Progressive dehydration of resting male subjects was accomplished by exposure to 43.3 C dry bulb, 29 C wet bulb for 12 hr. For control experiments, evaporative weight loss was replaced with 0.1% saline. For dehydrating subjects, the following relationships with evaporative weight losses were obtained: %Delta osmotic pressure = 1.14 (% evap wt loss) — 0.43; %Delta [Na+] = 1.37 (% evap wt loss) — 0.45; %Delta [K+] — 2.19 (% evap wt loss) — 1.29; %Delta hematocrit = 1.4 (%Delta evap wt loss) — 2.65. Comparison of dehydration with rehydration results indicated augmentation of plasma volume with fluids containing high concentrations of potassium. An average decrease in plasma volume of 13.6% (T-1824) from 2.5 to 11 hr after initial heat exposure in dehydrating subjects was accompanied by a 15.7% increase in total protein. Albumin increased 11.6% while globulin increase averaged 22.5%. Plasma protein fractions are not static during dehydration, probably due to augmentation of each protein fraction, particularly globulin. Measurement of plasma volume by T-1824 more likely indicates changes in protein concentration rather than plasma volume changes. A relationship between hematocrit changes and plasma albumin concentrations is suggested. plasma sodium; plasma potassium; plasma osmolarity; hematocrits; plasma albumin; plasma globulins Submitted on February 23, 1965

CHRISTENSEN propagated by using special cell types or techniques or both (320, 353, 372). In addition, a variety of in vitro detection systems, including enzyme immunoassays (149, 175, 333, 408), radioimmunoassays (137, 141, 181, 264), latex agglutination (140, 169), and nucleic acid hybridization techniques (116, 175), have been developed for their rapid detection. The detection and identification of these agents are important since viral gastroenteritis is the second most common clinical entity in developed countries, second only to viral upper respiratory tract illness (188). Worldwide, acute gastroenteritis and its associated dehydration afflicts almost 500 million children annually. In underdeveloped or developing countries, acute gastroenteritis, including viral gastroenteritis, is the leading cause of death of children under the age of 4 years (360). Since 1980, a wealth of literature has developed covering many aspects of these viruses and the infections they cause, including their molecular biology, epidemiology, immunology, and clinical features. In addition, detection tests for routine use have been developed for rotaviruses (310) and fecal adenoviruses (333) and experimental rotavirus vaccines have been developed (184, 377, 379, 380). Of these viruses, rotaviruses are the most common known cause of viral gastroenteritis in infants and young children, with the fastidious fecal adenoviruses most likely being the second most common cause in this age group (301, 369). Calici-, astro-, and coronaviruses are probably responsible for a minority of illness in the young age group (253, 302). In contrast, the Norwalk and Norwalk-like viruses have caused considerable numbers of outbreaks of gastroenteritis among older children, adolescents, and adults (136, 137, 189). ROTAVIRUSES Epidemiology Rotaviruses were first discovered in humans 15 years ago by Bishop et al. (18, 19) by the EM examination of duodenal

No abstract

The experiments reported are concerned with cardiovascular and sudomotor events preceding, accompanying, and following ingestion of water by five dehydrating subjects 8.75 hr after entrance into a heat chamber (43.3 C DB, 29 C WB). Certain skin areas such as the cheek showed increases in evaporative heat loss before subjects came in contact with water. This reflex could be initiated by saline ingestion but the degree of skin and oral temperature changes appeared to depend on tonicity of fluid ingested. The gustatory reflex was not thought to be the initiating agent for sudomotor responses. Increases in cutaneous blood flow appeared to begin almost as promptly as sweating responses but took considerably longer to develop. Ingestion of saline, though initiating a sweating response, did not alter heart rate, blood pressure, or cutaneous blood flow. It is suggested that fluid ingestion, regardless of tonicity, triggers reflex sweating over the body surface. Intensity and duration of this sudomotor response, as well as initiation of cardiovascular changes, apparently depend on tonicity of ingested fluid. cutaneous blood flow; skin temperature; regional sweating Submitted on November 27, 1964

During slowly rising ambient temperatures, digital vasodilatation often preceded that in forearm skin; the two vasodilatations proceeded together in spring but not in summer experiments. The curvilinear relation of local skin temperature to local skin blood flow in the forearm often showed an abrupt inflection, suggesting the appearance of an additional influence on the vessels; however, a regular relation to local sweating was not apparent, vasodilatation in forearm skin often continued to increase even when local skin temperature had stabilized or fallen slightly, and the forearm vascular events were prevented by local cooling. During repeat cycles of ambient temperature, complete dissociation of the cutaneous vascular events in finger and forearm and of forearm vasodilatation and sweating often occurred. Digital vasomotor waves were not accompanied by similar waves in forearm skin. Of multiple factors possibly controlling the forearm skin circulation, the local temperature seemed most important. The maximum vasodilatation in forearm during heat exposure was not augmented by acetyl-β-methylcholine. Submitted on January 18, 1960

Resting subjects were exposed for 12 hr to 43 C dry bulb, 28 C wet bulb, with and without rehydration. During dehydration, average weighted cutaneous opacity pulse amplitudes decreased 19.5%. An apparent relationship between calculated stroke volume and cutaneous pulse amplitudes existed. A 26% increase in heart rate offset decreases in perfusion per beat and probably contributed to a rise in diastolic pressure. Increases in skin temperature paralleled those of oral temperatures. In most subjects evaporative rates were slightly lower during dehydration. Certain dehydrating subjects maintained sweat rates at control levels but this did not prevent an increase in both oral and skin temperatures. Failure of temperature regulation in these experiments does not appear to be due to a decrease in heat transport or evaporation but rather to a lack of responsiveness of the sudomotor and vasomotor systems to increases in body temperature. Reasons for the temperature rise appear complex. evaporative weight loss; heat transport; skin temperature; temperature regulation Submitted on July 22, 1964

When seminude subjects were exposed to a slowly rising ambient temperature (25—45 C), the onset of cutaneous vasodilatation occurred simultaneously in the calf, forearm, cheek, and ear, and the further progress of the vasodilatation was similar in the last three regions. That in the calf and toe often differed from that in the forearm. Either the vasodilatation in the calf was small or it stabilized early while the forearm vessels continued to dilate markedly. One subject repeatedly presented an exception in that a marked vasodilatation in the calf considerably exceeded that in the forearm. He was a poor sweater and exhibited unusually high skin temperatures. The usual failure of the skin temperature to rise as much in the calf as in the forearm appeared to be closely related to the lesser cutaneous vasodilatation. There was no evidence that local sweating elicited local vasodilatation; on the contrary, evaporative cooling seemed to decrease the vasodilatation, particularly in the calf. The cutaneous vascular events were followed continuously in each region by means of photoelectric plethysmography. Submitted on December 27, 1960