Biomedical subjects

K C Kregel

Publications and source records attributed to K C Kregel.

42 records · Page 3Linked to original sources

PubMed1990

Arterial baroreceptor reflex modulation of sympathetic-cardiovascular adjustments to heat stress.

The purpose of this study was to determine if the arterial baroreceptor reflexes modulate the sympathocirculatory responses to acute heat stress. To address this, arterial pressure, heart rate, mesenteric and renal blood flow velocity (Doppler flow probes), arterial plasma norepinephrine, and colonic temperature were measured before and during whole body heating (42 degrees C ambient temperature) in groups of conscious, unrestrained rats with (sham) or without (sinoaortic deafferentation) intact arterial baroreceptor reflexes. Heating was stopped when a colonic temperature of 41 degrees C was attained. Baseline levels of arterial pressure were similar in the two groups, whereas heart rate was elevated in deafferented versus sham-operated rats (p less than 0.01). The increases above baseline for both arterial pressure (73 +/- 4 vs. 27 +/- 2 mm Hg) and heart rate (127 +/- 10 vs. 33 +/- 5 beats/min) were threefold to fourfold greater at the end of heating in the deafferented versus the sham group (p less than 0.01). Declines in mesenteric and renal blood flow were similar in the two groups during heating; however, deafferented rats had greater increases in both mesenteric and renal vascular resistance (p less than 0.05). Plasma norepinephrine was elevated at baseline in deafferented versus sham rats and increased in both groups during heating (p less than 0.01). The magnitude of the increase in plasma norepinephrine from baseline to 41 degrees C was fivefold greater in the deafferented versus the sham rats (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Circulatory responses to heat after celiac ganglionectomy or adrenal demedullation.

Chloraloseanesthetized rats were implanted with Doppler flow probes on the mesenteric, renal, and external caudal arteries and were exposed to an ambient temperature of 40 degrees C. Heart rate, core (Tc) and tail-skin temperatures, and mean arterial blood pressure (MAP) were also monitored. Before heating, the celiac ganglion was removed (ganglionectomy) from one group of animals (n = 11) and a bilateral adrenal demedullation was performed in a second group (n = 14). As Tc progressively increased from 37 degrees C to 43 degrees C, MAP rose to a plateau then fell precipitously as Tc exceeded 41 degrees C. Ganglionectomy eliminated the rise in mesenteric resistance (P less than 0.05) and attenuated the rise in MAP compared with an intact control group (n = 11). Ganglionectomy also increased the heating rate (P less than 0.05) and reduced heat tolerance time (P less than 0.05). Demedullation attenuated the rise in both mesenteric resistance and MAP (P less than 0.05) and increased the rate of heating (P less than 0.05) compared with controls (n = 10). Renal and caudal resistance changes were similar in all groups. These data show the importance of intact adrenal medullas and sympathetic innervation to the splanchnic region in contributing to thermal tolerance in the rat. However, neither factor alone can explain splanchnic vasoconstriction during severe heat stress.

Acclimatization↗

PubMed1988

Effects of changing hypothalamic temperature on eccrine sweating in the patas monkey.

Two male (10-13 kg) patas monkeys (Erythrocebus patas) were implanted with bilateral thermodes to control hypothalamic temperature. Animals were restrained in primate chairs and instrumented to yield hypothalamic (THYPO), colonic (Tc), and mean skin (Tsk) temperatures, chest sweat rate (mSW), and heart rate (HR). THYPO was monitored using a thermocouple inserted to the tip of a non-perfused thermode; mSW was measured using resistance hygrometry. After the monkey equilibrated to a selected ambient temperature, four thermodes were perfused with water from a temperature-controlled bath. Increasing THYPO from 37 to 41 degrees C increased mSW from 0.05 to 0.30 mg.cm-2.min-1. Reducing Tsk shifted the THYPO:mSW relationship to the right (p less than 0.05) without significantly altering its slope. Activity-induced changes in HR, when THYPO was constant, caused fluctuations in ongoing sweating that closely tracked HR. We conclude that mSW in the patas monkey is controlled by both peripheral and central thermal inputs and nonthermal factors.

Animals↗

PubMed1988

Peripheral vascular responses to hyperthermia in the rat.

To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70-150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10-15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.

Animals↗

PubMed1986

Effects of ingesting carbohydrate beverages during exercise in the heat.

Ingesting carbohydrate beverages during exercise in cool temperatures can improve endurance performance. However, because hyperosmotic solutions leave the stomach more slowly than water, carbohydrate beverages could be less effective in minimizing the dehydration and hyperthermia that accompany exercise in the heat. To determine the effect of osmotically different beverages on prolonged (2 h) treadmill exercise (65% VO2max) in the heat (T db = 35 degrees C), five male runners (age 24 to 41 yr) performed three separate runs drinking 200 ml every 20 min of either 10% glucose polymer (GP), 10% glucose (G), or saccharin-sweetened water (WH). A fourth run was performed in a cool (T db = 25 degrees C) room and included drinking saccharin-sweetened water (WC). Drink osmolalities (Osm) for runs GP, G, WH, and WC were 194, 586, 94, and 71 mmol . kg-1, respectively. No significant differences were observed between runs in the heat (GP, G, and WH) for heart rate, rectal and mean skin temperatures, sweat rate, percent change in plasma volume, and gastric residue volume. When compared to the WC run, both the GP and G runs yielded greater (P less than 0.05) declines in percent change in plasma volume, but only the G run had a greater (P less than 0.05) gastric residue volume. Neither plasma osmolality, total protein, nor [Na+] varied between runs. Plasma glucose, insulin, and respiratory exchange ratios were similar between the GP and G runs. However, the GP run yielded the lowest (P less than 0.05) plasma glycerol values. Although gastric residue volume (r = 0.68) and final percent change in plasma volume (r = 0.69) were significantly correlated with drink osmolality, thermoregulation was similar between runs in the heat despite the beverage consumed.

Adult↗

PubMedDate not supplied

Effects of opiate receptor drugs injected intracerebrally into the normovolemic and hypovolemic monkey.

Systemic injection of naloxone (NAL), an opioid-receptor antagonist, significantly elevates systolic blood pressure (SBP) in anesthetized hypovolemic monkeys, providing indirect evidence that endogenous opioids contribute to cardiovascular depression during shock. The purpose of this study was to identify specific centrally located opioid receptor sites that participate in SBP regulation under normovolemic and hypovolemic conditions. In 6 monkeys, bilateral guide cannulae were stereotaxically implanted above areas ranging from the diencephalon to the lower medulla. Microinjections (1 microliter) of D- Ala2-Met-enkephalinamide (DAME) (3.4-27.2 nM) into normovolemic unanesthetized monkeys reduced SBP by 10-65 mm Hg in a dose-related fashion. Subsequent injection of NAL (12.2 nM) attenuated this hypotensive response. Heart rate fell 20-40 bpm with DAME, but not in response to dose. In the anesthetized animal rendered hypotensive (SBP = 45 mm Hg) by hemorrhage. NAL injected into predetermined DAME-sensitive sites failed to increase SBP more than 5 mm Hg. Even consecutive injections into multiple sites elevated SBP only 20 mm Hg. We conclude that the centrally located opioid-sensitive sites tested exert only a mild influence in mediating hemorrhagic hypotension.

Animals↗