Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “COLD”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources

Cold light sources. Are they really cold?

Two light sources used in laparoscopy, both in the photo mode, proved capable of burning a hole in a standard paper surgical drape in less than five seconds. The relationship between power (in watts) and dial settings is not linear. Both of these sources have a maximum power density of 5.6 w/cm2, which far exceeds the 1.8 w/cm2 power density of the other light sources tested. Today, with the demand for increased illumination for photodocumentation , the physician must be cognizant of its potential hazards. Light sources will vary according to the type of source--tungsten, halogen or mercury arc. Each increase in wattage output will transmit a greater cable power density. Equipment should be checked for its potential to produce burns in routine use and, if defective, should be replaced.

Equipment Safety↗

Myocardial protection in diffuse coronary artery disease. Intermittent retrograde cold-blood cardioplegia at systemic normothermia versus intermittent antegrade cold-blood cardioplegia at moderate systemic hypothermia.

In order to determine the comparative merits of antegrade cardioplegia at moderate systemic hypothermia versus retrograde cardioplegia at systemic normothermia, we performed coronary artery bypass grafting using intermittent oxygenated blood cardioplegia in 2 sets of 50 consecutive patients with triple-vessel disease (complete occlusion of 1 coronary artery and greater than 90% narrowing of the other 2, with poor distal runoff). Group 1 had antegrade cardioplegia at moderate systemic hypothermia (28 degrees C). Group 2 had retrograde cardioplegia at systemic normothermia. This resulted in no deaths and in no differences in complication rates. Group 2's postoperative need for inotropic agents or vasodilators was significantly less (epinephrine, p < 0.0009; dopamine, p < 0.002; nitroglycerin, p < 0.001). Elevations of CKMB fraction were significantly more common in Group 1: 46% had CKMB levels greater than 9%, versus 16% of Group 2 patients (p < 0.0001). Intraoperative transesophageal echocardiography was performed in 39 Group-1 patients and in 42 Group-2 patients. Development of a new wall-motion abnormality after bypass was significantly only in Group 1 (p < 0.009, by chi 2 analysis). We conclude that retrograde cardioplegia at normothermia provides myocardial protection that equals or surpasses that of antegrade delivery at moderate systemic hypothermia, while avoiding the possible deleterious side effects of hypothermia.

Adult↗

Combined respiratory effects of cold air with SO(2) or NO(2) in single 1-hour exposures of hyperventilating guinea pigs.

The present study is a continuation of our previous experiments on repeated 10-min exposures of anesthetized, mechanically ventilated guinea pigs to clean cold dry air (Hälinen et al., 2000a), and to cold air plus gaseous air pollutants (Hälinen et al., 2000b). This time we made continuous 60-min exposures to clean cold dry air, cold air + SO(2) at 1 ppm, cold air + NO(2) at 1 ppm, and warm humid air + NO(2) at 1 ppm, and focused on responses at 10-60 min. Clean cold dry air and cold air + pollutants (n = 8-9 in each group) produced similar cooling in the guinea pig lower respiratory tract. The decreases in intratracheal temperature (T(tr)) reached a plateau at 20 min with mean maximal decreases of 9.7-11.3 degrees C from the pre-exposure control values of 36.0-37.3 degrees C. In contrast, there were progressive decreases in esophageal temperature (T(oe)) during the exposures, indicating constant conductive and evaporative heat losses from the tracheobronchial tissues. The mean maximal decreases in T(oe) were 1.2-1.4 degrees C from the preexposure control values of 37.8-38.0 degrees C. Clean cold dry air induced 4. 5-10.8% mean decreases in peak expiratory flow (PEF) at 10-60 min of exposure, which were statistically nonsignificant due to a relatively large variation between animals. Cold air + SO(2) at 1 ppm induced a mean decrease of 11.4% in PEF at 10 min (p <.05), which was spontaneously abolished during the next 10 min of exposure. Cold air + NO(2) at 1 ppm caused no decrease, but in fact small, nonsignificant increases in PEF at 30-60 min of exposure. Cold air + NO(2) at 1 ppm, and to some extent also cold air + SO(2) at 1 ppm, attenuated significantly the mechanical ventilation induced gradual decrease in tidal volume (V(T)), when compared to clean cold dry air exposure. Cold air + NO(2) at 1 ppm, but not warm humid air + NO(2) at 1 ppm, increased significantly the proportion of macrophages in the differential count of bronchoalveolar lavage fluid (BALF) white cells when compared to both clean warm humid air and cold dry air. None of the exposure conditions caused morphological or inflammatory changes in the respiratory tissues. In conclusion, continuous 60-min exposures to clean cold dry air, cold air + SO(2), and cold air + NO(2) produced weaker functional effects on the lower respiratory tract of guinea pigs than our previous consecutive 10-min exposures to these air conditions. After the first 10 min, there was a strong attenuation of the bronchoconstrictor responses, especially to cold air + NO(2) at 1 ppm. The small airway effects of prolonged mechanical ventilation were significantly modified by NO(2) at 1 ppm in both cold dry and warm humid breathing air. Finally, cold air + NO(2) at 1 ppm increased the proportion of macrophages in BALF white cells.

Air Pollutants↗