hematocrit and plasma oncotic pressure based on the dilution of the erythrocytes and the protein. Highly significant correlations were observed between the measured plasma volume (Y) and the plasma volume (X) calculated from hematocrit (Y = 0.95X + 0.22, r = 0.96) and the plasma oncotic pressure (Y = 0.86X + 0.46, r = 0.91). We therefore conclude that either hematocrit and plasma oncotic pressure measured continuously are reliable parameters for predicting the time course of the plasma volume change during an isotonic volume expansion of up to 15% of the initial blood volume.     

Motion sickness increases the risk of accidental hypothermia

Motion sickness (MS) has been found to increase body-core cooling during immersion in 28°C water, an effect ascribed to attenuation of the cold-induced peripheral vasoconstriction (Mekjavic et al. in J Physiol 535(2):619–623, 2001). The present study tested the hypothesis that a more profound cold stimulus would override the MS effect on peripheral vasoconstriction and hence on the core cooling rate. Eleven healthy subjects underwent two separate head-out immersions in 15°C water. In the control trial (CN), subjects were immersed after baseline measurements. In the MS-trial, subjects were rendered motion sick prior to immersion, by using a rotating chair in combination with a regimen of standardized head movements. During immersion in the MS-trial, subjects were exposed to an optokinetic stimulus (rotating drum). At 5-min intervals subjects rated their temperature perception, thermal comfort and MS discomfort. During immersion mean skin temperature, rectal temperature, the difference in temperature between the non-immersed right forearm and 3rd finger of the right hand (ΔT _ff), oxygen uptake and heart rate were recorded. In the MS-trial, rectal temperature decreased substantially faster (33%, P < 0.01). Also, the ΔT _ff response, an index of peripheral vasomotor tone, as well as the oxygen uptake, indicative of the shivering response, were significantly attenuated (P < 0.01 and P < 0.001, respectively) by MS. Thus, MS may predispose individuals to hypothermia by enhancing heat loss and attenuating heat production. This might have significant implications for survival in maritime accidents.     

Exogenous cysteamine increases basal pancreatic exocrine secretion in the rat

To determine whether exocrine pancreatic secretion is regulated by endogenous somatostatin, somatostatin deficiency was induced by cysteamine. Rats were subcutaneously administered a single dose of cysteamine (30 mg/100 g body weight) 12 hr before experiment. Anesthetized rats were prepared with cannulation into bile duct, pancreatic duct, duodenum, and jugular vein and pancreatic juice was collected. For in vitro study, isolated pancreata of rats, pretreated with cysteamine, were perfused with an intraarterial infusion of Krebs-Henseleit solution (37 degrees C) at 1.2 mL/min, and pancreatic juice was collected in 15-min samples. In vivo experiment of the rat, the mean basal pancreatic secretions, including volume, bicarbonate, and protein output were significantly increased from 18.4+/-0.5 microL/30 min, 0.58+/-0.05 microEq/30 min, and 214.0+/-26.1 microg/30 min to 51.6+/-3.7 microL/30 min, 1.52+/-0.11 microEq/30 min, and 569.8+/-128.9 microg/30 min, respectively (p<0.05). In the isolated perfused pancreas, cysteamine also resulted in a significant increase in basal pancreatic secretion (p<0.05). Simultaneous intraarterial infusion of octreotide (10 pmol/hr) to isolated pancreata partially reversed the effect of cysteamine on basal pancreatic secretion. These findings suggest that endogenous somatostatin play an important role on the regulation of basal pancreatic exocrine secretion.     

Tissue respiration and adenosinetriphosphatase activity in dogs in deep hypothermia

Summary The authors studied the intensity of tissue respiration (studied monometrically) and the adenosinetriphosphatase activity (by increase of inorganic phosphorus) in the brain, heart, and skeletal musculature of dogs in deep hypothermia depending on the length of circulatory arrest (30 and 60 minutes) and subsequent warming of the animals to normal temperature. Cooling (to 10° in the mediastinum) and subsequent warming was effected in 10–15 minutes by means of extracorporeal circulation. The tissue respiration and adenosinetriphosphatase activity showed a marked change especially in the brain tissue under the effect of deep hypothermia. Respiratory disturbances of all the tissues investigated were manifested by a reduction of the absorbed O₂, and by a drop of the CO₂ discharged; the decarboxylation process was disturbed more acutely as seen by the reduced respiratory quotient. A more marked depression of adenosinetriphosphatase activity was revealed in the tissues of cardiac and skeletal muscles following a 60 minute circulatory arrest. After the animals were warmed the tissue respiration and adenosinetriphosphatase activity augmented in all the tissues, indicating that the oxidative metabolic changes in conditions of deep hypothermia were reversible.(Presented by Academician A. N. Bakulev) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 55, No. 3, pp. 45–48, March 1963     

Exogenous lysophosphatidylcholine increases non-selective cation current in guinea-pig ventricular myocytes

Whole cell, patch-clamp studies were performed to examine the effect of lysophosphatidylcholine (LPC) on the membrane current in guinea-pig ventricular myocytes. The addition of 10 μM LPC to the external solution induced a membrane current which had a reversal potential of 0 mV. When Na⁺, the main cation in the external solution, was replaced by either K⁺, N-methyl-D-glucamine (NMG) or 90 mM Ca²⁺, LPC induced a current with the reversal potential near 0 mV, indicating that the current passed through a Ca²⁺-permeable non-selective cation channel. The order of the cationic permeability calculated from the reversal potential of the current was Cs⁺ > K⁺ > NMG > Na⁺ > Ca²⁺. Cl⁻ did not pass through the LPC-induced channel. The LPC-induced current was not blocked by Gd³⁺ in the external solution, nor by the absence of Ca²⁺ in the pipette solution. In conclusion, LPC induces a Ca²⁺-permeable non-selective cation channel in guinea-pig ventricular myocytes. Received: 11 September 1995/Received after revision: 3 January 1996/Accepted: 12 February 1996     

Oral ascorbic acid increases plasma oestradiol during postmenopausal hormone replacement therapy

OBJECTIVES: To study the possible interaction between ascorbic acid (AA) and oestradiol (E2) in postmenopausal women on hormone replacement therapy (HRT). METHODS: We studied 25 healthy postmenopausal women who had used percutaneous E2 gel at same dose for 10-12 months, at which time the plasma E2 concentrations were stabilized. The subjects were treated with 1000 mg of AA daily for 3 months and blood samples for assay of AA and E2 were taken at 0, 1 and 3 months. RESULTS: After 1 month of AA treatment, there was an overall increase of 20.8% in E2 levels in the group as a whole. Greater responses were seen in two subgroups. In women with initially the lowest plasma concentrations of AA (<70 micromol/l), there was an increase of 55% in plasma E2 levels which was close to significance (P=0.063). In another subgroup with initially the lowest E2 levels (<0.20 nmol/l) there was a marked and significant increase (from 0.13 to 0.26 nmol/l) in plasma E2 concentrations (P=0.028). CONCLUSIONS: Our results support early findings that AA may interact with oestrogen therapy. Possible interaction of AA with E2 at the level of antioxidation is discussed.