Cardiovascular functions of the unanesthetized small Indian mongoose, Herpestes auropunctatus.
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Biomedical subjects
Publications and source records attributed to Y C Lin.
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Twenty Holstein heifers in diestrus were given 30 mg of PGF2alpha Tham salt (im). Thereafter each of five heifers received no further treatment of 40 mug of GnRH (im) at 10, 30, or 50 hr after PGF2alpha. Serum progesterone decreased to less than 1 ng/ml at 24 hr after PGF2alpha and remained low throughout the remainder of the sampling period. Following PGF2alpha, estradiol concentrations increased gradually in serum but GnRH given at 30 hr after PGF2alpha abruptly decreased estradiol concentration. The magnitude of LH release induced by GnRH given at 30 or 50 hr after PGF2alpha was greater than that at 10 hr. All heifers exhibited behavioral estrus except those in group GnRH-50. Spontaneous LH peaks, which usually occur after PGF2alpha were observed in 5/5 (control), 4/5 (GnRH-10), 0/5 (GnRH-30), and 2/5 (GnRH-50) heifers. We conclude that pituitary responsiveness to GnRH increases with time after PGF2alpha and GnRH given at 30 hr completely inhibits and at 50 hr partially inhibits endogenous LH release.
Effects of helium on the isolated perfused rat heart were studied employing the Langendorff technique. The perfusate consisted of Krebs-Henseleit solution saturated with one of three gas mixtures: 1) 95% O2-5% CO2, 2) 50% O2-45% He-5% CO2, and 3) 50% o2-45% N2-5% CO2. Contractile indices measured revealed the performance of hearts with the helium mixture to be equivalent to those perfused with the 95% O2-5% CO2 mixture. Those perfused with the nitrogen gas mixture exhibited contractile activity lower than that in the other two groups. It was concluded that helium exerts a direct effect on the coronary vasculature of the isolated rat heart by reducing its resistance to flow. A greater oxygen delivery to hearts perfused with the He-saturated solution compared to the N2-perfused hearts may account for the difference in performance.
Apnea was initiated by clamping off the tracheal tube in 6 anesthetized dogs. Bradycardia, reduction in cardiac output and peripheral vasoconstriction developed gradually throughout the entire apneic period. O2 consumption during apnea was measured by monitoring the rate of O2 removal from the lung (VLO2), from the arterial blood (Va02), and from the venous blood (VV02). Total 02 consumption (VT02) was calculated by summing (VL02--Va02), VaQ2 and VV02-VL02, estimated by the product of arteriovenous O2 content difference and cardiac output, decreased continuously during apnea. At the end of 80 sec the rate of O2 removal from the lung was one-fourth of the pre-apneic rate, 5.29 +/- 0.51 ml-min-1kg-1. Oxygen disappearance form the blood was estimated by measuring arterial and venous O2 content at 20-sec intervals and by assuming a constant blood volume throughout the apneic period of 86 ml/kg, 25% of which is in the arterial tree and 75% of which is in the venous compartment. During the last 20 sec of an 80-sec apnea, VV02 represented 69% of VT02. The result indicated that VT02 during apnea was not significantly different from that of pre-apneic values. It is concluded from the present study that an oxygen conservation mechanism if existent, was not operative during an 80-sec apnea in the anesthetized dog.
The diving response was produced by submerging the head of the unanesthetized rat for 60 s, while it was confined in a mesh-wired cone. Heart rate and cardiac output decreased by 73% and 74% from the predive values, respectively, indicating insignificant change in stroke volume. Central systemic arterial blood pressure rose by 22% during diving and a fourfold increase in total peripheral resistance was observed. Blood flow to the coronary, cerebral, and bronchial circulations remained unchanged while a 95% reduction in the intestine and the spleen, a 97% reduction in the kidney, and greater than 99% reduction in the tail and skin were observed during diving. The blood flow reduction from predive values ranged from 50% for liver and skeletal muscle to 75% for the adrenals and 65% for the diaphragm. The redistribution of the drastically reduced cardiac output during head immersion in the rat is similar to that reported for diving mammals. It is suggested that the rat may serve as a useful cardiovascular model for further studies of the diving response in mammals.
This investigation was undertaken to study the effect of hydrostatic pressure on gastroesophageal dynamics during immersion in thermoneutral water to the neck. In 5 healthy male subjects (normal end-expiratory), gastric pressure (PG), esophageal pressure (PE), location and pressure of distal esophageal sphincter (des), location of respiratory inversion point (RIP), and gastroesophageal pH gradient were measured standing in air (A), standing in water to the neck (B), and standing in air with abdominal compression (C). The pressure was measured with a Honeywell esophageal catheter (model 31) with built-in pressure transducer. A Beckman stomach pH electrode (no. 39042) was positioned adjacent to the pressure transducer. PG increased from 4.6 +/- 0.6 (SE) mmHg in A to nearly 20 mmHg in B and C, while PE increased from -6.0 +/- 0.8 mmHg in A to -0.8 +/- 1.0 and -3.4 +/- 0.9 mmHg in B and C, respectively. However, PDES was always 11-15 mmHg higher than PG. The superior limit of DES was displaced cephalad by indicating a stretching of DES and a shortening of the esophagus. Qualitatively similar findings were obtained in C. In all experiments, the esophageal pH remained above 6, and no alteration in the amplitude of primary peristaltic waves was seen. It is concluded that a head-out immersion with increased gastroesophageal pressure gradient predisposes to gastric reflux in the absence of a competent DES mechanism.
Umbilical arterial and venous blood, and fetal testes were taken from 38 bovine fetuses at 90, 180 or 260 days of gestation. Concurrently blood also was taken from the jugular, and from the uterine artery and vein of the dams. Testosterone and androstenedione were determined by radioimmunoassays. Fetal testicular homogenates had 0.96 and 0.35 mug/g of testosterone and 0.39 and 0.50 mug/g of androstenedione at 180 and 260 days of gestation, respectively. Males had five to tenfold more serum testosterone and about twofold more androstenedione than female fetuses at each trimester of gestation. Male fetal blood testosterone decreased (P less than 0.01) from 2.7 to 0.3 ng/ml between 90 and 260 days of gestation. But, maternal testosterone and androstenedione increased (P less than 0.05) during gestation in cows with males, but not in cows with female fetuses. Testosterone was higher (P less 0.05) in cows carrying males than in cows with female fetuses. Androstenedione was higher in blood leaving the placenta on both the maternal and on the vetal sides suggesting placental synthesis of androstenedione.
After an intra-arterial injection of 10 mug GnRH into four bovine male fetuses, serum LH increased (P less than 0.01) 2-fold by 15 min and plateaued at approximately 11 ng/ml from 60 to 180 min. After GnRH in six female fetuses, LH increased (P less than 0.01) 7-fold by 15 min and plateaued at approximately 17 ng/ml from 60 to 180 min. Maternal serum LH was not significantly influenced (P greater than 0.05) by sex of fetus or administration of GnRH to the fetus. After GnRH in male fetuses, serum testosterone increased (P less than 0.05) and remained 2-fold greater than basal levels through 180 min. In contrast, serum testosterone from female fetuses averaged 370 +/- 60 pg/ml at injection and was unchanged after GnRH. Androgen synthesis was significantly increased during in vitro incubation of fetal testicular explants by the addition of LH. We conclude that GnRH causes release of LH from the bovine fetal pituitary as early as 120 days of age and that the testes respond with testosterone secretion after LH stimulation.
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Palytoxin (PTX) inhibited phasic tension production and initiated tonic contracture in isolated paced ventricle strips at concentrations greater than 10(-10) M. PTX-induced contracture was associated with increased 45Ca2+ uptake. PTX-induced additional 45Ca2+ uptake was completely blocked by 2 mM La3+. All observed PTX effects were enhanced by elevation of [Ca2+] o from 1.9 to 6 mM and this threefold increase in [Ca2+] o resulted in a threefold increase in isotope-determined Ca2+ uptake in presence of 10(-8) M PTX. It is concluded that the observed effects of PTX could be mediated by an increase in calcium permeability of myocardial cells.
For testing biological response of newborn Taiwan monkeys to infection of human adenovirus type 12 (Ad12) and simian virus 40 (SV40), 40 newborn Taiwan monkeys were inoculated with Ad12, Ad12, plus SV40, Ad12 supplemented with Ad12-induced hamster tumor tissue (Ad12 tumor) or control specimens (HeLa or African green monkey kidney cell lysate). Among them 26 survived including 8 newborn monkeys inoculated with control specimens. The survivors were observed for 4 years but no tumor was produced. The increase of body weight and intake of calories and protein in each test group during the first 12 wk were similar to those of corresponding control groups. Intrapulmonary inoculation of 108.2TCD50 of Ad12 with additional subcutaneous dose of Ad12 (108.8TCD50), Ad12 plus SV40 (108TCD50) or Ad12 plus Ad12 tumor killed 78% of newborn monkeys (7 of 9) in 18 days. The newborn could stand subcutaneous inoculation of SV40 (108TCD50) with 1 dose of Ad12 (108.8TCD50) or 3 doses of Ad12 (108.5, 108.5 and 108.2TCD50) at 24-hr intervals. When 108.8TCD50 or more Ad12 were inoculated, the virus could be isolated as late as 44 and 26 days from rectal and throat swab specimens respectively. The Ad12 neutralizing antibody in baby monkeys inoculated with multiple doses of Ad12 persisted, in low titer, longer than those injected with single high doses of Ad12, but anti-Ad12 T (tumor) antibody disappeared by 35 wk in both groups. Although SV40 antibody response was better than Ad12 antibody response in baby Taiwan monkeys, pre-infection of SV40 did not potentiate the production of anti-Ad12 T antibody.
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