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Biomedical subjects

G G Rogers

Publications and source records attributed to G G Rogers.

At least 37 records · Page 2Linked to original sources
PubMed1985

Creatine kinase release not associated with myocardial necrosis after short periods of coronary artery occlusion in conscious baboons.

The effects of 15 minute periods of coronary artery occlusion on plasma creatine kinase (CK) and CK-MB isoenzyme activity, regional myocardial function and subsequent myocardial necrosis were studied in six conscious baboons 2 to 3 weeks after recovery from instrumentation. Mid left anterior descending coronary artery occlusion induced complete loss of systolic wall thickening (ultrasound transit time technique) and decreases in epicardial (-93%) and endocardial (-96%) blood flows (microsphere technique). Reperfusion after 15 minutes resulted in complete recovery of regional function 24 hours later. Serial plasma enzyme activity revealed a significant increase in total CK from 71 +/- 11 to 976 +/- 158 U/liter and in CK-MB from levels that were too low to measure to 21.4 +/- 2.9 U/liter. At autopsy, neither gross pathologic evidence (triphenyltetrazolium chloride staining technique) nor histologic evidence of myocardial necrosis was observed. Thus, in the conscious baboon short episodes of myocardial ischemia are associated with a significant appearance of CK and CK-MB in the blood in the absence of cellular necrosis.

Animals↗
PubMed1985

Effects of coronary artery reperfusion on regional myocardial blood flow and function in conscious baboons.

The effects of coronary artery reperfusion initiated 1 hr and 3 hr after coronary artery occlusion were evaluated on measurements of overall and regional left ventricular function and on regional myocardial blood flow. These experiments were conducted in conscious baboons 2 to 3 weeks after recovery from instrumentation with a solid state left ventricular pressure gauge, aortic and left atrial catheters, a hydraulic occluder around the mid left anterior descending coronary artery, and pairs of ultrasonic transducers implanted in the endocardium of the left ventricular free wall or across the free wall to measure endocardial segment shortening and wall thickening, respectively. Coronary artery occlusion induced similar effects in both groups. At 1 hr after occlusion, the ischemic zone was characterized by severe and equal reductions in both endocardial (-97 +/- 1%) and epicardial (-95 +/- 4%) blood flows and complete loss of regional systolic function, which was replaced by paradoxical wall motion. Reperfusion initiated after 1 hr of ischemia was associated with a marked transient increase in endocardial (+386 +/- 51%) and epicardial (+544 +/- 79%) blood flows. During the subsequent 4 weeks, segment shortening and wall thickening tended to improve. However, at 4 weeks after reperfusion, segment shortening was still depressed by 45 +/- 12% and wall thickening by 58 +/- 14%. In contrast, reperfusion initiated after 3 hr of ischemia was not associated with a significant hyperemic response, and systolic segment shortening and wall thickening did not recover during the subsequent 4 week period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Effects of tiapamil on haemodynamics and myocardial salvage during myocardial infarction in the baboon.

We studied the effects of tiapamil during myocardial infarction in the anaesthetized baboon. 10 animals received placebo and 8 animals the drug. After basal measurements the left anterior descending coronary artery was ligated. Measurements were repeated at 15 min and 2-hourly until the 12th h after occlusion. Placebo or drug (1 mg X kg-1 and 50 micrograms X kg-1 X min-1) was administered 20 min after occlusion. Tiapamil decreased afterload by reducing peripheral resistance. Blood flow to the peripheral ischaemic zone was increased. These effects resulted in myocardial salvage manifest as a reduction in serum creatine kinase (MB) isoenzyme levels and less myocardial damage at 12 h than that predicted for the placebo group by S-T segment mapping 15 min after occlusion.

Animals↗
PubMed1978

Heat acclimatization by a method utilizing microclimate cooling.

A new approach to heat acclimatization has been shown to be feasible during laboratory experimentation. Wearing microclimate suits containing dry ice as the coolant, three groups of men were subjected to a moderate work rate in three different environments for 4 h/d for 8 d. Physiological responses on a subsequent heat tolerance test indicate that the group subjected to an environment of 32.0 degrees C W. B. and 33.5 degrees C D.B. were fully heat acclimatized. The 33/35 degrees C group were also well-acclimatized but developed dangerously high body temperatures during the first 2 d. Only partial acclimatization was achieved by the 31/33 degrees C group. The reason why the men acquire heat acclimatization while wearing the microclimate suits in a hot environment is probably that microclimate cooling does not prevent body temperature from rising--it only prevents it from rising excessively. It should be remembered that only one-third of the body is cooled while the rest shows the normal sweating response.

Acclimatization↗
PubMed1977

Effects of plasma ascorbic acid levels on heat acclimatization in man.

Thirteen male volunteers were heat acclimatized for 4 h/day for 10 consecutive days. Three to four hours before each heat exposure, four of the subjects received an oral dose of 250 ascorbic acid, five received 500 mg ascorbic acid, and the remaining four a placebo. Rectal temperature, heart rate, and sweat rate were measured hourly during exposure. Venous blood samples were collected before each administration of drug or placebo. On days 1, 2, 3, 5, 8, and 10, blood samples were also collected just prior to heat exposure and after two and four hours of exposure. In the subjects receiving ascorbic acid, total circulating plasma ascorbic acid increased over the first three or four days to a plateau level some fourfold higher than in the subjects receiving the placebo. The plateau level was the same in the subjects receiving 250 mg and 500 mg ascorbic acid. The increased ascorbic acid concentration was shown to be associated with a reduction in total sweat output, independent of rectal temperature, and a reduction in rectal temperature, independent of total sweat output. The results indicate that ascorbic acid may be effective in reducing heat strain in unacclimatized individuals.

Acclimatization↗
PubMed1976

Acclimatization in a hot, humid environment: energy exchange, body temperature, and sweating.

Four trained young men, worked for 4 h/day at 43-50% of their maximum aerobic capacity for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Their thermal status was assessed using direct calorimetry. As a group, the men showed classical acclimization responses, but there were marked individual differences. The calorimetric analysis revealed that reductions in strain were associated with minor changes in heat balance confined to the first and last hours of exposure. Events occurring within the first 4 days appeared to have little effect on body temperatures. Significant decreases in body temperature took place only when sweat and evaporation rate increased. A 10% increase in evaporation rate was accompanied by a 30% increase in sweat rate and a 200% increase in unevaporated sweat; thus, there is a wasteful overproduction of sweat. By the 10th day skin temperature was confined to the level necessary to evaporate sufficient sweat to achieve thermal balance with a fully wet body surface. The efficiency of heat transport within the body did not change with acclimatization.

Acclimatization↗
PubMed1976

Acclimization in a hot, humid environment: cardiovascular adjustments.

Four trained young men worked for 4 h/day at 40-50% of their maximum aerobic capacity first for 3 days at 25 degrees C db, 18 degrees C wb, and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. This portion of the study was mainly concerned with central circulatory changes during acclimatization. The central circulatory adaptation to work in heat could be divided into four distinct phases: phase I (day 1) was characterized by a progressive fall in stroke volume (SV) during heat exposure but cardiac output (CO) was maintained above control values by high heart rates. Phase II (days 2 and 3) was marked by increases in SV ande decreases in heart rate but with little change in CO from phase I. During phase III (days 4-8 of acclimatization), CO increased due to increases in SV. Phase IV (days 6-8) was associated with decreases in rectal and skin temperature towards control levels. SV and HR both decline in this phase so that CO was not elevated greatly above control levels. The results indicated that central circulatory and temperature regulating events are not casually associated in acclimatization.

Acclimatization↗
PubMed1976

Effect of ascorbic acid on rate of heat acclimatization.

There is some indication in the literature that ascorbic acid (vitamin C) may reduce the physiological responses to heat stress. Consequently, the effect of ascorbic acid ingestion on heat-strain indicators has been studied on a group of 60 mining recruits undergoing climatic room acclimatization. Of the 60 men, 19 received a daily dose of 250 mg ascorbic acid; 21 a daily dose of 500 mg ascorbic acid; and 20 received a placebo daily. Measurements of rectal temperature, heart rate, and hourly sweat rate were made on all subjects during the 4 h of heat exposure per day for 10 days. The wet bulb temperature was 32.2 degrees C, the dry bulb 33.9 degrees C, the air movement 0.4 m/s, and the work rate 35 W. The results indicate that the rate and degree of acclimatization, as assessed by 4th-h rectal temperature, is enhanced by ascorbic acid supplementation and that no differences in response could be shown between daily dosages of 250 and 500 mg of vitamin C.

Acclimatization↗