The original aim of this study was to observe whether the depressor drug clonidine inhibited the abnormal hindquarter tone in spontaneously hypertensive rats (SHR). In conscious SHR and normotensive control rats (NCR), hindquarter (terminal aortic) blood flow was observed with an implantd electromagnetic flow probe and mean arterial pressure with an indwelling catheter. Twenty minutes after intravenous injection of clonidine (5 μg/kg) when arterial pressure reached a steady lower level, hindquarter resistance (HQR), calculated as mean arterial pressure divided by hindquarter flow, did not decrease in SHR. Thus we were unable to obtain evidence for an inhibitory effect of clonidine on the abnormal hindquarter tone in SHR. In NCR, HQR increased significantly by clonidine. The decrease in arterial pressure on clonidine was greater in SHR than in NCR, presumably because the increase in HQR partially offset the hypotensive effect in NCR. It seems that the increase in HQR in NCR was induced by a reflexive excitation of regional sympathetic vasoconstrictor fibers, which, being the final common path for the abnormal hindquarter tone also, were already being excited in SHR before clonidine administration. This point was quantitatively verified.
This study was conducted to characterize Doppler blood flow signals in prostatic cancer using power Doppler imaging with a transrectal probe. Both the localization and vascularity of blood flow in the prostate were compared between patients with prostatic cancer and those with benign prostatic hyperplasia (BPH). The prominent accumulation of blood flow signals (hypervascular lesion) was recognized in all the cases with prostatic cancer, compared to only 2 (4%) of 47 with BPH (p<0.001). Power Doppler imaging is promising for the detection of prostatic cancer.
We investigated the roles of the mesothelium of the visceral pleura on hydraulic conductivity in dogs under normal conditions and condition of permeability pulmonary edema. Nineteen mongrel dogs were divided into following 4 groups: thoracotomy alone (control group, n=7); thoracotomy and striping of the mesothelium using Gelfilm (C+G group, n=4); injection of oleic acid to increase the permeability of the pulmonary vessels (OA group, n=4); injection of oleic acid and striping of the mesothelium (OA+G group, n=4). A hemispherical capsule filled with physiological saline was attached to the visceral pleura. The transpleural fluid flow (ΔV) was measured at given incremental or decremental hydrostatic pressures (ΔPcap) in the capsule. Hydraulic conductivity was calculated from the slope of linear regression line obtained from relationship between ΔPcap and the fluid flow rate (v) according to the Starling's equation. The conductivity obtained were 1.49±0.69 (nl·min−1·cmH2O−1·cm−2) in the control group, 1.37±0.88 in the C+G group, 3.75±0.74 in the OA+G group, and 7.07±2.49 in the OA+G group. The hydraulic conductivity was not increased by striping of the mesothelium (1.49±0.69 [nl·mm−1·cmH2O−1·cm−2] vs. 1.37±0.88, in the control group vs. C+G group, respectively). Visceral pleural hydraulic conductivity following OA injection was increased by striping of the mesothelium (3.75±0.74 vs. 7.07±2.49 in OA group vs. OA+G group, respectively). These findings suggest that the wall of pulmonary vessels acts as a barrier to movement of pleural effusion under normal conditions, whereas the mesothelium of the visceral pleura acts as that under condition of permeability pulmonary edema.
The central effects of capsaicin, veratrine, histamine and bradykinin were studied by injecting them directly into the cerebrospinal fluid and their peripheral effects were examined by injecting into femoral vein. Our experiments were performed in Na-pentobarbital-anaesthetized dogs. Tidal volume (VT), respiratory frequency (f/mm), systemic arterial pressure (BP) were recorded. A significant increase in f, and an initial apnea or hypoventilation followed by a significant increase in VT were observed with central and peripheral capsaicin. Vagotomy removed the peripheral VT response, but not the central one. While central capsaicin administration increased BP, peripheral administration decreased. After vagotomy, a significant increase was observed in BP for both administrations. Respiratory responses to central and peripheral administrations of veratrine were similar to those of capsaicin. Significant increases were observed in f and VT of the intact group in response to central and peripheral administration of histamine. Response to peripheral administration disappeared after vagotomy. While central and peripheral bradykinin increased VT significantly, there was no significant change in f. Vagotomy only removed the increase in VT in response to peripheral administration. In conclusion, respiratory responses to central administration of capsaicin and veratrine are due to direct effects of these substances on respiratory neurons. In peripheral administration, disappearance of the responses after vagotomy indicate that the responses are brought about by stimulation of the lung receptors.
BUF/Mna (B) rat is a mutated strain, having much larger thymus than WKY/ NCrj (W), ACI/NMs (A), and F344 (F) rats throughout their life-span. Rats of the latter 3 strains have normal sized thymuses, being less than 5.3 in the thymus to body weight ratio (mg/g), when they were killed at 6 weeks of age. Genetic segregation of large thymus size in the B strain at 6 weeks of age was studied by crossing B rats with W, A or F rats. All of 3 types of the Fl hybrid rats between the B strain and the other strains showed intermediate thymus ratios between those of both parental strains. In F2 rats between the B and W strains, the distribution of thymus ratios showed about 5 different peaks. These findings might indicate that two polymeric autosomal loci, thymus enlargement-1 (Ten-1) and thymus enlargement-2 (Ten-2), can enlarge the thymus size in B rats. Histometrically, whole thymus and cortex areas of the B rats were 2-5 times larger than the W rats during 6-12 weeks of age, but medulla areas were slightly different between the strains, showing that larger thymuses in B rats were mainly due to the enlarged cortex areas.
Serum secretory leukoprotease inhibitor (SLPI) is synthesized and secreted by serous cells in airway glands, and the serum level is speculated to reflect airway gland hyperplasia. To test this hypothesis, we measured the serum SLPI in 38 clinically stable patients with chronic bronchitis (3F and 35M; 58±2 years, mean±S.E.M.) (group CB), 24 patients with Sjögren's syndrome (24F; 52±3 years) (group SG), and compared it with 12 healthy control subjects (6F and 6M; 54±3 years) (group CN) using an enzyme-linked immunosorbent assay (ELISA). The serum SLPI from group CB (105±8 ng/ml) was significantly higher than that from group CN (60±2 ng/ml) and further, it significantly correlated with sputum volume per day. Although the mean value of serum SLPI from group SG (64±5 ng/ml) was not different from that from group CN, serum SLPI significantly correlated with the duration of respiratory symptoms (cough and/or sputum) in group SG. In conclusion, serum SPLI level reflects airway gland hyperplasia, suggesting that SLPI measurement is a possible laboratory method to estimate airway glandular hyperplasia.
We examined the gene expression of MASH-1, MATH-1, neuroD and NSCL-2 during neural differentiation of P19 embryonal carcinoma cells using reverse transcription-polymerase chain reaction and high performance liquid chromatography. These proteins are members of basic helix-loop-helix transcription factor family and their expressions are reported to be transient and restricted in the nervous system during early neurogenesis. Retinoic acid (RA; 1 μM)-treatment and aggregation for 4 days induced and greatly increased MASH-1, neuroD and NSCL-2 mRNA in P19 cells. The increases peaked at day 3, 4 and 5, respectively. RA-treatment increased MATH-1 mRNA slightly. mRNA of MAP2, a neural differentiation marker, were increased by RA-treatment and the increases reached to the plateau at day 5. The results indicate that the gene expression of MASH-1, MATH-1, neuroD and NSCL-2 during neural differentiation in P19 cells is transient and the order is similar to that in the mouse embryo nervous system as previously reported.
To evaluate serial changes in left ventricular diastolic filling patterns in preterm infants, we performed echocardiographic examinations in 18 very-low-birth weight infants and 20 fullterm infants before and after the closure of the ductus arteriosus. In the fullterm infants, the ductal closure induced significant decreases in the peak velocity and flow velocity integral of early diastole, first third filling fraction, and mitral stroke volume. In the preterm infants, by contrast, there were significant increases in the flow velocity integral of early diastole, first third filling fraction, and mitral stroke volume after the ductal closure. No differences following the ductal closure were found in the atrial phase of filling and peak filling rate normalized to stroke volume in either group. When the ductus arteriosus was open, essentially the same left-to-right shunting of the ductus arteriosus was detected in both preterm and fullterm infants, but the Doppler flow patterns of the patent foramen ovale were different: the fullterm infants had a single flow peak mainly during ventricular late systole and early diastole, but the preterm infants had two or three flow peaks with nearly equal amplitudes lasting from ventricular systole to diastole, which resembled the Doppler flow pattern of atrial septal defect. Only a faint Doppler flow signal of the foramen ovale was observed after the ductus arteriosus closed. Our results obtained from the preterms suggest that the left-to-right shunt through the foramen ovale may be one important factor to alter the Doppler transmitral filling patterns during the fetal to neonatal cardiovascular changes.
A 26-year-old woman ingested 0.9 g of mercuric chloride in a suicide attempt and developed hematemesis, melena and acute renal failure. Anuria persisted for 14 days. She was treated by plasma exchange, hemodialysis and peritoneal dialysis in combination with continued dimercaprol chelation. While hemodialysis was ineffective in removing the mercury, plasma exchange effectively eliminated mercury. After two plasma exchange therapies, mercury concentration in the blood decreased linearly on a log scale with half-lives of 23.1 days for whole blood and 19.1 days for plasma, using first-order kinetics. One month after ingestion, renal function recovered to normal as judged by serum creatine and blood urea nitrogen levels, although the β2-microglobulin level in urine was still elevated. At a follow-up examination four months later, renal function was found to be completely normal. This indicates that the renal damage caused by acute mercuric chloride poisoning may not be permanent.