Hand cold pressor test induces thermogenesis in upper thoracic regions as measured by skin surface infrared thermography

Levtova, N.; Benoit, E.-A.; Jhajj, A. K.; Narayana, T.; Purkayastha, D.; Salimi, A.; Kakon, G.; Maurice-Ventouris, M. E. I.; Kaffash Mohamadi, A. A.; Kizhner, T.; Khayargoli, P.; Darlington, P. J.

doi:10.1101/2022.03.22.485388

bioRxiv · 10.1101/2022.03.22.485388

Hand cold pressor test induces thermogenesis in upper thoracic regions as measured by skin surface infrared thermography

Levtova, N.·Benoit, E.-A.·Jhajj, A. K.·Narayana, T.·Purkayastha, D.·Salimi, A.·Kakon, G.·Maurice-Ventouris, M. E. I.·Kaffash Mohamadi, A. A.·Kizhner, T.·Khayargoli, P.·Darlington, P. J.

View original source ↗Export metadata ↓

Abstract

BackgroundCold exposure may cause health problems and impaired productivity in outdoor or cold-temperature workers. The cold pressor test (CPT) is a laboratory procedure that measures cardiovascular and thermoregulatory responses to acute cold exposure such as metabolic activity in brown adipose tissue. How the body responds to acute cold exposure of a hand is not completely understood. We tested the hypothesis that the upper thorax produces heat during a single hand-CPT, which restores warmth to the cold-expose appendage. ObjectivesThe objective was to measure skin temperature changes in the upper thoracic regions and the cold-exposed appendage during a CPT. The secondary objective was to determine if cardiovascular or psychological responses during CPT accounted for skin temperature changes. Methods50 healthy participants immersed their right hand up to wrist level in 4 {degrees}C water for three minutes. Surface skin temperatures were imaged by infrared thermography at baseline, during CPT, and in the recovery phase. Sublingual oral temperature and water bath temperature were recorded throughout the test. Cardiovascular responses were monitored by continuous finger pulse-wave plethysmography. Peak pain and peak stress were reported by the participants on a Likert scale. ResultsCPT increased the systolic blood pressure (+22 mmHg, p < 0.001), diastolic blood pressure (+15 mmHg, p < 0.001) and heart rate (+7 beats per minute, p = 0.024). During CPT, skin temperature increased on thoracic regions including mediastinal (+0.5{degrees}C, p < 0.021), sternal (+0.5{degrees}C, p < 0.002), right supraclavicular (+0.3{degrees}C, p < 0.042) and left supraclavicular (+0.3{degrees}C, p < 0.016) regions. During CPT, the hand was cooler on ventral (-14.6{degrees}C p < 0.001) and dorsal (-15.2{degrees}C p < 0.001) sides, and warmed up during recovery. The ventral forearm, dorsal forearm, antecubital fossa, and adjacent medial epicondyle region were significantly cooler throughout the recovery time. The oral temperature did not change during CPT. There were no correlations between the change in mediastinal skin temperature and the sex of the participant, or changes in cardiovascular parameters, peak pain, or peak stress values. ConclusionsLocalized hand cooling caused a rapid warming of the thorax, dissipation of cold in the forearm, and rewarming of the hand during recovery. Thermoregulation was not dependant on pain, stress, sex, or cardiovascular changes between participants. By understanding thermoregulation, better approaches can be developed to mitigate the negative impacts of cold exposure.

Explore related subjects

physiology Preprint

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

Levtova, N., Benoit, E.-A., Jhajj, A. K., Narayana, T., Purkayastha, D., Salimi, A., Kakon, G., Maurice-Ventouris, M. E. I., Kaffash Mohamadi, A. A., Kizhner, T., Khayargoli, P., Darlington, P. J.. 2022-03-22. Hand cold pressor test induces thermogenesis in upper thoracic regions as measured by skin surface infrared thermography. https://doi.org/10.1101/2022.03.22.485388

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

IBD-Derived Colonic Fibroblasts Exhibit an Osteopontin-Enriched Secretome, and Osteopontin Restrains Human Colonic Organoid Maturation

Background: Intestinal fibroblasts are extensively remodeled in inflammatory bowel disease (IBD), yet the soluble stromal signals that directly influence epithelial maturation remain incompletely understood. We examined whether fibroblasts derived from inflamed IBD colon display an osteopontin (OPN; SPP1)-enriched secretory phenotype and whether extracellular OPN directly modifies non-neoplastic human colonic epithelium. Methods: Conditioned media from 5 noninflamed-associated fibroblast (NAF) and 4 inflammatory-associated fibroblast (IAF) cultures were analyzed in the validated multi-donor cytokine-array matrix, with orthogonal SPP1 RT-qPCR validation in a complementary fibroblast cohort. Recombinant OPN was then tested in human colonic organoids from 3 donors using donor-resolved molecular and functional analyses under standard, fibroblast-conditioned, and WNT-modified culture conditions. Donor identity defined biological replication. Results: OPN showed the strongest positive rank-based separation between IAF and NAF cultures: all 4 IAF values were higher than all 5 NAF values (Cliff's delta=1.00; exact Mann-Whitney P=0.0159; median ratio=3.64; Benjamini-Hochberg q=.19). Fibroblast RT-qPCR showed approximately 10-fold higher mean SPP1 expression in IAF than NAF cultures (P<.05). In organoids, OPN consistently reduced KRT20, FABP1, CA2, and MUC2 from Day 5 to Day 9. SOX9, HES1, and NOTCH1 increased at Day 9, whereas LGR5 and ALDH provided no evidence of canonical stem-cell expansion. Organoid-area and EdU responses were modest and donor dependent. Conclusions: IBD-derived colonic fibroblasts can display an OPN-enriched secretory phenotype. In human colonic organoids, OPN is sufficient to impair epithelial maturation, whereas its effects on growth and proliferation are variable and depend on the surrounding niche.

physiology↗

bioRxiv2026

A multiscale analysis of liver lobule fibrosis and its impact on drug propagation and metabolism - a DLA approach

Employing DLA methods, this paper explores the self-assembly of collagen fibers and resulting fibrosis at three scales up to the scale of regular lobule models. This allows a mechanistic exploration of the effects of collagen on drug transport (flow and diffusion) and metabolism. In addition, this method permits an analysis of fiber growth characteristics. First, variations of the DLA method of Parkinson et al (1994) will be used to generate multiple explicit collagen microfibril self-assembly using DLA particles in one dimension using cubic grid blocks of (4 mm)3 in a 240 x 20 x 20 grid model. The second stage will be to assess the consequences of various densities of these fibers in three dimensions on flow reductions at a higher scale. Here we utilize DLA methods in cubic grid blocks of (80 nm)3 to mimic 3D collagen self-assembly of fibrils. We then apply a pressure gradient or specified flow rates across a spatially gridded version of these models to quantify flow effects. This region represents a local zone of liver tissue affected by fibrosis. Analytic models of fibrotic effects on flow are employed for comparison. A third stage explores the implications of fibrosis in a liver lobule model using multiple grid blocks of size 3200 mm to represent the lobule tissue. Here, a continuum model of fiber density is employed, based on the previous two scales. The model also includes the effects of additional grid blocks representing sinusoidal flow paths found in the lobule. We contrast and quantify drug propagation and metabolism of molecular dissolved versus nanoparticle delivery vehicles in fibrotic media, achieved by upscaling explicit collagen distributions to appropriate average values.

physiology↗

bioRxiv2026

Pulmonary pressure load shapes right ventricular molecular remodelling in dilated cardiomyopathy

Right ventricular (RV) adaptation to pulmonary hypertension determines outcome in dilated cardiomyopathy (DCM), but the molecular mechanisms of the transition to decompensation remain unclear. We analysed RV tissue from explanted hearts of patients with end-stage DCM using single-nucleus RNA sequencing (n=21), mass spectrometry and Olink Reveal proteomics (both n=44), and integrated these molecular profiles with echocardiographic and right-heart catheterisation measures to identify molecular correlates of RV dysfunction. Mean pulmonary arterial pressure was the dominant correlate of RV transcriptional remodelling, particularly in cardiomyocytes, where higher pressure was associated with contractile remodelling, autophagy, vesicle trafficking and glucose metabolism. In contrast, RV decompensation was characterised by immune activation and reduced oxidative phosphorylation exclusively at the proteomic level. Integrative multi-omics factor analysis (MOFA) further identified fibrosis as the dominant molecular program shared across transcriptomic and proteomic layers. Together, these findings indicate molecular adaptation to pressure load and tissue fibrosis during progression towards RV failure.

physiology↗