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Cardiovascular adjustments to exercise: hemodynamics and mechanisms.

The integrated response to severe exercise involves fourfold to fivefold increases in cardiac output, which are due primarily to increases in cardiac rate and to a lesser extent to augmentation of stroke volume. The increase in stroke volume is partly due to an increase in end-diastolic cardiac size (Frank-Starling mechanism) and secondarily due to a reduction in end-systolic cardiac size. The full role of the Frank-Starling mechanism is masked by the concomitant tachycardia. The reduction in end-systolic dimensions can be related to increased contractility, mediated by beta adrenergic stimulation. Beta adrenergic blockade prevents the inotropic response, the decrease in end-systolic dimensions, and approximately 50% of the tachycardia of exercise. The enhanced cardiac output is distributed preferentially to the exercising muscles including the heart. Blood flow to the heart increases fourfold to fivefold as well, mainly reflecting the augmented metabolic requirements of the myocardium due to near maximal increases in cardiac rate and contractility. Blood flow to the inactive viscera (e.g., kidney and gastrointestinal tract) is maintained during severe exercise in the normal dog. It is suggested that local autoregulatory mechanisms are responsible for maintained visceral flow in the face of neural and hormonal autonomic drive, which acts to constrict renal and mesenteric vessels and to reduce blood flow. However, in the presence of circulatory impairment, where oxygen delivery to the exercising muscles is impaired as occurs to complete heart block where normal heart rate increases during exercise are prevented, or in congestive right heart failure, where normal stroke volume increases during exercise are impaired, or in the presence of severe anemia, where oxygen-carrying capacity of the blood is limited, visceral blood flows are reduced drastically and blood is diverted to the exercising musculature. Thus,, visceral flow is normally maintained during severe exercise as long as all other compensatory mechanisms remain intact. However, when any other compensatory mechanism is disrupted (even the elimination of splenic reserve in the dog), reduction and diversion of visceral flow occur.

Adaptation, Physiological↗

Fatal bowel infarction and sepsis: an unusual complication of systemic strongyloidiasis.

A 58 year old Chinese male, one week after arriving in Canada from Hong Kong, presented with acute abdominal pain and diarrhoea which was rapidly followed by Escherichia coli infection causing septicaemia and meningitis. His past history revealed bronchial asthma for 15 years treated with steroids. At laparotomy, 7 days after the onset of symptoms, he was found to have extensive haemorrhagic infarction of the small bowel and right colon. Examination of the fibrosed mesenteric vessels revealed numerous filariform larvae of Strongyloides stercoralis, within the walls, and in all layers of bowel wall. The role of the parasite in the production of obliterative arteritis in this fatal case of haemorrhagic enteropathy is discussed. Clinical strongyloidiasis, in uncomplicated cases, varies from mild to severe with gastroenteritis, nausea, colicky abdominal pain, electrolyte imbalance and symptoms of malabsorption syndrome (MARCIAL-ROJAS, 1971). In malnourished individuals and patients with debilitating infections, either newly acquired or asymptomatic latent infection with S. stercoralis can assume severe dimensions (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). Similarly, in patients on steroid (CRUZ et al., 1966; WILLIS and MWOKOLO, 1966; NEEFE et al., 1973) and immunosuppressive therapy for lymphomatous diseases or deficient in immune response (ROGERS and NELSON, 1966; RIVERA et al., 1970), systemic strongyloidiasis is often fatal. The increased frequency of auto-infection in such patients with a breached immune barrier is, however, unclear. Further complications of this infection due to severe enterocolitis result in sepsis, bacteraemia and meningitis (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). This paper presents a fatal case of S. stercoralis infection which illustrates an uncommon if not unique, mechanism in its production of haemorrhagic enteropathy leading to sepsis and death.

Colon↗

Response of the cardiovascular system to catecholamines in rats given small doses of lead.

Experiments were done in order to assess the influence of low level lead poisoning in rats upon the responses of the rat cardiovascular system to perturbation by norepinephrine, epinephrine, and isoproterenol administration. Wistar rats were given lead acetate (50.0 mg/kg) via stomach tube once weekly for 5 weeks. Control rats were given sodium acetate similarly; both groups of rats were on a regular animal food diet during the experiment. At the end of the sixth week 2 types of responses were determined. Under urethane anesthesia, the response of mean arterial pressure and heart rate in control and lead-poisoned animals to various catecholamines was measured. Also the response of perfusion pressure in isolated mesenteric vessels, to catecholamines, was measured for vessels having been obtained from control and lead poisoned animals. Our results indicate that lead-treated rats, as compared to controls, have augmented and prolonged pressor responses to epinephrine and norepinephrine; less pronounced depression of arterial pressure in response to epinephrine and isoproterenol; and more pronounced tachycardia in response to isoproterenol. In the lead-treated rats, more pronounced vasoconstriction was observed in the perfusion studies upon administration of exogenous norepinephrine. Small doses of lead intensified alpha receptor response, diminished beta receptor response in blood vessels, and increased positive chronotropic action of isoproterenol.

Animals↗

Ultrasound in the study of atherosclerosis.

Ultrasound has come to play an increasingly important role in investigating atherosclerosis. The simple, continuous wave directional devices may be used to measure limb blood pressure and assess velocity patterns from accessible arteries. The recent combined B-mode and pulsed Doppler systems are being used regularly to study the carotid bifurcation in the neck. With improvements in image resolution, Doppler technology and signal processing methods, it is now feasible to evaluate the morphology of the plaque and accurately predict the degree of stenosis by the recorded velocity changes in the residual lumen. By the development of transducers of low transmitting frequency (less than 5 mHz), it is now possible to evaluate arteries at greater depth such as the renal and mesenteric vessels. Duplex scanning promises to become the definitive, noninvasive method of assessing both the anatomy and flow characteristics of all major arteries outside the thorax and skull that are common sites for the development of atherosclerosis.

Arterial Occlusive Diseases↗

Effects of pindolol on vascular smooth muscle.

Pindolol is a non-selective beta-adrenoceptor blocking agent with relatively marked intrinsic sympathomimetic activity. Stimulant effects in isolated, perfused mesenteric vessels (beta 2) equal those of isoprenaline. Effects on guinea-pig atria (beta 1) are negligible and those on guinea-pig trachea (beta 1 and beta 2) and cat atria (beta 1 and beta 2) are equivalent to 40-50% of the maximum effects of isoprenaline. It is concluded that the intrinsic sympathomimetic activity of pindolol is exerted principally on the beta 2-adrenoceptor. The beta-adrenoceptor blocking effect of pindolol is largely confined to the (-)enantiomer, whereas its stimulant effects are shared equally by the (+) and (-)enantiomers. Removal of the side chain hydroxyl group of pindolol does not diminish stimulant activity, but abolishes blocking activity. Pindolol-induced stimulation and blockade of beta-adrenoceptors may be brought about by different configurations of the molecule. Vasodilator effects observed in vitro and in vivo suggest that beta-adrenoceptor stimulation may make an important contribution to the antihypertensive effect of pindolol in man.

Animals↗

Induction of endometriosis in mice: a new model sensitive to estrogen.

Endometriosis consists of the growth of endometrial tissue outside the uterus. A rat model of endometriosis is available to evaluate the potential for environmental chemicals to promote the disease but may be relatively insensitive for the evaluation of the hazard of certain compounds. Our objective, which was to develop a mouse model for endometriosis, was based on (a) the promotion of endometriosis in primates by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), (b) the apparent relationship between endometriosis and immunodeficiency, and (c) evidence that humoral immunity is suppressed in mice but not rats following TCDD exposure. In the mouse model, slices of uterus were sutured to intestinal mesenteric vessels. By 3 weeks after surgery, these sites were cyst-like structures. The growth of the sites was hormone dependent. In intact mice, sites measured 3.60 +/- 0.22 mm; vehicle and estrone (0.5 microgram/day) treatments produced site diameters of 0.95 +/- 0.128 and 5.28 +/- 0.355 mm, respectively. This new mouse model provides a sensitive and useful technique for future studies of the potential for specific xenobiotics to promote the development of endometriosis.

Animals↗

Laparoscopic procedures for small bowel disease.

Small bowel procedures such as placement of feeding jejunostomy, diagnosis of small bowel ischaemia and obstruction, bowel resection and lysis of adhesions can all be performed laparoscopically. Diagnostic laparoscopy can be performed with low complication rates, and can help avoid unnecessary laparotomy. The open method of trocar placement is preferred in patients with adhesions or distended bowel due to obstruction or ileus. Feeding jejunostomy can be placed by laparoscopically assisted methods, pulling the jejunum out or completely laparoscopically. The latter requires fixation of the jejunum to the abdominal wall by transabdominal sutures or T-fasteners. The T-fastener technique for feeding jejunostomy is simple to perform, safe and effective. Small bowel ischaemia can be difficult to diagnose laparoscopically. Fluorescein and ultrasound Doppler examination of the small bowel may be as useful as in laparotomy, but there is little clinical experience with these techniques. Laparoscopically assisted small bowel resection involves intraperitoneal division of the mesenteric vessels and exteriorization of the small bowel through a small abdominal incision, followed by resection and anastomosis. The causes of small bowel obstruction can be diagnosed laparoscopically, and adhesions can be lysed under laparoscopic guidance. The laparoscopic approach is replacing laparotomy for many small bowel procedures. Improvements in instruments and experience in laparoscopic procedures will continue to make these procedures easier and safer to perform.

Enteral Nutrition↗

Midgut carcinoid tumours: surgical treatment and prognosis.

Midgut carcinoids originating in the small intestine are the most common cause of the carcinoid syndrome. These tumours typically progress slowly and have an extended disease course, and although they often present with metastases at diagnosis, surgical treatment has become increasingly important for their management. Surgery should include efforts to remove mesenteric metastases, which may cause severe long-term abdominal complications with typical fibrotic intestinal entrapment and small-bowel ischaemia due to compression of mesenteric vessels. Attempts should also be made to surgically remove or ablate liver metastases, since this may provide considerable palliation of the carcinoid syndrome. For patients with the carcinoid syndrome surgery is combined with continuous biotherapy with long-acting somatostatin analogues, which may alleviate symptoms and stabilize disease or slow progression. Favourable survival and appreciable quality of life can be expected with this combined treatment, even in patients with advanced midgut carcinoids.

Biopsy, Needle↗

A role for the central histaminergic system in the leptin-mediated increase in cardiovascular dynamics.

The central nervous system (CNS) histaminergic neurons have been shown to regulate feeding behavior and are a target of leptin in the brain. The present study aimed to examine the involvement of the histaminergic system in the leptin-mediated regulation of cardiovascular dynamics. We investigated the cardiovascular responses to the CNS administration of histamine, leptin and alpha-melanocyte stimulating hormone (alpha-MSH) both in the presence and absence of the histamine H1 antagonist, chlorpheniramine. The intracerebroventricular (i.c.v.) administration of histamine resulted in an immediate increase in both mean arterial pressure (MAP) and heart rate (HR) and vasoconstricted the iliac, renal and superior mesenteric vessels. The i.c.v. pretreatment with chlorpheniramine attenuated the histamine-induced increase in MAP, HR and decreased vascular conductance. The i.c.v. administration of leptin increased MAP and HR and decreased vascular conductance. The i.c.v. pretreatment with chlorpheniramine decreased the leptin-induced increase in MAP and the leptin-mediated iliac vasoconstriction. The i.c.v. administration of alpha-MSH also increased MAP, HR and decreased vascular conductance. However, pretreatment with chlorpheniramine did not influence the central alpha-MSH-mediated increase in MAP, HR and decreased vascular conductance. These results indicate that the central histaminergic system mediated by H1 receptors have a role in the central signaling pathway and is involved in leptin's regulation of cardiovascular dynamics. It appears that leptin directly or indirectly stimulates histaminergic neurons that lead to increased cardiovascular activity.

Analysis of Variance↗

Helical CT diagnosis of small bowel obstruction in the acute clinical setting.

Definite confirmation or exclusion closed loop obstruction (CLO) is one of the most difficult tasks the radiologist has to face in the clinical practice. Aim of this retrospective work was to study the value of spiral computed tomography (CT) in the diagnosis of closed loop obstruction complicated by intestinal ischemia. The state of the art CT signs of closed loop obstruction were taken into consideration. Serrated beaks with poor or no contrast enhancement of the bowel walls, ascites or engorgement of the mesenteric vasculature allowed the CT diagnosis of CLO complicated by ischaemia. U or C-sharped of dilated loops, radial distribution of the mesenteric vessels, beaks and whirls suggested CLO, but did not help differentiate CLO from strangulation. CLO is a dynamic entity which may regress or need laparotomy depending on the time and degree of rotation of the incarcerated loops. CT is a reliable imaging modality able to differentiate CLO from strangulation, which is rarely simple and obvious. Detection of ischemic changes in the bowel walls and/or attached mesentery on CT scans imply strangulation highlighting the need for laparotomy; if only signs of CLO are detected, the existence and/or development of strangulation cannot be predicted.

Acute Disease↗

Schistosoma bovis: plasminogen binding in adults and the identification of plasminogen-binding proteins from the worm tegument.

Schistosoma bovis is a ruminant haematic parasite that lives for years in the mesenteric vessels of the host. The aim of this work was to investigate the ability of adult S. bovis worms to interact with plasminogen, a central component in the host fibrinolytic system. Confocal microscopy analysis revealed that plasminogen bound to the tegument surface of the male-but not female-S. bovis worms and that this binding was strongly dependent on lysine residues. It was also observed that a protein extract of the worm tegument (TG) had the capacity to generate plasmin and to enhance the plasmin generation by the tissue-type plasminogen activator. Proteomic analysis of the TG extract identified 10 plasminogen-binding proteins, among which the major ones were enolase, glyceraldehyde-3-phosphate dehydrogenase and actin. This study represents the first report about the binding of plasminogen to Schistosoma sp. proteins.

Actins↗

Is there a role for staging laparoscopy in patients with locally advanced, unresectable pancreatic adenocarcinoma?

The study objective was to determine the incidence of laparoscopically detected metastasis in patients with radiographically staged locally advanced adenocarcinoma of the pancreas. Patients with locally advanced pancreatic cancer are considered candidates for novel treatment protocols. Stratification of patients into locally advanced disease versus metastatic disease is imperative to accurately evaluate treatment outcome. Between 1994 and 2000, 100 consecutive patients undergoing staging laparoscopy with radiologic evidence of unresectable locally advanced pancreatic cancer were identified from a prospective database. All patients had preoperative contrast-enhanced, thin-cut computed tomography scanning or magnetic resonance imaging and had no evidence of detectable metastatic disease. There were 53 men and 47 women, with a median age of 64 years. The disease site was the pancreatic head in 69 cases and the body or tail in 31. Radiographic assessment of nonresectability was due to encasement of the celiac or hepatic artery in 37 patients, of the portal vein and superior mesenteric vessels in 56, and extrapancreatic extension in 7. Laparoscopy identified metastatic disease in 37% of patients, not seen on preoperative imaging. Peritoneal disease was noted in 12 cases and liver metastasis in 18 cases, and 7 patients had both. Neither the primary tumor size nor location influenced the incidence of metastatic disease. Standard imaging modalities failed to detect metastatic disease in 37% of patients who were considered to have locally advanced pancreatic cancer. Patients considered for treatment protocols for locally unresectable pancreatic cancer should be staged laparoscopically before initiation of therapy.

Adenocarcinoma↗

Transanal one-stage endorectal pull-through for Hirschsprung's disease: a multicenter study.

BACKGROUND/PURPOSE: Transanal endorectal pull-through (TEPT) is the latest development in treatment of Hirschsprung's disease (HD). This prospective study was designed to evaluate the safety and efficacy of 1 stage TEPT technique in the management of patients with HD. METHODS: One hundred forty-nine children (116 boys and 33 girls) aged 8 days to 14 years underwent 1 stage TEPT procedure over an 18-month period at 5 Egyptian academic pediatric surgical centers and affiliated hospitals. Median follow-up was 12 months (range, 3 to 21 months). These patients were evaluated with regard to age, sex, length of the aganglionic segment, intraoperative details, and postoperative functional results or complications. An electromyogram (EMG), endorectal ultrasound scan, and lower gastrointestinal (GI) motility studies were reserved for patients with postoperative problems with bowel control. RESULTS: Mean operating time was 120.2 +/- 27.8 minutes (range, 60 to 210 minutes). The average length of resected bowel was 26.8 +/- 12.4 cm (range, 15 to 45 cm). Thirteen patients required laparotomy because of extension of aganglionic segment beyond the sigmoid colon in 9, tear in the mesenteric vessels in 2, and difficulties in getting to the submucosal plane in 2. Three deaths (2%) occurred 3 days, 4 days, and 4 weeks postoperatively, respectively. Postoperative complications included transient perianal excoriation in 48 patients (30 were <3 months of age), enterocolitis (n = 26), anastomotic stricture (n = 7), recurrent constipation (n = 6), hypoganglionosis at distal end of pulled through segment (n = 2), cuff abscess (n = 3), anastomotic leak (n = 1), adhesive bowel obstruction (n = 1), and rectal prolapse (n = 1). Complete anorectal continence was noted in 35 of 42 (83.3%) children older than 3 years, whereas soiling and frequent accidents still occur in 7, who showed a steady improvement in their continence status. CONCLUSIONS: One-stage TEPT technique is both feasible and safe technique in properly selected children with rectosigmoid HD in all ages. The technique is easily learned and is associated with excellent clinical results.

Adolescent↗

Conservative treatment of a mesenteric lymphangiomyomatosis in an 11-year-old girl with a long follow-up period.

The authors report the case of a 11-year-old girl admitted for a mesenteric tumor discovered during an appendicectomy. The abdominal Doppler echography and computed tomography (CT) scan showed a 8 x 6 x 7-cm multinodular mass involved in the mesenterium. Biological markers and iodine 131 meta-iodobenzylguanidine (MIBG) scintigraphy results were normal. Percutaneous biopsies were performed. Pathology results showed perilymphatic proliferation of smooth muscle cells leading to cystic lesions. No sign of malignancy was seen. Laparotomy showed a multinodular fixed mass involved from the root of the mesenterium. The superior mesenteric vessels were encircled by the tumor, which could not be resected completely. Partial resection was performed. The pathology and the immunohistochemical tests confirmed the diagnosis of lymphangiomyomatosis. At 21 years of age, she remains asymptomatic. An echography and CT scan showed the mass remaining unchanged in size and echopattern. Lymphangiomyomatosis (LMA) is thought to affect exclusively women in their reproductive life, and the steroid hormones are supposed to play an essential role in the pathology and in the behavior of this condition. Infantile LMA is exceptional. The patient reported is remarkable for her young age, the location of the tumor, her long history, and her benign course. Because the tumor is supposed to be hormone dependent, the surge of oestrogen in this 21-year-old woman may initiate the extensive form of lymphangiomyomatosis with pulmonary involvement, the prognosis of which is extremely poor.

Appendectomy↗

Trefoil factor family peptide 3 prevents the development and promotes healing of ischemia-reperfusion injury in weanling rats.

BACKGROUND/PURPOSE: Although the pathogenesis of necrotizing enterocolitis (NEC) is not completely defined, ischemia appears to be one of the most important causative factors. Trefoil factor family peptide 3 (TFF3) is a peptide normally expressed in the small bowel and colon and is involved in the maintenance and repair of mucosal integrity. The authors hypothesized that monomeric (TFF3 Ser57) and dimeric (TFF3 Cys57) recombinant TFF3 may prevent the development and accelerate healing of intestinal ischemia-reperfusion injury in weanling rats. METHODS: Intestinal injury was induced in 18-day-old rats by occlusion of the superior mesenteric vessels for 60 minutes. To examine the protective effect, rats were given 3 microg/g of TFF3 Ser57 or TFF3 Cys57 by subcutaneous or enteral administration 30 minutes before the vascular occlusion. To examine the healing effect, rats were given 3 microg/g of TFF3 Ser57 or TFF3 Cys57 by subcutaneous or enteral administration 60 minutes after the beginning of reperfusion. Samples from small bowel and colon were collected for morphometric analysis after 3 hours of reperfusion. Mucosal damage was assessed by the Chiu score. RESULTS: Both forms of TFF3 reduced the amount of damage when administered before the ischemia. Administration of TFF3 Ser57 and TFF3 Cys57 after the beginning of reperfusion significantly increased the villous height and decreased the Chiu score in the small intestine and colon. CONCLUSIONS: TFF3 Ser57 monomer and TFF3 Cys57 dimer prevent the development and promote healing of ischemia-reperfusion injury in weanling rats. There are no differences between the routes of administration of TFF3.

Animals↗

Interstitial cells of Cajal in dysmotility in intestinal ischemia and reperfusion injury in rats.

BACKGROUND: Intestinal ischemia and reperfusion (I/R) injury is an obligatory occurrence in small bowel transplantation. I/R may impair the normal gastrointestinal motility. Interstitial cells of Cajal (ICC) are known as pacemaker cells in the gastrointestinal tract. The aim of this study was to assess the role of ICC in the gastrointestinal motility in a rat model of I/R injury. MATERIALS AND METHODS: Wistar rats were subjected to 30- or 80-min intestinal ischemia by occluding the mesenteric vessels followed by reperfusion. Small intestinal segments were resected at 12 h or 4 days. The spontaneous mechanical activity was evaluated by organ bath technique. Immunopositivity of c-Kit and PGP9.5 at the level of the myenteric plexus was evaluated as markers of ICC and enteric nerves, respectively. RESULTS: In the bowel segment with 80-min ischemia followed by 12-h reperfusion, muscles showed a 25% reduction (P < 0.05) in the frequency of contractions compared to that with 30-min ischemia followed by 12-h reperfusion, whereas amplitude of contractions was not significantly different. This change was associated with a 70% decrease (P < 0.01) of c-Kit immunopositivity. These changes of intestinal motility pattern and distribution of c-Kit-positive cells were both recovered from 80-min ischemia followed by 4 days reperfusion. In contrast, the immunopositivity of PGP9.5 was not affected in any I/R injury group. CONCLUSIONS: Transient functional changes in ICC were induced by prolonged I/R injury but they recovered after 4 days, suggesting a central role of ICC in both disrupting and restoring the normal gastrointestinal motility in I/R injury.

Animals↗

Understanding trends in inpatient surgical volume: vascular interventions, 1980-2000.

OBJECTIVE: To help understand past and future trends in vascular intervention, we examined changes in the rate of utilization, patient demographics, and length of stay from 1980 to 2000. METHODS: We reviewed the ICD-9 codes for all vascular procedures using the National Hospital Discharge Survey of non-federal United States hospitals (1980-2000). RESULTS: The number of vascular procedures performed in this country increased from 412,557 in 1980 to 801,537 in 2000 (per capita increase of >50%). This increase was most evident in elderly patients (>75 years, 67% per capita increase in discharges). Long hospital stays (> or =7 days) for vascular procedures fell 41%, and short hospital stays (<24 hours) increased 15% over the period of study. The frequency of abdominal aortic aneurysm repairs remained relatively constant. Except for an interval in the late 1980s, and a minor decrease from 1997 to 2000, the frequency of carotid endartarectomy rose dramatically (69%). Lower extremity revascularizations increased steadily until 1990 but then declined 12%. From 1995 to 2000, there was a 27% per capita decrease in the number of renal-mesenteric operations. Correspondingly, over the past 5 years there has been a 979% growth in the number of percutaneous/endovascular interventions. Despite a substantial number of interventions for lower extremity vascular disease, there was a concomitant increase in the number of major and minor amputations. CONCLUSION: Interventions for vascular disease have increased dramatically, with a major shift toward less invasive treatments, particularly for the renal and mesenteric vessels and the lower extremities. These trends in procedural use suggest that vascular surgeons need to embrace catheter-based approaches if they want to remain leaders in the treatment of peripheral vascular diseases.

Adolescent↗

Debunking a myth: neurohormonal and vagal modulation of sleep centers, not redistribution of blood flow, may account for postprandial somnolence.

It is widely believed that postprandial somnolence is caused by redistribution of blood flow from cerebral to mesenteric vessels after a meal. This belief persists despite its apparent contradiction with a well-known neurophysiologic principle that cerebral perfusion is preferentially maintained under a wide range of physiologic states. For instance, during exercise when a large amount of perfusion is diverted to muscles, blood flow to the brain is maintained. Furthermore, recent evidence suggests that there is no measurable change of blood flow in the common carotid artery during postprandial states. We propose an alternative hypothesis that postprandial release of gut-brain hormones and activation of vagal afferents may play a role in postprandial somnolence through modulation of sleep centers such as the hypothalamus. Feeding alters the milieu of hormones such as melatonin and orexins and also promotes central vagal activation. Emerging evidence suggest that these pathways are also modulators of neural sleep centers. Potential adaptive explanations of postprandial somnolence are explored from a Darwinian perspective.

Adaptation, Physiological↗