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PubMed1991

Vasopressin response to haemorrhage in rats: effect of hypoxia and water restriction.

1. The aim of the present study was to determine the effect of water restriction and/or hypoxia on the vasopressin response to haemorrhage in conscious rats. 2. Male, Long-Evans rats (n = 39) were prepared with chronically indwelling femoral artery and vein catheters and exposed to 24 h of one of the following: normoxia with ad lib drinking water (N + W); normoxia with water restriction (N - W); hypoxia with ad lib drinking water (H + W); and hypoxia with water restriction (H - W). At the end of 24 h, a 15 mL/kg arterial haemorrhage was performed. 3. Water restricted rats had elevated pre-haemorrhage vasopressin levels. Haemorrhage induced an increase in vasopressin in all groups. Water restriction (N - W) or hypoxia (H + W) each augmented the vasopressin response to haemorrhage. However, the combination of hypoxia and water restriction (H - W) failed to augment the vasopressin response to haemorrhage as compared to normoxic, water replete (N + W) rats. 4. Hypoxia or water restriction per se augment the vasopressin response to haemorrhage. This augmented vasopressin response to haemorrhage is not maintained when hypoxia and water restriction are combined.

Animals↗

PubMed1998

Echocardiographic Aspects of Restrictive Cardiomyopathy: Their Relationship with Pathophysiology.

BACKGROUND AND METHODS: We studied 17 patients with restrictive cardiomyopathy; eight had biventricular restriction (type A), four had left ventricular restriction (type B), and five had only right ventricular restriction (type C). RESULTS: Type A disease was characterized by pulmonary and systemic venous congestion. The restrictive pattern was found in the inlet of both ventricles. Both atria were enormous, with small or normal-size ventricles. Differential diagnosis included constrictive pericarditis and systolic pump dysfunction. Type B restriction disease was characterized by venous pulmonary congestion, pulmonary hypertension, and important dilatation of the left atrium and right cavities with a small or normal-size left ventricle; the restrictive pattern was found only in the affected left ventricle. CONCLUSIONS: The clinical picture resembles that of rheumatic mitral valve disease with right ventricular failure. Type C disease had restriction only in the inlet of right ventricle, with giant right atrium, systemic venous hypertension with low flow, and normal pressure of pulmonary artery and left heart. Differential diagnosis included Ebstein's anomaly of tricuspid valve. The etiology of type A disease was amyloid, endomyocardial fibrosis of ventricles and idiopathic interstitial fibrosis. Asymmetric types were always caused by Davies' disease.

Journal Article↗

PubMed1979

Metabolic effects of blood flow restriction in adipose tissue.

The metabolic effects of blood flow restriction were studied in isolated blood-perfused canine subcutaneous adipose tissue. Blood flow restriction (on the average to 20 per cent of control flow) was caused by either mechanical clamping of the arterial inflow or by i.a. injections of methoxamine or angiotensin. Glucose uptake in the adipose tissue was reduced during blood flow restriction. This was partially compensated for by a period of increased glucose uptake following restoration of flow. Blood flow restriction also caused an increase in the venous lactate/pyruvate ratio. The basal lipolytic rate was decreased during blood flow restriction. Lipolysis induced by brief (5 min) sympathetic nerve stimulation (4 Hz) was not inhibited by blood flow restriction as the total amount of glycerol released from the tissue was unaffected. The outflow rate was reduced during blood flow restriction, but glycerol trapped within the tissue was apparently not reutilized by the fat cells as it was released upon flow restroation. FFA outflow following nerve stimulation was, however, inhibited suggesting increased reutilization of FFA within the tissue. This increased reutilization may ultimately be caused by the observed change in red./ox.-balance and/or by the limited carrier capacity (albumin) available during blood flow restriction. Three main conclusions may be drawn from the present results. Firstly, plasma levels of glycerol and FFA do not necessarily reflect adipose tissue lipolysis at a given moment. Secondly, the decreased adipose tissue blood flow seems to be a major cause of the lowered FFA-levels during hemorrhage. Thirdly, in contrast to hemorrhage, even severe reduction of adipose tissue blood flow is insufficient to cause irreversible ischemic damage.

Adipose Tissue↗

PubMed1981

Evidence for Plasmid Linkage of Restriction and Modification in Streptococcus cremoris KH.

Restriction and modification have been demonstrated in Streptococcus cremoris KH cells when infected by Streptococcus lactis C2 phage (designated c2) at an efficiency of plating of 2 x 10. The growth of c2 phage through KH cells produces modified progeny phage capable of unrestricted growth on KH cells. The ability of single-colony isolates of S. cremoris KH cultures to restrict and modify c2 phage was found to be variable. From 2 to 6.5% of colonies isolated were partially deficient in restrictive capacity, permitting a greater plaquing ability by c2 phage of 1.8 to 2.9 log cycles. No completely restrictionless mutants were isolated from 1,000 colonies examined. Mutants were shown to be deficient in both restriction and modification capabilities of the same specificity. The frequent occurrence of a genotypic change that resulted in the loss of both restriction and modification capacities indicated the involvement of plasmid deoxyribonucleic acid in genetically determining this specific restriction and modification system. S. cremoris KH was found to harbor 11 plasmid molecules, with molecular weights (x10) estimated to be 50, 41, 24, 18, 10, 7.4, 3.3, 3.0, 2.8, 2.5, and 1.5. Of the 27 mutants examined, 25 were missing the 10-megadalton plasmid. This consistent plasmid difference among the majority of mutants isolated supports the involvement of this plasmid in restriction and modification. Plasmid linkage of restriction and modification systems provides a genetic mechanism for the rapid development of phage-sensitive starter cultures due to the inherent instability of extrachromosomal elements.

Journal Article↗

PubMed1990

DNA Hybridization Probe for Use in Determining Restricted Nodulation among Bradyrhizobium japonicum Serocluster 123 Field Isolates.

Several soybean plant introduction (PI) genotypes have recently been described which restrict nodulation of Bradyrhizobium japonicum serocluster 123 in an apparently serogroup-specific manner. While PI 371607 restricts nodulation of strains in serogroup 123 and some in serogroup 127, those in serogroup 129 are not restricted. When DNA regions within and around the B. japonicum I-110 common nodulation genes were used as probes to genomic DNA from the serogroup strains USDA 123, USDA 127, and USDA 129, several of the probes differentially hybridized to the nodulation-restricted and -unrestricted strains. One of the gene regions, cloned in plasmid pMJS12, was subsequently shown to hybridize to 4.6-kilobase EcoRI fragments from DNAs from nodulation-restricted strains and to larger fragments in nodulation-unrestricted strains. To determine if the different hybridization patterns could be used to predict nodulation restriction, we hybridized pMJS12 to EcoRI-digested genomic DNAs from uncharacterized serocluster 123 field isolates. Of the 36 strains examined, 15 were found to have single, major, 4.6-kilobase hybridizing EcoRI fragments. When tested for nodulation, 80% (12 of 15) of the strains were correctly predicted to be restricted for nodulation of the PI genotypes. In addition, hybridization patterns obtained with pMJS12 and nodulation phenotypes on PI 371607 indicated that there are at least three types of serogroup 127 strains. Our results suggest that the pMJS12 gene probe may be useful in selecting compatible host-strain combinations and in determining the suitability of field sites for the placement of soybean genotypes containing restrictive nodulation alleles.

Journal Article↗

PubMed1968

Conditional temperature-sensitive restriction of Pseudomonas bacteriophge CB3.

Restriction of Pseudomonas bacteriophage CB3 growth on some Pseudomonas aeruginosa hosts was studied. On restricting hosts, growth of this phage was severely inhibited below 32 C and hence was temperature-sensitive. Investigation of this phenomenon revealed that restricting hosts were not killed as a consequence of their infection under nonpermissive conditions. The ability of some hosts to restrict showed segregation in sexual crosses between restricting and nonrestricting hosts. However, the pattern of restriction among various hosts differed with the phage in question when other phages were compared with CB3. Temperature-shift experiments indicated that blockage of an early event in the phage lytic cycle occurred when restricting conditions were imposed on cells infected with CB3. This blockage could be eliminated by holding at permissive conditions until the cold-sensitive step was bypassed or by pulsing restricting cells for 5 min at 37 C.

Bacteriophages↗

PubMed1969

Site of host restriction of simian virus 40 mutants in an established African green monkey kidney cell line.

A previously described large-plaque morphology mutant of SV40 (SV-L) in primary African green monkey kidney (AGMK) cells has been shown to be restricted in the established AGMK line CV-1. The site of restriction is an early step in infection, involving the virus particle. A block in penetration or uncoating has been tentatively proposed. Restriction is observed in a number of other established lines, including monkey, human, and mouse. Independent large-plaque mutants were isolated in AGMK and their properties were compared with SV-L (temperature restriction, host restriction, and virion antigen). They can be separated into two classes. Both are restricted on CV-1, though to a lesser degree than SV-L. Further-more, both are coat mutants as determined by immunological analysis of their virions, suggesting a relationship between coat mutants associated with large-plaque morphology in AGMK and host restriction in established cell lines. Temperature restriction is seen with one but not the other of the mutants.

Adsorption↗

PubMed1985

Nucleoprotein and membrane protein genes are associated with restriction of replication of influenza A/Mallard/NY/78 virus and its reassortants in squirrel monkey respiratory tract.

An avian influenza A virus, A/Mallard/NY/6750/78(H2N2), was restricted in in replication in the respiratory tract of squirrel monkeys. Avian-human influenza A reassortant viruses possessing the six RNA segments coding for nonsurface proteins (i.e., internal genes) of this avian virus were as restricted in replication in squirrel monkeys as their avian influenza parent. These findings indicated that restriction of replication of the avian influenza virus is a function of one or more of its internal genes. For an investigation of which of the avian influenza genes was responsible for restricted replication in the respiratory tract of primates, reassortant viruses were produced that contained human influenza virus surface antigens from the A/Udorn/72(H3N2) virus and one or more of the internal genes derived from the avian influenza virus parent. Avian-human reassortant influenza A viruses containing only the nucleoprotein or matrix protein RNA segment from the avian influenza virus parent were as restricted in their growth as an avian-human influenza reassortant virus containing each of the six avian influenza internal genes. In addition, an avian-human influenza reassortant virus possessing only the avian RNA 1 and nonstructural genes (which by themselves do not specify restricted replication) manifested a significant reduction of virus replication in squirrel monkey tracheas. Thus, the avian nucleoprotein and matrix genes appear to play a major role in the host range restriction exhibited by the A/Mallard/78 virus and its reassortants, but the combination of RNA 1 and nonstructural genes also contributes to restriction of replication.

Animals↗

PubMed2006

Restrictive diastolic filling predicts death after acute myocardial infarction: systematic review and meta-analysis of prospective studies.

OBJECTIVE: To determine, through a systematic review and meta-analysis, the magnitude of the survival deficit associated with a restrictive filling pattern after acute myocardial infarction (AMI). METHODS: Online databases were searched for prospective echocardiography outcome studies of patients after AMI. All authors were contacted to seek confirmation of their data. Restrictive filling was compared with all non-restrictive filling patterns. Review Manager Version 4.2.7 software was used for analysis. RESULTS: 3855 patients in 16 studies were identified. Follow up varied from two weeks to five years (> 1 year, 10 studies; and > 4 years, four studies). 776 (20%) of patients had a restrictive filling pattern at baseline. 580 patients died (247 in the restrictive group), and the overall odds ratio for death (restrictive filling worse) was 4.10 (95% confidence interval 3.38 to 4.99). CONCLUSIONS: Mortality is about four times higher in patients with a restrictive filling pattern than in those with non-restrictive filling patterns after AMI. Echocardiographic assessment of diastolic filling pattern is an important part of the echocardiographic assessment of patients after myocardial infarction and provides important prognostic information about such patients.

Diastole↗

PubMed1999

Medical restrictions to driving: the awareness of patients and doctors.

The study was set up to investigate the awareness of elderly patients and medical doctors of medical restrictions to driving. Separate questionnaires were completed by patients and doctors. All were interviewed face-to-face, without prior warning and their immediate answers were recorded. In total, 150 elderly patients from the acute elderly care wards, rehabilitation wards and day hospital, and 50 doctors (including all grades from consultant to junior house officer) were interviewed. The main outcome measures were numbers of patients currently driving and previously driving; patients' awareness of how their medical condition affected their ability to drive; doctors' spontaneous knowledge of medical conditions which restrict driving, current licensing policy, and restrictions for five specific medical conditions (epilepsy, myocardial infarction, stroke, 5-cm abdominal aortic aneurysm, and diabetes). Only 21 patients were current drivers, and six of these should not have been driving. While 103 perceived themselves eligible to drive, 46 had medical restrictions to driving. Seventeen of the 47 patients who perceived themselves not eligible to drive possibly did not have restrictions to driving. Doctors' knowledge of the current licensing policy and action to be taken if a patient was not eligible to drive was very poor. Knowledge of medical restrictions to driving was scanty, with few doctors giving the correct driving restrictions for the five specific conditions. We recommend that education of doctors regarding medical restrictions to driving should begin at an undergraduate level and be continued throughout their postgraduate career.

Age Factors↗

PubMed1989

Transient reduction of metabolic rate by food restriction.

It is widely held that restriction of food intake leads to a decrease in metabolic rate, and this effect has been implicated as the mechanism by which food restriction retards aging in laboratory rodents. Data on which this belief is based were obtained mostly from studies of basal metabolic rate after acute rather than chronic food restriction. In contrast we previously reported no effect of chronic food restriction on metabolic rate measured under usual living conditions. The present study examines changes in metabolic rate immediately after restriction of food so as to include the initial response to decreased intake of food. Two groups of specific pathogen-free Fischer 344 rats were housed under barrier conditions from 6 to 24 wk of age. Restricted rats were fed 60% of food consumed by rats eating ad libitum. Metabolic rate was measured indirectly by gas analysis with rats under normal daily living conditions (24MR) and basal metabolic rate (BMR) was also measured. Both 24MR and BMR decreased after food restriction, but this decrease was transient, so that within a few weeks metabolic rate of restricted rats was the same as that of rats fed ad libitum.

Aging↗

PubMed1996

Adaptations of intestinal nutrient transport to chronic caloric restriction in mice.

Lifelong caloric restriction increases median and maximum life span and retards the aging process in many organ systems of rodents. Because the small intestine absorbs a reduced amount of nutrients each day, does lifelong caloric restriction induce adaptations in intestinal nutrient transport? We initially compared intestinal transport of sugars and amino acids between 24-mo-old mice allowed free access to food [ad libitum (AL)] and those provided a calorically restricted [40% less than ad libitum (CR)] diet since 3 mo of age. We found that CR mice had significantly greater transport rates for D-glucose, D-fructose, and several amino acids and had significantly lower villus heights. Total intestinal absorptive capacities for D-glucose, D-fructose, and L-proline were each 40-50% greater in CR mice; absorptive capacity normalized to metabolic mass (body weight 0.75) was approximately 80% greater in CR mice. Comparison of uptakes in aged AL and CR mice with previously published results in young AL mice suggests that caloric restriction delays age-related decreases in nutrient transport. In contrast to published studies in hibernation and starvation, chronic caloric restriction enhances not only uptake per milligram but also uptake per centimeter. We then switched 24-mo-old AL mice to a calorie-restricted diet for 1 mo and found that short-term caloric restriction has no effect on intestinal nutrient transport, intestinal mass, and total absorptive capacity. Thus chronic but not short-term caloric restriction increases intestinal nutrient transport rates in aged mice, and the main mechanism underlying these increases is enhanced transport rates per unit intestinal tissue weight.

Adaptation, Physiological↗

PubMed2002

Cardioprotective effect of ischemic preconditioning is preserved in food-restricted senescent rats.

Ischemic preconditioning (PC) has been proposed as an endogenous form of protection against-ischemia reperfusion injury. We have shown that PC does not prevent postischemic dysfunction in the aging heart. This phenomenon could be due to the reduction of cardiac norepinephrine release, and it has also been previously demonstrated that age-related decrease of norepinephrine release from cardiac adrenergic nerves may be restored by caloric restriction. We investigated the effects on mechanical parameters of PC against 20 min of global ischemia followed by 40 min of reperfusion in isolated hearts from adult (6 mo) and "ad libitum"-fed and food-restricted senescent (24 mo) rats. Norepinephrine release in coronary effluent was determined by high-performance liquid chromatography. Final recovery of percent developed pressure was significantly improved after PC in adult hearts versus unconditioned controls (85.2 +/- 19% vs. 51.5 +/- 10%, P < 0.01). The effect of PC on developed pressure recovery was absent in ad libitum-fed rats, but it was restored in food-restricted senescent hearts (66.6 +/- 13% vs. 38.3 +/- 11%, P < 0.05). Accordingly, norepinephrine release significantly increased after PC in both adult and in food-restricted senescent hearts, and depletion of myocardial norepinephrine stores by reserpine abolished the PC effect in both adult and in food-restricted senescent hearts. We conclude that PC reduces postischemic dysfunction in the hearts from adult and food-restricted but not in ad libitum-fed senescent rats. Despite the possibility of multiple age-related mechanisms, the protection afforded by PC was correlated with increased norepinephrine release, and it was blocked by reserpine in both adult and food-restricted senescent hearts. Thus caloric restriction may restore PC in the aging heart probably via increased norepinephrine release.

Adrenergic Uptake Inhibitors↗

PubMed2005

Defending body mass during food restriction in Acomys russatus: a desert rodent that does not store food.

Golden spiny mice, which inhabit rocky deserts and do not store food, must therefore employ physiological means to cope with periods of food shortage. Here we studied the physiological means used by golden spiny mice for conserving energy during food restriction and refeeding and the mechanism by which food consumption may influence thermoregulatory mechanisms and metabolic rate. As comparison, we studied the response to food restriction of another rocky desert rodent, Wagner's gerbil, which accumulates large seed caches. Ten out of 12 food-restricted spiny mice (resistant) were able to defend their body mass after an initial decrease, as opposed to Wagner's gerbils (n = 6). Two of the spiny mice (nonresistant) kept losing weight, and their food restriction was halted. In four resistant and two nonresistant spiny mice, we measured heart rate, body temperature, and oxygen consumption during food restriction. The resistant spiny mice significantly (P < 0.05) reduced energy expenditure and entered daily torpor. The nonresistant spiny mice did not reduce their energy expenditure. The gerbils' response to food restriction was similar to that of the nonresistant spiny mice. Resistant spiny mice leptin levels dropped significantly (n = 6, P < 0.05) after 24 h of food restriction, and continued to decrease throughout food restriction, as did body fat. During refeeding, although the golden spiny mice gained fat, leptin levels were not correlated with body mass (r(2) = 0.014). It is possible that this low correlation allows them to continue eating and accumulate fat when food is plentiful.

Activity Cycles↗

PubMed1988

Effects of food restriction and hyperoxia on rat survival and lung polyamine metabolism.

We fed Sprague-Dawley rats either freely or by restricting them to 20% of their usual diet for 21 days. In one experiment, we refed half of the food-restricted rats for 12 h, then exposed the three groups to air or 85% O2 for 5 days. The mortalities in 85% O2 were 100, 33, and 0% for the food-restricted, restricted-refed, and freely fed groups, respectively. In air lung polyamine contents and glucose 6-phosphate dehydrogenase and NADP-dependent isocitrate dehydrogenase activities were significantly lower with food restriction. After hyperoxia, lung polyamine and protein contents and enzyme activities were increased in the two surviving groups, but spermine and DNA contents of refed rats did not increase. In a second experiment, we exposed rats to 60% O2 and found that DNA synthesis of food-restricted rats was lower than the freely fed rats in air and remained low after hyperoxia. We conclude that food restriction increases the mortality from 85% O2 and is associated with lower DNA synthesis and polyamine content. We speculate that food-restricted animals may accumulate greater lung injury partly because of a compromised repair process.

Animals↗

PubMed1995

Effect of exercise and food restriction on selected markers of the acute phase response in hamsters.

Acute aerobic exercise has been shown to elicit physiological changes characteristic of the acute phase response (APR), a nonspecific host defense response. Regular evocation of these changes may prime the immune system to improve resistance to disease. Because food deprivation is associated with an impaired APR, food restriction may prevent these beneficial changes. We tested the hypotheses that voluntary exercise elicits an APR and that food restriction modifies this response in four groups of hamsters: ad libitum-fed sedentary, ad libitum-fed exercised, food-restricted sedentary, and food-restricted exercised. Five variables altered during an APR were examined: core temperature, serum iron, serum interleukin-6, serum amyloid A, and serum glucocorticoids measured by biotelemetry, colorimetric analysis, B-9 cell growth assay, indirect enzyme-linked immunosorbent assay, and radioimmunoassay, respectively. Blood was drawn during the hamsters' inactive period after 19-20 days of access to running wheels. Resting core temperature was elevated by exercise and depressed by food restriction (P < 0.01). Iron was depressed by food restriction (P < 0.01). Cortisol, but not corticosterone, was elevated by food restriction (P < 0.001). There were no significant differences among groups in interleukin-6 (P > 0.49) or serum amyloid A (P > 0.29). We conclude that there is little evidence that voluntary exercise or exercise combined with food restriction causes an APR in hamsters.

Acute-Phase Reaction↗

PubMed2000

Effect of sleep restriction on orthostatic cardiovascular control in humans.

We hypothesized that sleep restriction (4 consecutive nights, 4 h sleep/night) attenuates orthostatic tolerance. The effect of sleep restriction on cardiovascular responses to simulated orthostasis, arterial baroreflex gain, and heart rate variability was evaluated in 10 healthy volunteers. Arterial baroreflex gain was determined from heart rate responses to nitroprusside-phenylephrine injections, and orthostatic tolerance was tested via lower body negative pressure (LBNP). A Finapres device measured finger arterial pressure. No difference in baroreflex function, heart rate variability, or LBNP tolerance was observed with sleep restriction (P > 0.3). Systolic pressure was greater at -60 mmHg LBNP after sleep restriction than before sleep restriction (110 +/- 6 and 124 +/- 3 mmHg before and after sleep restriction, respectively, P = 0.038), whereas heart rate decreased (108 +/- 8 and 99 +/- 8 beats/min before and after sleep restriction, respectively, P = 0.028). These data demonstrate that sleep restriction produces subtle changes in cardiovascular responses to simulated orthostasis, but these changes do not compromise orthostatic tolerance.

Adult↗

PubMed2006

Combination therapy of androgen-independent prostate cancer using a prostate restricted replicative adenovirus and a replication-defective adenovirus encoding human endostatin-angiostatin fusion gene.

Although prostate-restricted replicative adenovirus has exhibited significant antitumor efficacy in preclinical studies, it is necessary to develop more potent adenoviruses for prostate cancer gene therapy. We evaluated the synergistic killing effect of prostate-restricted replicative adenovirus and AdEndoAngio, a replication-defective adenovirus expressing the endostatin-angiostatin fusion protein (EndoAngio). When coadministered with AdEndoAngio, prostate-restricted replicative adenovirus significantly elevated EndoAngio expression, suggesting that AdEndoAngio coreplicates with prostate-restricted replicative adenovirus. Conditioned medium from prostate cancer cells infected by prostate-restricted replicative adenovirus plus AdEndoAngio inhibited the growth, tubular network formation, and migration of human umbilical vein endothelial cells better than conditioned medium from prostate cancer cells infected by AdEndoAngio alone. Furthermore, in vivo animal studies showed that the coadministration of prostate-restricted replicative adenovirus plus AdEndoAngio resulted in the complete regression of seven out of eight treated androgen-independent CWR22rv tumors, with a tumor nodule maintaining a small size for 14 weeks. The residual single tumor exhibited extreme pathologic features together with more endostatin-reactive antibody-labeled tumor cells and fewer CD31-reactive antibody-labeled capillaries than the AdEndoAngio-treated tumors. These results show that combination therapy using prostate-restricted replicative adenovirus together with antiangiogenic therapy has more potent antitumor effects and advantages than single prostate-restricted replicative adenovirus and deserves more extensive investigation.

Adenoviridae↗